Calcium Stacking

Anyone got experience with calcium stacking for bone/teeth density in juveniles? I'm not interested in minimum dietary supplementation for prevention/cure of ortho/dental problems. I'm talking safe maximum stacking whilst avoiding toxicity.

Turns out my vet is a fucking asshole and would rather see me trial and error and almost kill my dogs than give me the information (I wouldn't do that FYI thats why I'm asking)... and I'm having trouble finding exact toxicity levels due to the varying ingredients in supplements eg. some contain phosphorous or flouride which pose a separate issue, vitamins for absorption or lactose based products which impede digestion.

If you have any recommendations on a maximum doseage with a specific supplement, that'd be awesome if not a recommendation on a supplement I can utilize with no other additives would also help me a bundle too since I'd be able to work it out on my own - cheers J

 

bump!!!!!!

 

one gram of crushed eggshell for every pound of meat will give the correct calcium/phosphorous ratio.

 

I feed Raw. Bones loaded with Calcium. Whole eggs (shell and all) If you are trying to add bone mass (size and structure), you may have to add something with new blood.

McCoy

 

First off, to much of a vitamin is just as crazy as to little of a vitamin. Next thing pedigree has more to do with structure of bones and teeth compared to any calcium stacking or what ever. Never seen a bulldog calcium stacked and seen plenty of bulldogs that could bite a 2X4 in half. I just can't imagine the benefits of what you are trying to accomplish. I could be wrong, I could be right but I do know one thing that my second sentence is true to a T. Maybe this will help you out.

http://www.peteducation.com/article.cfm?c=2&aid=652

 

• Control of calcium is complex and is influenced by the actions of parathyroid hormone (PTH) and vitamin D and the interaction of these hormones with the gut, bone, kidneys, and parathyroid glands.
• Derangement in the function of these can lead to hypercalcemia.
• Secretory productions of some neoplastic cells can also disturb calcium homeostasis.

SYSTEMS AFFECTED

• Renal/Urologic—high levels of calcium are toxic to the renal tubules and can cause polyuria and polydipsia (PU/PD) and renal failure; can also lead to urolithiasis and associated lower urinary tract disease
• Gastrointestinal—reduces excitability of smooth muscle and can alter gastrointestinal function
• Neuromuscular—depressed skeletal muscle contractility causes weakness.
• Cardiovascular—hypertension and altered cardiac contractility

SIGNALMENT

• Dog and cat
• Primary hyperparathyroidism in the keeshond and Siamese cat

SIGNS

General Comments

• Depend on the cause of hypercalcemia
• Patients with underlying neoplasia, renal failure, or hypoadrenocorticism generally appear ill.
• Patients with primary hyperparathyroidism show mild clinical signs, if any, due solely to the effects of hypercalcemia.
• Signs become apparent when hypercalcemia is severe and chronic.

Historical Findings

• PU/PD—most common in dogs
• Anorexia
• Lethargy—most common in cats
• Vomiting
• Constipation
• Weakness
• Stupor and coma—severe cases

Physical Examination Findings

• Lymphadenopathy or abdominal organomegaly in patients with lymphosarcoma
• Usually unremarkable in dogs with primary hyperparathyroidism
• Parathyroid gland adenoma—not palpable in dogs; often palpable in cats with primary hyperparathyroidism

CAUSES

• Neoplasia—lymphosarcoma (most common in dogs, less common in cats), anal sac apocrine gland adenocarcinoma (dogs), multiple myeloma, lymphocytic leukemia, metastatic bone tumor, fibrosarcoma (cats), various types of carcinoma
• Primary hyperparathyroidism
• Renal failure—acute or chronic
• Blastomycosis
• Hypoadrenocorticism
• Vitamin D rodenticide intoxication—no longer marketed in the United States

RISK FACTORS

• Keeshond breed—hyperparathyroidism
• Renal failure
• Neoplasia
• Use of calcium supplements or calcium-containing intestinal phosphate binders
• Use of calcitriol or other vitamin D preparations

 

DIFFERENTIAL DIAGNOSIS

• History should include exposure to rat poison and any previous response to steroids.
• History of waxing/waning illness suggests hypoadrenocorticism.
• Complete lymph node, rectal, and abdominal palpation may raise index of suspicion for lymphosarcoma and other neoplasia.
• Assessment of hydration status, renal palpation, and urinary history points toward lower urinary tract disease or renal failure.

LABORATORY FINDINGS

Drugs That May Alter Laboratory Results

• Oxalate, citrate, and EDTA anticoagulants bind calcium and falsely lower calcium measurement.
• Vitamin D preparations and thiazide diuretics can raise serum calcium concentrations.

Disorders That May Alter Laboratory Results

• Hemolysis and lipemia can falsely raise calcium concentrations.
• Hypoalbuminemia can falsely lower total calcium concentration.

Valid If Run in Human Laboratory?

