References for Supplements for Home Cooked Diet

 

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"The Waltham Book of Clinical Nutrition of the Dog and Cat" - 1994 W. Jean Dodds, DVM

Fat-soluble vitamins: Vitamin E, "Earl Mindell's Nutrition & Health for Dogs" by Earl Mindell, R. Ph., Ph.D. & Elizabeth Renaghan pages. 38-39

Water-soluble vitamins: B-Complex, "Earl Mindell's Nutrition & Health for Dogs" by Earl Mindell, R.Ph.D., Elizabeth Renaghan pages 30-32;

Water-soluble vitamins: Vitamin C, "Earl Mindell's Nutrition & Health for Dogs" by Earl Mindell, R.Ph., Ph.D. & Elizabeth Renaghan) pages 33-36

Fat-soluble vitamins: VITAMIN A, "Earl Mindell's Nutrition & Health for Dogs" by Earl Mindell, R. Ph., Ph.D. & Elizabeth Renaghan pages 36-38

Exp Neurol. 1989 May;104(2):113-7.
Anticonvulsant effects of MK-801 and glycine on hippocampal afterdischarge. Peterson SL, Boehnke LE.
Department of Medical Pharmacology and Toxicology, Texas A&M University, College Station 77843.

The effects of glycine and MK-801 on hippocampal seizure threshold and afterdischarge (AD) were determined in freely moving rats implanted with intracranial electrodes. The 0.25 mg/kg (ip) dose of MK-801 significantly reduced the primary hippocampal and cortical AD but induced neurological deficit in 4 of 16 rats. The 0.25 mg/kg MK-801 dose also significantly increased the seizure threshold as compared to the vehicle control treatment and reduced the rebound cortical AD as compared to the control (nondrug) seizure response. The 40 mmol/kg (po) glycine dose significantly reduced the rebound hippocampal and cortical AD without inducing neurological deficit. The 40 mmol/kg glycine dose did not significantly alter the response to the ineffective 0.125 mg/kg MK-801 dose. These results demonstrate the differential effects of MK-801 and glycine on primary and rebound hippocampal AD, respectively, which further establishes the independence of the hippocampal seizure AD parameters. The lack of interaction between MK-801 and glycine was unexpected considering that glycine potentiates MK-801 receptor binding as well as the activity of other anticonvulsants.

Brain Res. 1989 Mar 20;482(2):247-51.
Age-dependent changes in brain glycine concentration and strychnine-induced seizures in the rat.
Hunter C, Chung E, Van Woert MH.
Graduate Program in Biomedical Sciences, Mount Sinai School of Medicine, New York, NY 10029.

Glycine levels and receptor binding were measured in the medulla and spinal cord of 2-month, 10-month, and 24-month-old Fischer 344 rats. The behavioral response to the administration of the glycine antagonist, strychnine, was also evaluated in 2- and 24-month-old animals to investigate the relevance of these parameters to the susceptibility to seizures. Significant reductions in glycine in both the spinal cord and medulla occurred from 2 to 24 months of age. The glycine precursors, serine and threonine, were decreased only in the spinal cord. [3H]Strychnine binding was also decreased by 38% and 34% in the medulla and spinal cord, respectively, of 24-month-old rats compared to 2-month-olds. [3H]GABA binding was similarly reduced while no age-related changes in [3H]diazepam binding in the spinal cord were detected. Comparison of 2- and 24-month-old animals after systemic injection of 1.75 mg/kg strychnine showed that senescent animals have a higher incidence of seizures and mortality compared to young animals. Decreases in glycinergic neurotransmission may lower strychnine seizure threshold in the aged animal.

Eur J Pharmacol. 1988 Jun 10;150(3):381-4.
The glycine-prodrug, milacemide, increases the seizure threshold due to hyperbaric oxygen; prevention by 1-deprenyl.
Youdim MB, Kerem D, Duvdevani Y.
Rappaport Family Research Institute, Faculty of Medicine, Technion, Haifa, Israel.

