TEMPLATE
CATEGORY
NAME
TAG
USE
L
Defects in GCLC are the cau
L
Reproductive function
L
Liver function test
H
associated with blood clottin SLC4A1 defects = spherocyt to chronic hemolytic anemia
OCCURS: 2 Blood Works™
Activator
Blood Works™
Hormone
Blood Works™
Gene
Blood Works™
Genome
Blood Works™
Activator
Glutamate cysteine ligase, catalytic subunit Gonadotropic releasing hormone Gamma-glutamyl transpeptidase Protein C Solute carrier family 4, anion exchanger, member 1
H
TECHNICIAN NOTES: Glutamate Cysteine Ligase (GCL), previously known as gamma-glutamylcysteine synthetase (GCS), is the first enzyme of the cellular glutathione (GSH) biosynthetic pathway that catalyzes the chemical reaction: L-glutamate + L-cysteine + ATP ßàgamma-glutamyl cysteine + ADP + Pi GSH, and by extension GCL, is critical to cell survival. Nearly every eukaryotic cell, from plants to yeast to humans, expresses a form of the GCL protein for the purpose of synthesizing GSH (Glutathione). To further highlight the critical nature of this enzyme, genetic knockdown of GCL results in embryonic lethality. Furthermore, dysregulation of GCL enzymatic function and activity is known to be involved in the vast majority of human diseases, such as diabetes, Parkinson's disease, Alzheimers disease, COPD, HIV/AIDS, and cancer. This typically involves impaired function leading to decreased GSH biosynthesis, reduced cellular antioxidant capacity, and the induction of oxidative stress. However, in cancer, GCL expression and activity is enhanced, which serves to both support the high level of cell proliferation and confer resistance to many chemotherapeutic agents. https://en.wikipedia.org/wiki/Glutamate%E2%80%93cysteine_ligase Gonadotropin-releasing hormone Gonadotropin-releasing hormone (GnRH) insensitivity is a rare autosomal recessive genetic and endocrine syndrome which is characterized by inactivating mutations of the gonadotropin-releasing hormone receptor (GnRHR) and thus an insensitivity of the receptor
to gonadotropin-releasing hormone (GnRH), resulting in a partial or complete loss of the ability of the gonads (sex gland or reproductive gland) to synthesize the sex hormones. https://en.wikipedia.org/wiki/Gonadotropin-releasing_hormone_insensitivity Gamma-glutamyl transpeptidase Gamma-glutamyltransferase (also Îł-glutamyltransferase, GGT, gamma-GT is a transferase(a type of enzyme) that catalyzes the transfer of gamma-glutamyl functional groups from molecules such as glutathione to an acceptor that may be an amino acid, a peptide or water (forming glutamate). GGT plays a key role in the gamma-glutamyl cycle, a pathway for the synthesis and degradation of glutathione and drug and xenobiotic detoxification. Other lines of evidence indicate that GGT can also exert a pro-oxidant role, with regulatory effects at various levels in cellular signal transduction and cellular pathophysiology. This transferase is found in many tissues, the most notable one being the liver, and has significance in medicine as a diagnostic marker. https://en.wikipedia.org/wiki/Gamma-glutamyl_transpeptidase Protein C Protein C, also known as autoprothrombin IIA and blood coagulation factor XIV, is a zymogen, the activated form of which plays an important role in regulating anticoagulation, inflammation, cell death, and maintaining the permeability of blood vessel walls in humans and other animals. The zymogenic form of protein C is a vitamin K-dependent glycoprotein that circulates in blood plasma. The protein C zymogen is activated when it binds to thrombin, another protein heavily involved in coagulation, and protein C's activation is greatly promoted by the presence of thrombomodulin and endothelial protein C receptors (EPCRs). Because of EPCR's role, activated protein C is found primarily near endothelial cells (i.e., those that make up the walls of blood vessels), and it is these cells and leukocytes (white blood cells) that APC affects. Because of the crucial role that protein C plays as an anticoagulant, those with deficiencies in protein C, or some kind of resistance to APC, suffer from a significantly increased risk of forming dangerous blood clots (thrombosis). Anion exchanger 1 AE1 in human red blood cells has been shown to transport a variety of inorganic and organic anions. The AE1-catalyzed process is physiologically important in red blood cells. https://en.wikipedia.org/wiki/Anion_exchanger_family#Anion_exchanger_1 Anemia implies a reduction in the O2-carrying capacity of the blood and is usually characterized by low hematocrit level. Excessive loss of erythrocytes, deficiency in the hemoglobin content of erythrocytes, and a decreased rate of erythropoiesis cause anemia. Hemolytic anemia is caused by rupture of excessive numbers of circulating erythrocytes. Hemolysis occurs because erythrocytes are defective or because otherwise normal cells are induced to rupture by external factors. Although anemia is a common clinical problem, the chronic manifestation of the disorder normally leads to hyperkinetic circulation, chamber dilation, and finally the development of left ventricular hypertrophy. Hence, severe anemia may lead to the deterioration of the heart ventricle function seen in heart failure, a major cause of mortality. Cardiac hypertrophy in anion exchanger 1-null mutant mice with severe hemolytic anemia
