The Choosing Wisely project is an effort by the American Board of Internal Medicine Foundation to encourage physicians and patients to choose diagnostic and therapeutic interventions in a rational, evidence-based way. Specialists make recommendations about tests and treatments in their area of expertise. The most recent recommendation list comes from the American College of Medical Toxicology and the American Academy of Clinical Toxicology. It contains a number of recommendations relevant to potential toxins, and the first highlists the dangers of unregulated herbal remedies and homeopathy.
Holy cow, that is profound! Might such information from such a distinguished group of individuals serve as a legitimate means for combatting the loons — especially those in congress — who continue to adulterate our world with their illegitimate crap, ignorance and mysticism in regards to alternative health options?
And, what will the response be of the mindless minions who populate the veterinary homeopathy club? Denial, of course; because, how can wishful thinking, observational bias and water be toxic?
Animals are promoted by the veterinary profession to have “special ” toxins.
See
http://www.nytimes.com/2013/11/05/science/poisonous-to-pets.html?ref=health&_r=0
I question a lot of these “special” dog toxins when the ld 50 for the has not been shown to be significantly different from the human ld50. But it does bring up another reason not to use a herbal supplement in a dog or cat when DNA testing of herbal supplements are often shown to be not what they seem to be on the label.
See
http://www.nytimes.com/2013/11/05/science/herbal-supplements-are-often-not-what-they-seem.html?ref=health
Right now the FDA has issued a dog jerky treat warning. Dogs are dying apparently from jerky treats whose ingredients come from china. The FDA so far has not found a common reason that links these deaths. Some vets speculate it may be that jerky is safe for humans but not dogs. Dog have been eating grapes since the Romans started making wine but the profession now promotes a special grape toxicity in dogs but not humans or cats.
Art Malernee
Fla Lic 1820
Well, the idea that certain substances may be toxic for some species and not others does rest on at least some plausible foundation. Xylitol is ubiquitous in human foods and yet is unquestionable severly toxic in at least some dogs. And cats have demonstrably different abilities to detoxify substances compared with herbivorous or omnivorous species likely due to an evolutuonary history that had little selection pressure for detoxification in an obligate carnivore. The toxicity of specific substances needs to be established individually, of course, but it is reasonable to avoid most potential toxins even if the evidence is not strong, especially given that there is no benefit or need for most of the commonly identified substances (xylitol, grapes, anti-freeze, rat poison, snail bait, chocolate, etc).
I attended a toxicology lecture at UC Davis a couple summers ago in which grapes were discussed, and it was fascinating. Due to their geographic location adjacent to wine country, they have treated many dogs who had severe toxicity reactions after eating grapes; however, they are also aware of dogs who live on vineyards and have eaten large quantities of grapes for years and not had any reaction at all. Mysterious. But why risk it, as skeptvet has pointed out, no reason it’s necessary for dogs to eat things like grapes.
I believe that it’s one thing if people want to take risks themselves with random herbs and magic, but it’s criminally irresponsible to essentially experiment on animals and children…
Here is an article this week about pet jerky
http://well.blogs.nytimes.com/2013/11/04/concerns-about-jerky-pet-treats/?ref=health&_r=0
Here is a response to the xylitol controversy the links no longer work. Xylitol is still used in dog medications the last time I checked. I will see if I can fix the document link.
Xlear, Inc. Issues Response to JAVMA Report on Dogs and Xylitol
Market Wire, October, 2006
12Next
Xlear, Inc., a leading manufacturer of xylitol products, issued the following statement in response to the clinical report on xylitol and dogs published in the October 1, 2006 issue of the Journal of the American Veterinary Medical Association (JAVMA).
Reports and articles about xylitol and dogs have propagated across the Internet during the past several months. While Xlear does not manufacture xylitol products for pets, nor recommend giving xylitol to dogs, we feel that there have been some misconceptions reported in recent papers and statements about xylitol that need to be addressed.
