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0347066 2137493 410067663 A 01/26642
12/1989 10/1984 3/1998 4/2001
Heath, "Pulmonary Vascular Disease" Medical Clinics of North
America vol. 61(6), pp. 1279-1307 (1997).*
Hirsch, "The Treatment of Obesity with Drugs" The American
Journal of Clinical Nutrition, pp. 2-4, (Jan. 1998).*
San Juan, Puerot Rico, Dec. 15, 2000 "PRNewswire".
Brain Res Jun. 12, 1999;831 (l-2):229-36, Transport mechanisms
for the antidepressant citalopram in brain microvessal endothelium;
written by B. Rochat, P. Baumann, KL Andus.
(Continued) Primary Examiner—Vickie Kim
(7'4) Attorney, Agent, or Firm—Patterson, Thuente, Skaar & Christensen, PA.
The comprehensive pharmacologic therapy for treatment of obesity including Cysteine is a procedure which involves the administration of a desired therapeutic range of Diethylpropion and/or Phentermine in combination with a SSRI medication and nutritional supplementation for brief and long durations which may be 12 months or more. The preferred procedure involves the administration of drugs in combination which are identified as: Citalopram (Celexa) and Phentermine; Citalopram (Celexa) and Diethylpropion; Citalopram (Celexa), Phentermine, and Diethylpropion. In addition nutritional supplementation such as a multivitamin, 5-Hydroxytryptophan, Cysteine, vitamin B6, vitamin C, Tyrosine, Calcium, and Lysine may be used to enhance the performance of the weight loss treatment program.
18 Claims, 1 Drawing Sheet
Psychomharmacol Bull 1997;33(1): 109-12, Plasma levels of citalopram enantiomers and metabolites in elderly patients; written by JP Foglia, BG Pollock, MA Kirshner, J Rosen, R Sweet, and B Mulsant.
Abstract from: Clin Neuropharmacol Mar.-Apr. 2000;23(2):90-7;
Neuropharmacology of paradoxic weight gain with selective
serotonin reuptake inhibitors; written by BH Harvey and CD Bower.
Abstract from: Clin Psychiatry 2000;61 Suppl ll(l-2):37-41,
Weight gain and antidepressants; M Fava.
Abstract from: J Clin Psychiatry Nov. 2000;61(ll):863-7,
Fluoxetine versus sertraline and paroxetine in major depressive
disorder: changes in weight with long-term treatment; written by M
Fava, R Judge, SL Hoog, ME Nilsson, and SC Koke.
Abstract from: Int clin psychopharmacol Nov. 1999; 14(6):329-37;
Efficacy and tolerability of mirtazapine versus citalopram: a double-
blind, randomized study in patients with major depressive disorder.
Nordic Antidepressant Study Group; written by E Leinonen, J
Skarstein, K Behnke, H Agren, and JT Helsdingen.
Excerpt from: Anchors (US Patent 5,795,895) book, "Safer than
Phen-fen", p. 82; written by Michael Anchors, M.D., Ph.D., Aug.
Budavari et al., The Merck Index, 1989, Merck & Co., Inc., 11th
Edition, pp. 2321 and 4116.
Riley et al., Facts and Comparisons®, 1999, pp. 239, 264(d), and 264(td).
The Medical Clinics of North America, vol. 61/No. 6, Nov. 1977; Pulmonary Vascular Disease, written by Donald Heath and Paul Smith, pp. iii and 1279-1307.
The American Journal of Clinical Nutrition, Jan. 1998—vol. 67—No. 1; Treatment of Obesity with Drugs; written by Jules Hirsch.
Archives of Internal Medicine, Jan. 12, 1998, vol. 158, p. 102; Asymptomatic Mitral and Aortic Valve Disease Is Seen in Half of the Patients Taking 'Phen-Fen'; written by Griffen et al. The Medical Letter® On Drugs and Therapeutics, vol. 36 (Issue 936), Nov. 25, 1994, pp. 107-108; Fluoxetine (Prozac) and Other Drugs for Treatment of Obesity.