The novel glycine-prodrug anticonvulsant, milacemide (2-N-pentylaminoacetamide) (500 mg/kg), significantly increased (greater than 400% the seizure threshold induced by hyperbaric oxygen (4.5 atmosphere). This effect was significantly reduced by the selective inhibition of monoamine oxidase B by 1-deprenyl (2.0 mg/kg). 1-Deprenyl alone hardly affected the seizure threshold. These results suggest that, in the brain, milacemide is oxidized to glycine and that this reaction is mediated primarily by monoamine oxidase B. However, the interaction of milacemide metabolites (glycine amide, pentanoate and glycine) as antagonists of receptors of the glutamate NMDA (N-methyl-D-aspartate) subtype cannot be excluded.

Vet Hum Toxicol. 1985 Apr;27(2):97-9.
Effects of glycine and other inhibitory amino acid neurotransmitters on strychnine convulsive threshold in mice.
Sangiah S.

The effects of glycine and other inhibitory amino acid neurotransmitters on strychnine convulsive threshold were studied in mice. The mean intravenous threshold dose for strychnine to produce its convulsive effects in briefly restrained mice was determined to be 1.386 +/- 0.035 mg/kg. The dose of strychnine produced 100% postconvulsive mortality in all the mice tested. Intraperitoneal administration of various doses (100-500 mg/kg) of glycine, beta-alanine and L-threonine, 15-20 minutes prior to strychnine infusion produced an increase of 13.92%, 25.73% and 17.15% respectively in strychnine convulsive threshold in mice. Diazepam, known to produce its anticonvulsant, sedative and muscle relaxant effects through its interaction either with central GABA or glycine receptors was found to be the most potent (48.39%) in increasing strychnine convulsive threshold. Taurine and Baclofen were found to be ineffective in raising strychnine convulsive threshold in mice. These observations favor the possible use of either glycine or beta-alanine in addition to diazepam in treating clinical cases of strychnine neurotoxicoses.

4: Adv Neurol. 1986;43:119-25.
Biotin-responsive encephalopathy with myoclonus, ataxia, and seizures.
Bressman S, Fahn S, Eisenberg M, Brin M, Maltese W.

Prominent neurological abnormalities, including myoclonus, seizures, ataxia, and hearing loss, have been noted in juvenile-onset biotin-responsive MCD. The underlying defect in many of these patients, who generally present in the first year of life, appears to be a deficiency of biotinidase. We have presented a young woman with adult-onset myoclonus, ataxia, hearing loss, seizures, hemianopia, and hemiparesis who responded to pharmacologic dosages of biotin. Although she displayed many of the clinical and biochemical features of juvenile-onset MCD, she did not have a biotinidase deficiency, and the underlying defect remains to be determined. Because of her response to biotin, we have advocated that other patients with unexplained myoclonus syndromes be evaluated for biotin-dependent carboxylase deficiencies and undergo a therapeutic trial with biotin.

Br Med J. 1979 Sep 1;2(6189):521-3.
Decreased serum 24,25-dihydroxy vitamin D concentrations in children receiving chronic anticonvulsant therapy.
Weisman Y, Fattal A, Eisenberg Z, Harel S, Spirer Z, Harell A.

Serum 24,25-dihydroxy vitamin D (24,25(OH)2D) and 25-hydroxy vitamin D (25-OHD) concentrations and the ratio between the two were measured in 31 Israeli children and adolescents receiving long-term treatment with phenobarbitone or phenytoin and in controls. 24,25 (OH)2D concentrations were significantly depressed in the patients, although the 25-OHD concentrations were similar to those in the healthy controls. In four patients with radiological evidence of osteopenia very low serum 24,25(OH)2D concentrations and serum 24,25(OH)2D: 25-OHD ratios were recorded. The findings suggest that 24,25(OH)2D deficiency may play an important part in the pathogenesis of osteomalacia in patients treated with anticonvulsant drugs and provide further indirect evidence that 24,25(OH)2D is important for normal bone structure.