First, xylitol has been used in a number of animal studies and the results of which have been included in the World Health Organization’s review of the safety and toxicology of xylitol. In several of the studies, up to 20 percent of the total caloric intake for dogs was comprised of xylitol. These studies were conducted during a full-year time period, and after the study, the animals were sacrificed and histology studies conducted on their organs. No abnormalities were noted. Other studies have also shown xylitol to be safe. Please see the following:
— http://www.inchem.org/documents/jecfa/j … 12je22.htm
— http://www.inchem.org/documents/jecfa/j … 13je11.htm
While I can see why the manufacturer of xylitol might want to minimize concerns about the product, there is direct experimental evidence supporting the clinical reports of toxicity, so I find this perspective less than credible. Dose is important, as with any toxicosis, and there are reports of low-doses not causing biochemical changes or clinical signs. And it may be that not all dogs are equally susceptible. But it would be inaccurate to state that there is not good evidence to support the claim that xylitol is toxic in dogs.
Experimental acute toxicity of xylitol in dogs.
J Vet Pharmacol Ther. October 2009;32(5):465-9.
Z Xia1; Y He; J Yu
Article Abstract
The Cases of xylitol poisoning in dogs are increasing as a result of ingestion of xylitol-containing products. Eighteen adult, clinically normal Pekingese dogs were orally dosed with 1 or 4 g/kg xylitol in aqueous solution. Blood samples were collected before and after dosing. Plasma insulin concentrations of both treated groups rose sharply from 20 min after xylitol dosing, peaking at 40 min. Hypoglycemia followed the increase in insulin concentration, with blood glucose values started to decrease 30 min after dosing. Other plasma biochemistry changes associated with xylitol administration were increased alanine aminotransferase and aspartate aminotransferase activities, hypophosphatemia, hypokalemia, and hypercalcemia. Plasma sodium and chloride concentrations remained normal. This study established a biochemical basis for diagnosis and treatment of xylitol poisoning in dogs.
Xia ZhaoFei; Cai LiYuan; He YuYing; Wan JianQing; Yu JinHai
Toxicological and Environmental Chemistry2013 95 2 337-343
Xylitol poisoning of dogs is associated with increased glycogenolysis, coagulopathy, and oxidative stress.
Abstract
Clinical cases of xylitol poisoning in dogs have been frequently reported in recent years. Following our previous study of acute xylitol toxicity in dogs, we further investigated alterations of blood coagulation, glycogenolysis, and antioxidant status in xylitol poisoning. Twelve adult, clinically healthy, crossbreed dogs were orally dosed with 4 g kg-1 xylitol in aqueous solution. Plasma glucagon and lactate levels increased, while pyruvate concentrations decreased after xylitol dosing. Xylitol-dosed dogs developed coagulopathy, characterized by prolonged prothrombin time, activated partial thromboplastin time and thrombin time, and decreased fibrinogen levels, probably secondary to impaired liver function, which was observed in our previous study. The plasma concentrations of vitamin E, vitamin C, superoxide dismutase, and the reduced form of glutathione peroxidase were decreased, while malondialdehyde levels were increased, suggesting oxidative stress.
Not to mention reports from animal poison control center databases.
As for grapes, Art, are you denying that grape toxicity does not exist in dogs?
I have seen xylitol as an ingredient in an over-the-counter oral health rinse for dogs & cats, but I assumed it’s because anyone can sell almost anything OTC for pets nowadays. Art, you’re saying it’s used in actual legitimate medications?
BTW, is there any research on tea tree oil’s safety for dogs or cats?