Archives of Internal Medicine, May 11, 1998, vol. 158, pp. 12781279; The "Phen-Pro" Diet Drug Combination is Not Associated With Valvular Heart Disease; written by Griffen et al. Deposition Transcripts of Dr. Martin C. Hinz (vol. I of Nov. 17, 2004; and vol. II of Feb. 24. 2005).
Deposition Transcripts of Gottfried Kellermann, which is also on behalf of Neuroscience (vol. I of Nov. 23, 2004; and vol. II of Nov. 24, 2004).
Deposition Transcript of Dr. William Wilson—Nov. 12, 2004.
Deposition Transcript of Dave Peterson—Feb. 28, 2005.
Abell et al., "Placebo Controlled Double-Blind Trial of
Fluvoxamine Maleate in the Obese", Journal of Psychosomatic
Research, 30(2): 143-164 (1986).
Bouchard et al. "Gitalopram and Viloxazine in the treatment of depression by means of slow drop infusion A double-linked comparative trial", Journal of Affective Disorders, 46:51-58 (1997). Marek et al., "A comparison of trazodone and fluoxetine: implications for serotonergic mechanis of antidepressant action", Psychopharmacology 109:2-11 (1992).
Van Praag, "In Search of the Mode of Action of Antidepressants 5-HTP/Tyrosine Mixtures in Depressions", Neuropharmacology 22(38):443-440 (1983).
U.S. Appl. No. 09/523,114, filed Mar. 10, 2000, Hinz.
U.S. Appl. No. 11/282,965, filed Nov. 18, 2005, Hinz.
U.S. Appl. No. 11/353,644, filed Feb. 14, 2006, Hinz.
U.S. Appl. No. 11/353,643, filed Feb. 14, 2006, Hinz.
Agundez et al, "Modulation of CyPlA2 enzyme activity by
indoleamines: inhibition by serotonin and tryptamine",
Pharmacogentics, 8:251-258 (1998).
Andrews et al, "The Effects of 5-hydraoxytryptophan and 5-hydroxytryptamine on Dopamine Synthesis and Release in Rat Brain Striatal Synaptosomes", Journal of Neurochemistry, 30:465470 (1978).
Avarello, "Serotonin Syndrome: a reported case", Neuro Sci, 23:S55-S56 (2002).
Barfholome et al., "L-dopa and 5-hydroxytryptophan Therapy in Phenylalanine-Hydroxylase Activity", The Lancet 2(Nov. 22): 1042-1043 (1975).
Bouyer et al., "Modification of Spontaneous ECoG and Behavior in Cat by Monoamine Precursors", Psychopharmacology, 65:49-54 (1979).
Coppen et al. "Levodopa and L-tryptophan Lherapy in
Parkinsonism", The Lancet, Mar. 25, (1972).
Dunner et al., "Affective Disorder: Studies with Amine Precursors",
Am J. Psychiatry, 132(2): 180-183 (1975).
Gelenberg et al. 'Tyrosine for the treatment of depression", Nutr.
Health, 3(3): 163-73 (1984).
Hurley etal., Pyrrolo [l,4]benzodiazepine Antibiotics. Biosynthesis of the Antitumr Antibiotic 11-Demefhyltomaymycin and its Biologically Inactive metabolity Oxotomaymycin to Streptomyces achromogene, Biochemistry, 15(17):3760-3769 (1976). Kramarcy et al, "Effects of Drug-Inducted Changes in Brian Monoamines on Aggression and Motor Behavior in Mice", European Journal of Pharmacology, 99:141-151 (1984). Li Kam Wa et al., "Renal metabolism and effects of the glutamyl derivates of L-dopa and 5-dydroxytryptophan in man", Clinical Science, 91:177-185 (1996).
Lindstrom, "Aromatic-L-Amino-Acid Decarboxylase Activity in Mouse Pancreatic Islets", Biochimica et Biophysica Acta, 884: 276-281 (1986).