Yes CBC/BIOCHEMISTRY/URINALYSIS

• Serum calcium—total calcium concentration depends on binding proteins; adjusted (corrected) calcium can be estimated by the following formulas: Corrected Ca = Ca (mg/dL) - albumin (g/dL) + 3.5 or Corrected Ca = Ca (mg/dL) -[0.4 × total protein (g/dL)] + 3.3
• Azotemia and isosthenuria help define degree of renal impairment.
• Serum phosphorus is usually low or low-normal in patients with primary hyperparathyroidism or hypercalcemia associated with malignancy.
• Hyperphosphatemia in the absence of azotemia suggests a nonparathyroid cause of hypercalcemia.
• Combination of hyperphosphatemia and azotemia is difficult to interpret, since renal failure can be the cause or effect of hypercalcemia.
• Hyperkalemia and hyponatremia suggest hypoadrenocorticism.
• Hyperglobulinemia is associated with multiple myeloma.
• Cytopenias are seen in patients with myelophthisic disease.

OTHER LABORATORY TESTS

• Serum ionized calcium is high in patients with primary hyperparathyroidism or hypercalcemia associated with malignancy; usually normal or low in patients with hypercalcemia associated with renal failure
• Serum PTH measurement—intact molecule and two-site assay methods have the greatest specificity; high-normal or high concentration suggests primary hyperparathyroidism; low concentration suggests neoplasia.
• Serum PTH-rp measurement is often high in patients with hypercalcemia associated with malignancy.
• Vitamin D assays are not readily available.

IMAGING

• Radiography is useful for assessing renal size and shape, urolithiasis, bone lysis, and occult neoplasia.
• Ultrasonography valuable for assessing renal architecture, abdominal lymphadenopathy, and urolithiasis

DIAGNOSTIC PROCEDURES

• Cytologic examination of fine-needle aspirate of lymph nodes to confirm lymphosarcoma
• Examination of bone marrow aspirate to confirm occult hematopoietic neoplasia
• ACTH stimulation testing to confirm hypoadrenocorticism

Treatment

• Inpatient care because of the deleterious effects of hypercalcemia and the need for fluid therapy
• Consider severe hypercalcemia a medical emergency.

Medications

DRUGS OF CHOICE

• Normal saline—fluid of choice
• Avoid calcium-containing fluids.
• Diuretics (furosemide) and corticosteroids can be useful.

CONTRAINDICATIONS

• Do not use glucocorticoids until the diagnosis of lymphoma is excluded; they can obfuscate the diagnosis; if hypoadrenocorticism is suspected, do not give glucocorticoids until after ACTH stimulation testing.
• Thiazide diuretics can cause calcium retention.

PRECAUTIONS

N/A POSSIBLE INTERACTIONS

Avoid the use of calcium- or phosphorus-containing compounds; they can cause soft tissue mineralization in severely hypercalcemic and hyperphosphatemic patients. ALTERNATIVE DRUGS

• Sodium bicarbonate (1–4 mEq/kg) may be useful in combination with other treatments.
• Mithramycin has been used in severe hypercalcemic crises; avoid its use if possible, because of associated nephrotoxicity and hepatotoxicity.
• Calcitonin may be useful in the treatment of hypervitaminosis D.

Follow-Up

PATIENT MONITORING

• Serum calcium every 12 h
• Renal function tests—the first sign of tubular damage may be casts in the urine sediment.
• Must monitor urine output, particularly if oliguric renal failure is suspected, in which case urine output should be measured carefully; oliguria cannot be determined unless the patient is fully hydrated.
• Hydration status must be monitored; indicators of overhydration include increased body weight, increased central venous pressure, and edema (pulmonary or subcutaneous).

POSSIBLE COMPLICATIONS

• Irreversible renal failure
• Soft tissue mineralization

Miscellaneous

ASSOCIATED CONDITIONS

Calcium-containing urolithiasis AGE-RELATED FACTORS

• Mild elevations in calcium and phosphorus may be normal in growing animals.
• Middle-aged and older dogs and cats are at increased risk for cancer.

ZOONOTIC POTENTIAL

N/A PREGNANCY

A fetus is at the same risk as the dam; do not alter treatment because of pregnancy. SYNONYMS

N/A SEE ALSO

• Hyperparathyroidism
• Renal Failure, Acute
• Renal Failure, Chronic

ABBREVIATIONS

• Ca = calcium
• PTH = parathyroid hormone
• PTH-rp = parathyroid hormone–related peptide

Suggested Readings

• Chew DJ, Nagode LA, Carothers M. Disorders of calcium: hypercalcemia and hypocalcemia. In: DiBartola SP, ed. Fluid therapy in small animal practice.Philadelphia: Saunders 1992;116–176.
• Feldman EC. Disorders of the parathyroid glands, In: Ettinger SJ, Feldman EC, eds. Textbook of veterinary internal medicine. 4th ed.Philadelphia: Saunders, 1994;1437–1464.