Here is one of the world health broken Links
http://www.inchem.org/documents/jecfa/jecmono/v12je22.htm
INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY WORLD HEALTH ORGANIZATION SUMMARY OF TOXICOLOGICAL DATA OF CERTAIN FOOD ADDITIVES WHO FOOD ADDITIVES SERIES NO. 12
Dog In short-term study five dogs were dosed 10 g xylitol/kg/day by intravenous infusion during seven weeks. Blood chemistry and urinalyses were investigated weekly. Plasma glucose content was reduced to 64 mg % after six weeks. A slight increase in plasma lactate and a significant increase of SGPT and Alk. Pase was observed. Also an increased urinary loss was observed. No effect of xylitol on plasma insulin levels and no oxalate crystals in the kidneys were observed (Meng, 1974). A six weeks toxicity experiment with one female and one male dog (5.5-6 kg) per group was carried out. The concentration was during the experiment increased from 5% after two weeks to 20%. Food consumption was recorded twice daily and body weights twice a week. At the end of the experiment gross pathology was carried out, and brain, heart, liver, lungs, pituitary, spleen, pancreas, thymus, prostate/uterus, kidneys, thyroids, adrenals and testes/ovaries were weighed. No histopathological investigation was carried out. Except for a tendency to increased liver weights in the xylitol groups no effects are observed. This study is not an adequate toxicity study, but has to be seen as preliminary experiment (Hummler, 1974). In a long-term toxicity study eight female and eight male beagle dogs per group, weighing 6-9 kg, were fed 0, 2, 5, 10 and 20% dietary xylitol during two years. The total amounts of carbohydrates were kept constant. In addition animals receiving 20% sorbitol and 20% sucrose were used as sugar controls. Body weight and food consumption was recorded weekly, while water consumption was recorded over five day periods at the weeks one to four, 9-12, 21-24, 35-38 and 46-49. Ophthalmoscopy, dental examination and a full neurological examination of four male and four female dogs were carried out at 13, 26, 39, 50, 64 and 76 weeks. Haematology, biochemistry and urinalyses were carried out at the beginning of the experiment and at 12, 26, 38, 50, 64 and 76 weeks. The haematology included erythrocyte sedimentation rate, PCV, Hb, RBC, reticulocyte count, MCHC, MCV, WBC, differential count, platelet count, prothrombin index, whole blood clotting time. The biochemistry included determination of total protein, Al, GPT, GOT, total LDH, alpha-HBDH, bilirubin, uric acid, cholesterol, lactate and insulin in serum and urea xylitol, glucose concentration and total reducing substances in plasma. Sodium, potassium, chloride and bicarbonate were also detected in the blood. Urinalyses consisted of estimations of Ph, protein, reducing substances, glucose, ketones, bile pigments, urobiligen and Hb. On completion of 52 weeks, two male and two female dogs per group were sacrificed for interim study, while the remaining dogs will be killed after two years’ dosing. The weights of brain, liver, kidneys, pituitary, thyroid, spleen, heart, lungs, adrenals, ovaries, testes, uterus, thymus, prostate, pancreas were recorded. Histopathology of these organs and of aorta, trachea, lymph nodes, gall bladder, urinary bladder, salivary glands, oesophagus, duodenum, stomach, jenunum, ileum, skin, skeletal muscle, mammary glands, tongue, eye with optic nerve and sciatic nerve was performed. The food intake and weight gain of the 20% xylitol group were increased. A dose-related increase of SAP and SGPT and a decreased lactate level was noticed, while in the 20% xylitol dose group also the total serum protein was significantly increased. At 52 weeks a tendency to increased cholesterol content in serum was observed. Except a dose related decrease in the pituitary of the xylitol dose groups no effects on organ weights, in gross necropsy and histopathology were observed.
There have been some case reports of toxicity in dogs and cats, as well as some limited research suggesting topical use may have beneficial effects, but a clear safe and effective dose hasn’t been established since there is very little research available.
Bischoff, K.; Guale, F.. Journal of Veterinary Diagnostic Investigation1998 10 2 208-210
Australian tea tree (Melaleuca alternifolia) oil poisoning in three purebred cats.