Lindstrom et al., "Aromatic amino acids and pancreatic islet function: a comparison of L-tryptophan and L-5-hydroxytryptophan", Molecular and Cellular Endocrinology, 48: 121-126 (1986). Malone et al., "Treatment (Rx) of 76 Pateitns with Primary Fibromyalgia (1° FM) with Combined Dopaminergic and Serotonergic Drugs", Arthritus & Rhuematism, 39:S92 (1996) (Abstract).
Mathiau et al, "Absence of Serotonergic Innervation form Raphe Nuclie in Rat Cerebral Blood Bessesl - II. Lack of Trypfhophan Hydroxylase Activity In Vitro" Neuroscience, 52(3): 657-665 (1993).
Meyers, "Use of Neurotransmitter Precursors for Treatment of Depression", Alternative Medicine Review, 5(1): 64-71 (2000). Niedens et al, "First fungal aromatic L-amino acid decarboxylase from a paclitaxel-producing Penicillium raistrickii", Mycologia, 91(4):61-26 (1999) (Abstract).
Rabey et al., "L-trypotphan Administration in L-Dopa-Induced Hallucinations in Elderly Parkinsonian Patients" Gerontology, 23: 438-444 (1977).
Sawaki et al., "Some correlations between Procaine-Induces Convulsions and Monamines in the Spinal Cord of Rats", Japan, J. Pharmacol, 51:369-376 (1989).
Schlosberg et al., "Effects of L-Dopa and L-5-Hydroxytryptophan on Locomotor Activity of the Rat after Selective or combined destruction of Central Catecholamine and Serotonin Neurons", The Journal of Pharmacology and Experimental Therapeutics, 211(2):296-304 (1979).
Shintaku et al., "Diagnosis and treatment of 6-pyruvoyltetrahydropterin synthase deficience", Brain & Development, 22:S118-S121 (2000).
Sternberg et al, "Development of Scleroderma-like Illness during
Therapy with L-5-hydroxytryptophan and Carbidopa", The New
England Journal of Medicine, 303(14):782-787 (1980).
Tanaka et al., "Hyperphenylalaninemia Due to Impared
Dihydrobiopterin Biosynthesis", Eur. J. Pediatr, 136:275-280
Thurmond et al, "Effects of Dietary Tyronsine, Phenylamlanine, and
Tryptophan on Aggression in Mice", Pharmacoogy Biochemistry &
Behavior, 6:475-478 (1997).
Trulson et al., "Behavorial Effects of Serotonergic and Dopaminergic Drugs in Cats Following Chronic Amphetamine Administration", European Journal of Pharmacology, 99: 313-324 (1984).
Weitbrecht and et al., "Der Einfluss von 1-Tryptophan auf die L-Dopa-Resportion", DtschMed Wochenschr, 101(l):20-22 (1976). Dave Peterson Affidavit dated Apr. 11, 2005.
* cited by examiner
THERAPY FOR TREATMENT OF OBESITY
This application is a Divisional Application from application Ser. No. 09/947,941, filed Sep. 6, 2001 which will issue on Jul. 6, 2004, as U.S. Pat. No. 6,759,437, which application is a Continuation-In-Part Patent Application of application Ser. No. 09/412,701 filed Oct. 4, 1999, which issued as U.S. Pat. No. 6,403,657 on Jun. 11, 2002, the entire contents of which are hereby incorporated herein by reference in their entireties.
BACKGROUND OF THE INVENTION
Research has identified that long term use of medications for treatment of obesity in patients has resulted in many problems. The two most significant problems encountered by patients using medications to assist in weight loss, assuming the absence of irreversible side effects from the medications, are that:
The medications stop working during therapy where at least 40% to 50% of patients quit losing weight (plateau) on an average of 3.3 months into therapy; and 5% to 8% of patients who receive drug therapy for weight problems experience the complication where the medications fail to assist in appetite suppression where the patient therefore does not lose significant weight.