J Am Vet Med Assoc. 1993 Apr 15;202(8):1276-8.
Seizures and acute death attributable to hypovitaminosis A and suspected hypovitaminosis D in feeder pigs.
Lakritz J, George LW, Moore J.
Department of Veterinary Anatomy and Cell Biology, School of Veterinary Medicine, University of California, Davis 95616.

Clinical signs that included lethargy, inappetence, diarrhea, and vomiting and that progressed to seizures were observed in 40 feeder pigs that were approximately 70 days old. The pigs were fed ground red wheat and whole milk and were housed in a barn that did not allow exposure to direct sunlight. Analysis of samples of feed obtained from the farm indicated inadequate quantities of calcium and phosphorus as well as a low ratio of these 2 nutrients. Serum and tissue concentrations of vitamin A were less than normal. Low serum calcium concentrations, high serum phosphorus concentrations, and high alkaline phosphatase and creatine kinase activities were compatible with low vitamin D concentrations.

Brain Res Bull. 1992 Jan;28(1):27-38.
Pattern of neuronal death in the rat hippocampus after status epilepticus. Relationship to calcium binding protein content and ischemic vulnerability.
Freund TF, Ylinen A, Miettinen R, Pitkanen A, Lahtinen H, Baimbridge KG, Riekkinen PJ.
Department of Functional Neuroanatomy, Hungarian Academy of Sciences, Budapest.

The pattern of hippocampal cell death has been studied following hippocampal seizure activity and status epilepticus induced by 110-min stimulation of the perforant pathway in awake rats. The order of vulnerability of principal cells in the different hippocampal subfields--as determined by silver impregnation--was found to be very similar to the pattern found in ischemia; i.e., dentate hilus greater than CA1, subiculum greater than CA3c greater than CA3a,b greater than dentate granule cells. The hilar somatostatin-containing cells were the most vulnerable cell type, whereas all other subpopulations of nonprincipal neurons--visualized by immunocytochemistry for the calcium binding proteins parvalbumin and calbindin--were remarkably resistant. Pyramidal cells in the CA3 region containing neither of the examined calcium binding proteins were more resistant to overexcitation than CA1 pyramidal cells, most of which do contain calbindin. This indicates that no simple relationship exists between vulnerability in status epilepticus and neuronal calcium binding protein content, and that local and/or systemic hypoxia during status epilepticus may be responsible for the ischemic pattern of cell death.

Brain Dev. 1991;13(2):132-4.
Hypocalcemic focal seizures in a one-month-old infant of a mother with a low circulating level of vitamin D.
Oki J, Takedatsu M, Itoh J, Yano K, Cho K, Okuno A.
Department of Pediatrics, Asahikawa Medical College, Japan.

We present a case of a one-month-old infant with hypocalcemia and rickets, with symptoms of focal seizures. The ictal EEG showed left occipital spikes spreading over all of the left hemisphere. From the laboratory studies, we concluded that a low maternal circulating level of vitamin D would cause infantile hypocalcemia and rickets, while immature renal response to parathyroid hormone and transient hypoparathyroidism in infancy would induce hyperphosphatemia. Hypocalcemia may be an important factor in the cause of focal seizures which start even after the age of one month. Further, investigation of maternal vitamin D levels should be done in infantile hypocalcemia.

Arch Invest Med (Mex). 1988 Apr-Jun;19(2):165-71.
Serum parathormone, 25 hydroxycholecalciferol and magnesium concentrations in infants with seizures associated with spontaneous hypocalcemia.
Villalpando S, Campos-Pahua J, Esquivel S, Mondragon L, Urquieta B, Larracilla J.

J Fam Pract. 1984 Jun;18(6):873-7.
Prevalence of hypocalcemia and elevated serum alkaline phosphatase in patients receiving chronic anticonvulsant therapy.
Schmitt BP, Nordlund DJ, Rodgers LA.