Abstract
Three Angora cats with severe flea infestations were shaved and treated with pure M. alternifolia oil (about 120 ml between all 3 cats). Within 5 h of treatment 2 cats were hypothermic and dehydrated, all developed nervous signs and one was comatose. The cats were bathed in mild detergent, given activated charcoal and dexamethasone orally and the dehydrated cats were given fluid therapy. The comatose cat improved over days 2 and 3 but remained ataxic and obtunded. On day 3 it began regulating its body temperature but died of an undiagnosed caused later that evening. The other 2 cats recovered at 24 and 48 h after treatment.
Reichling, J.; Fitzi, J.; Hellmann, K.; Wegener, T.; Bucher, S.; Saller, R.Deutsche Tierärztliche Wochenschrift2004 111 10 408-414Topical tea tree oil effective in canine localised pruritic dermatitis – a multi-centre randomised double-blind controlled clinical trial in the veterinary practice.
Abstract
Tea tree oil, a volatile oil, is well known for its broad antibacterial and antifungal activity. A standardised and stabilised 10% tea tree oil cream was tested against a commercial skin care cream (control cream) in the management of canine localised acute and chronic dermatitis. Fifty-seven dogs with clinical manifestations of mostly pruritic skin lesions or alterations, skin fold pyodermas and other forms of dermatitis, corroborated by predominantly positive fungal and bacterial skin isolates, were enrolled by seven practising veterinarians and randomly allocated to two study groups (28:29) and were treated twice daily with a blinded topical preparation. After 10 days of treatment, success rates of 71% for the tea tree oil cream and 41% for the control cream (over-all efficacy documented by the veterinary investigator) differed significantly (p=0.04), favouring tea tree oil cream treatment. Accordingly on day 10, the tea tree oil cream caused significantly faster relief than the control cream (p=0.04) for two common clinical dermatitis signs, pruritus (occurring in 84% of dogs) and alopecia. Only one adverse event was reported in the tea tree oil group (suspected not to be causally related to the study drug) and none in the control cream group. The tested herbal cream appears to be a fast-acting safe alternative to conventional therapy for symptomatic treatment of canine localised dermatitis with pruritus
Art, that’s a nearly 40-year-old study – today we have different manufacturing processes, different sources and different batches and xylitol is in numerous products. I would guess if it is in some medications, that the dose is low enough not to cause clinical effects. As skeptvet said, of course, an xylitol manufacturer is going to cite a source in their favor. Like Hershey’s denies cocoa mulch is dangerous to dogs. And so on.
The same applies to thousands of “natural” product manufacturers who claim their tea-tree-oil products are simply natural and wouldn’t hurt a fly, despite reports available to suggest otherwise. The common problem with the “natural” products is either inert ingredients or proprietary use, which means we have no idea the source, the concentration, etc.
Thanks for the tea tree oil research info; that’s pretty severe in the Persians. I have only heard anecdotes about skin reactions. Good to know!
Sorry, Angoras.
Like Hershey’s denies cocoa mulch is dangerous to dogs. And so on.>>>
do you have any credible data that the ld50 is any different for Cocoa ingestion in a dog vs human? My read is the ld50s are about the same.
Art, don’t you ever see xylitol or chocolate toxicosis in your practice? If you have a dog or cat come in with clinical signs and a history of eating one of these substances do you discount the relevance of the substance ingestion and search for a different explanation for the symptoms?
“In dogs, the LD50 for theobromine is approximately 250-500 mg/kg, however deaths have occurred following ingestion of 115 mg/kg. The half-life of theobromine is very long in dogs (17.5 hours) compared to other species. This may help to account for the susceptibility of canines to theobromine toxicity.”
https://www.addl.purdue.edu/newsletters/2000/spring/choc.shtml
Other sources have the LD50 in dogs as even lower. In humans, LD50 is about 1,000 mg/kg.
Here’s a table for example: http://chem.sis.nlm.nih.gov/chemidplus/jsp/common/Toxicity.jsp?calledFrom=lite
Skeptvet, what is the cut-off for links to be considered spam? This is only the second time any of my posts “awaiting moderation” has occurred by including links, just wondering what the cut-off is?