In the past long term treatment, defined as treatment longer than 3 months to many years, with medications, has raised safety issues including, medication intolerability by the patient, medication side effects and most important ineffectiveness of the drugs or the cessation of benefit of the drugs which in turn causes the patient to fall out of appetite suppression and terminate weight loss.
A weight loss procedure using SSRI medication is disclosed in U.S. Pat. No. 5,795,895. The potential for patients to obtain goal weight loss under the process of U.S. Pat. No. 5,795,895 is low, and the failure of the drugs to provide a desired level of performance is at the heart of the problem.
In the past obesity or weight management procedures, as noted in U.S. Pat. No. 5,795,895, implement a single dosing
medications have unique chemical properties making the outcome of treatment of patients uncertain. In addition not all medications function to assist in weight loss. In the past SSRI (selective Serotonin Reuptake Inhibitor) medications
5 which have been used in weight loss include Fluoxetine Hydrochloride (Prozac), Sertraline (Zoloft), Fluvoxamine Maleate (Luvox), and Trazodone Hydrochloride (Desyrel).
The treatment programs for obesity as known also teach away from the use of alternative dosing procedures to
10 effectuate weight loss. Specifically U.S. Pat. No. 5,795,895 teaches that an SSRI medication never needs to be raised to improve the anorexiant effect of weight loss and that the SSRI medication level administered to a patient may be raised to assist in the treatment of coexisting conditions such
15 as depression.
It is therefore desirable to have a weight loss treatment program for a patient which provides for an effective therapeutic range of available medication to enhance desired weight loss. It is also desirable to provide a weight loss program which minimizes the percent of individuals who do not initially respond to the medication treatment regime or who cease to continue to receive the beneficial effects of the weight loss program following the initiation of the medication treatment due to nutritional deficiencies. These and
other problems are solved by the disclosed Comprehensive Pharmacologic Therapy For Treatment Of Obesity.
A problem has been known in the past where drugs which work on norepinephrine stop working after a period of time
30 when used in treating patients for weight loss. As stated in Wurtman et. al in U.S. Pat. No. 4,885,312.
Indirect-acting sympathomimetic amines (such as Phentermine) function by releasing stored norepinephrine from sympathetic nerve endings. The major problem with their
35 use is that after a few doses, they often stop functioning, i.e., tachyphylaxis sets in. Tachyphylaxis is known to be associated with partial depletion of the norepinephrine in the nerve endings, leading to the supposition that there are releasable and non-releasable pools of norepinephrine and
40 that when the drugs cease functioning, it is because the releasable pools have been severely depleted. The chemical pathway involved is:
Tyrosine dopa »- dopamine norepinephrine »- epinephrine
schedule of SSRI medication for a patient. A single dosing schedule of SSRI medication is not optimal for a desired level of weight loss performance. Individuals frequently fail 55 to lose a desired amount of weight when alternative doses of medication are unavailable.
Second, patients receiving treatment for weight loss through the use of medication frequently experience complications such as a cessation of performance of the medi- 60 cation due to a "nutritional deficiency". Frequently it is difficult to predict which patients are likely to experience unacceptable performance of weight loss medication due to "nutritional deficiencies" associated with calorie deficit's.
It is also problematic to predict the outcome of medication 65 treatment upon individuals receiving Norepinephrine medications such as Phentermine and/or Diethylpropion. These
Dopa, doparnuie, norepinephrine, and epinephrine are known as "catecholamines". Chemically the enzyme "Tyrosine Hydroxylase" limits the rate of formation of catecholamines. Another problem as known is to identify a way to increase the amounts of Tyrosine Hydroxylase or it's activity in a patient receiving treatment for obesity. No procedure is known which uses a dietary precursor approach to increase amounts of Tyrosine Hydroxylase and it's activity in a patient receiving treatment for obesity. No procedure is known to increase catecholamine levels in a patient by providing the precursor needed for the formation of Tyrosine Hydroxylase.
Catecholamine formation is regulated by a feed back loop involving norepinephrine and Tyrosine Hydroxylase. In this loop norepinephrine binds to each of the four legs of the