“Cumulative exposure to cadmium has been associated with elevations in blood pressure and renal dysfunction in human beings and rodents”. This introductory statement in a paper entitled “Association of urinary cadmium excretion with feline hypertension” by N.C. Finch, H. M. Syme and J. Elliot (1) from my alma mater, the Royal Veterinary College London, raises an important question. Other than cigarette smoke, possible environmental sources of cadmium in afflicted cats were not identified or suggested by these authors. They acknowledged that hypertension caused by kidney disease could increase cadmium excretion in the urine, but that there was no relationship between renal function and cadmium excretion. Furthermore, causality could not be inferred in so far as cadmium causing hypertension or hypertension resulting in more cadmium being excreted.
Suffice it to say, hypertension in cats, as in humans and other animals, must be controlled to prevent damage to the eyes, heart, kidneys and other internal organs, and the findings of this clinical research study calls for a full assessment of cadmium levels in manufactured cat foods.
I recall over 30 years ago that the U.S. Department of Agriculture expressed concern over humans consuming the livers of slaughtered laying hens because of high cadmium levels. Cadmium residues in the livers of aged beef and dairy cattle were also a concern in some European countries at that time. Today, state authorities from Alaska to Main advise moose hunters not to eat the livers and kidneys of mature bulls because of high cadmium levels acquired from consuming willow and other vegetation that concentrate cadmium present in various soils. Human and domestic animal sources of cadmium include crop contamination from various soils and chemical fertilizers and from cadmium being concentrated in consumed animal parts (see below)…
According to Health Canada (www.hc.gc.ca) “A maximum acceptable concentration of 0.005 mg/L (5 µg/L) for cadmium in drinking water has been established for humans on the basis of health considerations. Food is the main source of cadmium intake for individuals who are not occupationally exposed. A joint FAO/WHO expert committee has estimated a provisional tolerable weekly intake of cadmium for an adult to be from 0.4 to 0.5 mg. Because it would be difficult to reduce cadmium intake in food, intake from water should be as low as possible. Certain shellfish, such as crabs and oysters, may concentrate cadmium to extremely high levels in certain tissues, even if they inhabit waters containing low levels of cadmium. Cadmium may also concentrate in the kidney and liver of swine, sheep, and cattle (2). Reported concentrations of cadmium in foodstuffs vary widely; concentrations in most foods average about 0.05 mg/kg on a wet-weight basis (3). Concentrations in beef livers, kidneys, and brown crabmeat can reach 0.2, 1.6, and 21.0 mg/kg, respectively (4). More detailed data are available from the national food monitoring program of the Department of National Health and Welfare,
( Department of National Health and Welfare. Unpublished data, Health Protection Branch, Ottawa 1978). Average cadmium concentrations, on a fresh-weight edible part basis, ranged from 0.1 (0.01 to 0.13) mg/kg for meat and poultry to 0.60 (0.13 to 2.78) mg/kg for beef kidney. Of the 16 food types listed, a mean concentration of 0.05 mg/kg was exceeded in beef (0.6 mg/kg) and pork (0.26 mg/kg) kidneys, and in beef (0.15 mg/kg), pork (0.09 mg/kg), and chicken (0.06 mg/kg) livers.
One analysis of pet foods– SpexCertiPrep, a laboratory standards company, “Trace Metal Analysis of Commercial Pet Food for Toxic Metals by ICP and ICP-MS.” By R. Obenauf et al (www.spexcsp.com) reported: pet food levels of cadmuim ranged from 1.8-130 parts per billion with a mean of 42 compared to human grade tuna at 36, sardines at 14 and chicken at 1.8 ppb. Toxic metal levels were gnerally higher in dry versus canned cat and dog foods. ( 1 ppb= 1 microgram/Kg or 0.001 mg/Kg).
According to EVISA (5) “Cadmium appears to be the largest single contributor to autoimmune thyroid disease. It is a very powerful and toxic metal which seems to be placed at the very center of the thyroid story —Not only does cadmium appear to play a very pivotal role in thyroid disease, it is a very unique mineral. It is extremely toxic and has toxic biological effects at concentrations smaller than almost any commonly found mineral. Despite this great toxicity, there is some evidence that cadmium is an essential nutrient with biological function. One of the greatest effects of cadmium is that it depletes selenium in the body because selenium is essential for cadmium removal. Selenium atoms combine with cadmium atoms and are escorted out of the body via the bile system. When selenium is depleted by cadmium, there is less selenium to form the deiodinase enzymes which convert T4 to T3, resulting in low T3 and hypothyroidism. Also there is less selenium to form glutathione peroxidase, one of the body’s prime antioxidants. This results in greater levels of reactive oxygen species and hydrogen peroxide, which lead to an increased production of thyroid hormone and damage to the thyroid gland”.
Dr. W. Jean Dodds sent me an additional important consideration, writing that:
“A second mineral of importance to thyroid function when over-supplemented is iodine. Even though the effect of iodine deficiency in promoting goiter and hypothyroidism has been known for decades, one should not automatically supplement a hypothyroid or normal dog’s diet with iodine. Many people unwittingly do this by feeding extra kelp or seaweed. This supplementation can result in excessive iodine intake, which can in turn cause the thyroid gland to overproduce T4 and T3. This then provokes an immune-mediated response in the body, where the immune system actually attacks the thyroid gland and inhibits hormone output. Such a response can suppress thyroid levels by up to 25 percent, causing hypothyroidism as well as autoimmune thyroiditis (6)”.
These observations from an expert panel of scientists and scientific publications warrant closer scrutiny of the roles excess cadmium (and iodine especially in sea food ingredients in pet foods) may play in the epidemic of thyroid disease in cats, manifested as hyperthyroidism, and in dogs as hypothyroidism, many cases being identified as autoimmune thyroid disease.
As a precautionary measure to reduce consumption of potentially toxic substances (such as cadmium as well as lead, cobalt, chromium, arsenic, mercury, selenium, copper, fluoride and uranium) which gradually accumulate in various body parts, the internal organs, especially livers and kidneys, bones and fats (which can also accumulate lipophilic pesticides and dioxins) of mature animals should not be recycled into the human, companion animal and farmed animal (including farmed fish) food chain. Mature animals– ‘spent’ breeder-sows and other species kept for breeding purposes, spent egg-laying hens and also horses, —should not be included in pet foods or livestock and fish feed because of this age-related bio-accumulation of toxic substances .High in the aquatic food-chain carnivorous fish and long-lived marine life that both concentrate such toxic chemicals (and also bromide compounds from fire-retardant treated materials and endocrine disrupting chemicals in plastics that are a major ocean pollutants) should likewise be considered unfit food items for human and non-human consumption..
I appreciate the helpful comments of Margaret Gates with www.feline-nutrition.org in the completion of this brief review.