I really don’t know. Most posts with links are held for manual approval. I try to get to them a couple times a day, but it may sometimes be a day before I can approve a post. I also get hundreds of spam messages sent automatically to my spam folder every day, so I can’t go through those looking for legitimate comments.
If a post with links is rejected outright, or if it is held for moderation and doesn’t get approved within 24 hours, feel free to send a message to me about it.
Thanks, skeptvet, will keep that in mind, it’s not a big deal. I can imagine the spam you get on a daily basis, what a job!
there is concerns regarding the safety of administering oral dental care products containing xylitol
(BreathaLyser
College of Veterinary Medicine, Saskatoon, Saskatchewan.
Materials and Methods:
A randomized, double blind, placebo controlled study was performed where fifteen crossbred dogs of mixed ages (mean years:
3.1, range 2-7 years), weight (mean kg: 24.8, range 16-40) and sex (females: 8, males: 7) were randomly divided into three
groups and their drinking water was treated for 14 days with either: a) commercial care product (BreathaLyser Plus, imRex Inc.,
London, ON, Canada), b) BreathaLyser Plus containing five times the amount of xylitol recommended by the manufacturer, or
c) placebo (purified water coloured to match solutions (a) and (b)). At the start of the study, there were no differences between
the three groups for breed, sex, age, or weight. Throughout the trial, all dogs were maintained in the same environment and fed
the same commercial dog food (Iams Adult, Iams Company, Dayton, Ohio, USA). No food supplementations such as treats or
chew toys were given during the study.
All dogs in this study were examined for general health and acclimatized to the facilities for eight days before entering the study.
On day 0, samples for complete blood count, and clinical chemistry (Na, K, Na:K ratio, Cl, HCO3, Anion Gap, Ca, P, Mg, Urea,
Creatinine, Glucose, Total Bilirubin, Cholesterol, AP, ALT, GGT, GLDH, CK, Total Protein Albumin, Globulin, A:G Ration,
SDH) were collected at approximately seven hours after feeding. All samples were performed at an independent diagnostic laboratory
(Prairie Diagnostic Services, Saskatoon, Saskatchewan). Each study group was then placed on drinking water containing
the appropriate test product and maintained on the treated water for 24 hours per day for 14 days. The principal investigator
and all study and laboratory personnel were blind as to which test article was being administered to each group. Prior to
feeding on the following day, each animal had blood collected for glucose analysis. Animals were fed and subsequent blood
samples for glucose were obtained at two-hour intervals for a total of four samples for each animal. The animals were observed
throughout the study period for any adverse effects or behavioral changes. On the last day of the study (day 14), blood samples
were once again collected for complete blood count and blood chemistry at approximately seven hours after feeding, and the
dogs were then returned to normal drinking water. Data are expressed as mean ± standard error of the mean (SEM). Differences
among treatment were tested using repeated measures analysis of variance (ANOVA) followed by Tukey’s posteriori test, as
appropriate. Differences were considered to be significantly different if p<0.05.
Results:
All dogs freely accepted and drank the water with the study additives. Throughout the study there were no noteworthy abnormal
findings for CBC or clinical blood chemistry. No adverse events were observed or reported. All glucose samples from all
treatment groups were within the normal range during the entire study (Fig. 1). Blood glucose showed a diel variation in all treatment
groups on the first day of treatment, with blood glucose in the lower end of the normal range in the morning sample taken
before feeding the dogs (Fig. 1). The blood glucose then rose as the dogs fed throughout the rest of the day, but without any difference
detected among treatment groups (Fig.1). However, there was a minor, but statistically significant increase in blood glucose
at day 14 in the dogs from the 5 times treated group compared to the control group (Fig. 1). Analyses of liver function tests
(AP, ALT, GGT) demonstrated no significant effect of xylitol treatment at any time during the study (Table 1).