Residents of an institution for the developmentally disabled in northwest Ohio receiving anticonvulsant therapy for six months or more with phenobarbital or phenytoin or both were studied for the prevalence of hypocalcemia and elevated alkaline phosphatase level. Fifty-six residents were identified. Sixteen (29 percent) were hypocalcemic. Fifteen (27 percent) had elevated serum alkaline phosphatase levels. Twenty-three residents received vitamin D supplementation (400 IU/d) in addition to a normal dietary intake of calcium and vitamin D. The mean serum calcium level was identical (8.65 mg/dL) for those receiving and not receiving additional vitamin D. This study corroborates the findings of prior studies suggesting an association between anticonvulsant usage and mineral and bone abnormalities. The causal nature of this association, its clinical significance, and its management require further investigation.

Brain Res. 1984 Apr 23;298(1):125-9.
Administration of 1,25-dihydroxyvitamin D3 results in the elevation of hippocampal seizure threshold levels in rats.
Siegel A, Malkowitz L, Moskovits MJ, Christakos S.

Electrical stimulation of the dorsal hippocampal formation of the rat was employed to determine the effect of 1,25-dihydroxyvitamin D3 1,25-(OH)2D3), the hormonal form of vitamin D, on induced seizure thresholds. Stereotaxic injection of 100 micrograms or 50 micrograms 1,25-dihydroxyvitamin D3 in 2 microliter propylene glycol into the hippocampus resulted in a significant elevation in seizure threshold in all animals treated. 1,25-dihydroxyvitamin D3-induced increases were noted within 5-10 min and lasted at least 120-180 min after injection when the experiments were terminated. Intravenous injection of 1,25-(OH)2D3 also resulted in a significant elevation of seizure threshold; however, the increase was transient, lasting only 30 min. This effect was specific since 200 micrograms vitamin D3 or 200 micrograms 25-hydroxyvitamin D3 (25-(OH)D3), injected into the hippocampus, had no effect on seizure threshold levels. This investigation represents the first direct demonstration of a role for 1,25-(OH)2D3 in the regulation of seizure activity and suggests, along with the previously demonstrated presence of immunoreactive vitamin D-dependent calcium binding protein and receptors for 1,25-dihydroxyvitamin D3 in the brain, that the vitamin D endocrine system may play a significant role in the physiological mechanisms underlying convulsive disorders.

Bone. 1995 Aug;17(2 Suppl):107S-111S.
Noncalcemic actions of 1,25-dihydroxyvitamin D3 and clinical applications.
Holick MF.

Department of Medicine, Boston University Medical Center, MA 02118, USA. Vitamin D is absolutely essential for the maintenance of a healthy skeleton. Without vitamin D, children develop rickets and adults exacerbate their osteoporosis and develop osteomalacia. Casual exposure to sunlight is the major source of vitamin D for most people. During exposure to sunlight, ultraviolet B photons photolyze cutaneous stores of 7-dehydrocholesterol to previtamin D3. Previtamin D3 undergoes a thermal isomerization to form vitamin D3. Increased skin pigmentation, changes in latitude, time of day, sunscreen use, and aging can have a marked influence on the cutaneous production of vitamin D3. Once vitamin D3 is formed in the skin or ingested in the diet, it must be hydroxylated in the liver and kidney to 1,25-dihydroxyvitamin D3 [1,25(OH)2D3].

It is now recognized that a wide variety of tissues and cells, both related to calcium metabolism and unrelated to calcium metabolism, are target sites for 1,25(OH)2D3. 1,25(OH)2D3 stimulates intestinal calcium absorption and mobilizes stem cells to mobilize calcium stores from bone. Noncalcemic tissues that possess receptors for 1,25(OH)2D3 respond to the hormone in a variety of ways. Of great interest is that 1,25(OH)2D3 is a potent antiproliferative and prodifferentiation mediator. As a result, 1,25(OH)2D3 and its analogs have wide clinical application in such diverse clinical disorders as rheumatoid and psoriatic arthritis; diabetes mellitus type I; hypertension; cardiac arrhythmias; seizure disorders; cancers of the breast, prostate, and colon; some leukemias and myeloproliferative disorders; chemotherapy-induced hair loss; and skin rejuvenation as well as skin diseases like psoriasis and ichthyosis.

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