“In dogs, the LD50 for theobromine is approximately 250-500 mg/kg, >>>
I have seen this promotion on the Internet but have never seen a citation linked to a prospective dog trial like rodent theobromine ld 50 citations linked to prospective trials. so I would want to see the prospective data to see how the 250-500 estimate was created. I suspect from what I have read dogs absorb oral theobromine slower than other animals. I am not sure if that would increase or decrease the ld50 but would result in different data depending on when measurements were taken due to different absorption times. A prospective ld50 for monkeys and dogs I would guess may have been done in the days before the Internet and strong animal testing laws but the only prospective ones I can find is for rodents.
The old saying is “the dose makes the Posion” but if the ld50 really is different a EBM guideline needs to be different for a dog weighing the same as a human getting identical dose of Chochlate per pound of body weight. Here is what I give my clients.
UF VETERINARIANS OFFER PET SAFETY TIPS FOR THE HOLIDAYS
Dec. 4, 1998
by Sarah Carey
——————————————————————————–
GAINESVILLE — Pet owners should keep in mind their animals’ safety during the holiday season, when hazards increase, say University of Florida veterinarians.
Drunk drivers, electrical cords and baking chocolate all pose a greater-than-usual threat to animals at this time of year because they become more common, said Michael Schaer, professor with the UF College of Veterinary Medicine’s small animal clinical sciences department.
“Keep your animals on leashes and away from roads in order to avoid encounters with drunken drivers,” Schaer said.
Holiday-related dietary indiscretions, including feeding animals baking chocolate, can prove toxic to pets, he added. Chocolate cooking bars are high in a chemical called theobromine, a stimulant which can be fatal to a small animal.
“Use common sense,” Schaer said. “Keep cooking chocolate bars in a place where your dog or cat can’t get to them.”
He added that regular chocolate candy does not pose a theobromine toxicity risk.
For more information, contact Sarah Carey, director of public relations, UF College of Veterinary Medicine, (352) 392-4700, ext. 5206
Sent from my iPad
Several resources cite the same paper (Gans, J.H., Korson, R., Cater, M.R. & Ackerly, C.C. (1980) Effects of short-term and
long-term theobromine administration to male dogs. Toxicol. appl. Phannacol., 53,481-496) which identifies the LD50 in dogs as 300mg/kg.
ABSTRACT Thirty-three dogs were each given a single oral dose of theobromine which ranged from 15 to 1000 mg/kg. Three dogs died, one each given theobromine 300, 500, and 1000 mg/kg. Ten dogs were continued on theobromine (75 to 150 mg/kg/day) for periods of 21 or 28 days; seven died and the others were killed with pentobarbital sodium. None had thymic or testicular atrophy, as has been reported in rats, but a degenerative, fibrotic cardiomyopathy limited to the right atrial appendage occurred in 6 of these 10 dogs. Theobromine was given to two groups of dogs for 1 year in doses of 25 and 50 mg/kg/day, respectively. Other dogs were given theobromine 25 or 50 mg/kg/day for 4 months and the dose was then increased to 100 or 150 mg/kg/day for 8 months. Three dogs (one each at 50, 100, and 150 mg/kg/day) died during the course of the year. The right atrial appendage of one, the dog at 100 mg/kg/day, was obliterated by fibrosis, but no heart lesions were found in the other two dogs. At the end of 1 year all surviving dogs including controls were killed and subjected to complete necropsies. As in the short-term study, the only gross and microscopic change associated with theobromine was a fibrotic lesion in the right atrium of the heart, in three of five dogs given theobromine 150 mg/kg/day and in two of the four dogs given 100 mg/kg/day. Plasma theobromine concentrations were determined during the last 2 months of the year. While right atrial cardiomyopathy occurred in dogs given theobromine 100 or 150 mg/kg/day, a clear relationship between dose, plasma concentration, frequency, and severity of the lesion could not be determined.
This LD50 is quite a bit lower than the 950-1356mg/kg reported for rats (and the 1000mg/kg reported for humans, though I’m sure this has not been determined through a prospective study!).
And there are plenty of case reports of individual dogs dying after consumption of chocolate:
Veterinary Record1994 134 11 284 Strachan, E. R.; Bennett, A. Theobromine poisoning in dogs.
Abstract
One evening, 2 healthy 4-year-old dogs ate a (8 oz) 225 g tin of cocoa powder. The following morning one dogs was dead; the other was shivering but apparently well, but it had a sudden convulsion, collapsed and died in acute cardiac failure later. PM examination revealed cyanosis, cardiac arrest, severe congestion of stomach, intestines and liver and unclotted haemorrhagic fluid in the peritoneal and thoracic cavities. Theobromine was identified in the blood (250 mg/litre) and serum (140 mg/litre). Theobromine, a small amount of caffeine and cocoa powder were detected in gastric contents. The lethal dose of cocoa was believed to be 0.2 oz/kg bodyweight (100 mg/kg of pure theobromine), in these dogs 0.15 oz/kg bodyweight was lethal.
Glauberg, A.; Blumenthal, H. P. Journal of the American Animal Hospital Association1983 19 2 246-248 Chocolate poisoning in the dog.
Abstract
A Springer Spaniel weighing 20.9 kg developed generalized seizures and died after 15 hours after ingestion of two pounds of chocolate. The dog’s symptoms and the serum theobromine concentration of 133 mg/litre immediately post mortem point to an intoxication with this dimethyl xanthine as the cause of death. Supportive data is presented on the pharmacokinetics of theobromine in dog and man. Possible interventions in suspected theobromine intoxication from chocolate are also discussed.
So it seems pretty implausible that theobromine would not be any more toxic to dogs than to humans.
A tangential but important issue here, of course, is how do we decide when something is meaningfully toxic. The LD50 is intended as a standard that allows comparison across species, but it is pretty worthless from a clinical perspective. For one thing, if we require non-survival prospective studies to validate any concern about toxicity for every substance, we’ll be poisoning a lot of dogs. The precautionary principle doesn’t seem unreasonable in this instance. And in the “real world” we’re often less concerned about mortality than about preventing exposures that require medical therapy, and the associated cost. Avoiding something that might be a risk to reduce the chances of a toxicosis even without definitive evidence seems appropriate if that substance has no known value anyway.
Skepvet, here is a prospective coyote ld50 study that I think supports you are right and I am wrong about “special” dog chocolate toxicity where the human/dog ld50 are not about the same.
I could not find any prospective monkey studies but the prospective rodent studies do show the ld50 is much higher for mice.
See
http://digitalcommons.unl.edu/cgi/viewcontent.cgi?article=1014&context=icwdm_usdanwrc
Art Malernee Dvm
Fla Lic 1820
Art, have you never treated a chocolate-poisoned dog? I understand your skeptic nature, but theobromine and caffeine toxicity in dogs has been well known for a long time. If you haven’t treated a chocolate-poisoned dog lately, perhaps it is due to pet-owner awareness and that prevention, based on clinical data and other studies, is working.
V.t.
Do you treat dogs that have eaten regular chocolate candy for theobromine toxicity? If so how? Since skeptvet has convinced me with the data that dogs and humans most likely do not have similar ld50s I no longer can look at the human recommendations and treat dogs following EBM human theobromine guides for small humans. I must admitt I have not seen theobromine toxicity in dogs eating regular chocolate candy. Most of these dogs are vomiting if they ate the entire sack. Even in the coyote bait trials the ones that threw up the bait did not have theobromine toxicity symptoms. Maybe if the dogs did not vomit my observation would be different.
In that study, initial combinations and dosing did present vomiting and some coyotes in fact died hours later. Of course when they increased the combinations and dosing, the likelihood of death increased. They also used more or less pure mixtures from various sources, not exactly that which a chocolate company uses combined with other ingredients.
As for treatment, depending on the individual and symptoms, ipecac to induce vomiting, or activated charcoal, IV fluids, anti-seizure meds, cardiovascular monitoring and meds if necessary – plus or minus other meds all depending on symptoms, and response.