TEMPLATE
CATEGORY
NAME
TAG
USE
Muscle - jaw/mastication
Pterygoid-lateral
H
may be associated with TMJ
Checkpoint™
Muscle - jaw/mastication
Temporalis
H
may be associated with TMJ
Checkpoint™
Amino Acid
Asparagine
L
Source of energy to the body's
Checkpoint™
Amino Acid
Ornithine
L
Excessive consumption may c
Checkpoint™
Amino Acid
Ornithine
L
Inhibit during severe illnesse
Checkpoint™
Amino Acid
Ornithine
L
associated with affection and a
Checkpoint™
Amino Acid
Ornithine
L
Growth hormone and healing s
Checkpoint™
Muscle - eyelids
Orbicularis oculi
H
may be associated with TMJ
Checkpoint™
Biochemical
Hydroxy Methylbutyrate
L
May prevent exercise-induce
Checkpoint™
Amino Acid
Hydroxy Methylbutyrate (HMB) L
Prevent during immobilizatio
Checkpoint™
Amino Acid
Hydroxy Methylbutyrate (HMB) L
May increase muscle strengt
Checkpoint™
Mineral
Magnesium chloride
L
Body salt
Checkpoint™
Amino Acid
Taurine
L
May prevent convulsions
Checkpoint™
Amino Acid
Taurine
L
definciency contributes to spas
Checkpoint™
Amino Acid
Taurine
L
May increase muscle strength
Checkpoint™
Enzyme
Cellulase
H
Digests cellulose - alleviates
OCCURS: 5 Checkpoint™ OCCURS: 2
Technician Notes: Cellulase Cellulase is used as a treatment for phytobezoars, a form of cellulose bezoar found in the human stomach. A bezoar is a mass found trapped in the gastrointestinal system. Pharmacobezoars are composed of medications that don't properly dissolve in your digestive tract. Bezoars can cause lack of appetite, nausea, vomiting, weight loss and a feeling of fullness after eating only a little food. Bezoars can also cause gastric ulcers, intestinal bleeding and obstruction, leading to tissue death (gangrene) in a portion of the digestive tract. http://www.mayoclinic.org/diseases-conditions/gastroparesis/expert-answers/bezoars/faq-20058050
HMB Role of β-hydroxy-β-methylbutyrate (HMB) in leucine stimulation of muscle mitochondrial biogenesis HMB both stimulate mitochondrial biogenesis and fatty acid oxidation similarly to leucine. Both HMB and leucine increased mitochondrial biogenesis by ~30–35% http://www.fasebj.org/content/26/1_Supplement/251.6.short?utm_source=TrendMD&utm_medium=cpc&u tm_campaign=FASEB_J_TrendMD_0 A general hypothesis is proposed that HMB is metabolized to HMG-CoA in tissues such as muscle, mammary tissue, and certain immune cells and is used for de novo cholesterol synthesis. In times of stimulated growth and/or differentiation. HMG-CoA may be rate-limiting for cholesterol synthesis, which could limit cell growth or function. It is proposed that feeding HMB can provide a saturating source of cytosolic HMG-CoA for cholesterol synthesis and in turn allow for maximal cell growth and function. http://www.sciencedirect.com/science/article/pii/S095528639700048X
TEMPLATE
CATEGORY
NAME
TAG USE
Mapping Methylation™
Protein
MTRR
H
Part of 5-methyl fol
Mapping Methylation™
Protein
MTRR
H
aka - 5-methyltetra
Mapping Methylation™
Biochemical
Serotonin
H
modulator of appet
Mapping Methylation™
Biochemical
Serotonin
H
Modulator of appet
Mapping Methylation™
Biochemical
Pyruvic Acid
H
Involved in the Kre
Mapping Methylation™
Chemical
Sulfate
H
Salt of sulfuric ac
Mapping Methylation™
Vitamin
Citric Acid
H
Krebs Cycle compo
Mapping Methylation™
Biochemical
Isocitric Acid
H
Krebs Cycle compo
Mapping Methylation™
Enzyme cofactor
Coenzyme A
H
Krebs Cycle compo
Mapping Methylation™
Biochemical
FADH2
L
The energy in FAD
Mapping Methylation™
Genome
DHPR (Dihydropyridine Receptor)
L
Found in the transv
Mapping Methylation™
Biochemical
FAD flavin adenine dinucleotide
L
A redox cofactor in
OCCURS: 5
OCCURS: 4
OCCURS: 2
Mapping Methylation™
Genome
ACAT(acetyl-coenzyme A)
L
Involved with meth
Mapping Methylation™
Biochemical
NADH
L
Enhances Dopamin
Mapping Methylation™
Activator
ACE (angiotensin i-converting enzyme)
L
Catalyzes activatio
Mapping Methylation™
Vitamin compound
Nicotinamide adenine dinucleotide (NAD)
L
Krebs Cycle compo
Mapping Methylation™
Amino Acid
Arginine
L
Synthesized from
Mapping Methylation™
Amino Acid
Arginine
L
Stimulates the rel
Mapping Methylation™
Amino Acid
Arginine
L
Improves immune
Mapping Methylation™
Biochemical
cis-Aconitic Acid
L
Krebs Cycle compo
Mapping Methylation™
Biochemical
Adenosine Monophosphate
L
In the Krebs Cycle
Mapping Methylation™
Biochemical
Urea
H
Found in and extr
Mapping Methylation™
Biochemical
Nitric Oxide
H
Important in prote
Mapping Methylation™
Genome
VDR (Vitamin D Receptor)
L
Transcription factor
Mapping Methylation™
Mineral
Molybdenum
H
Deficiency may =
Mapping Methylation™
Mineral
Molybdenum
H
Cofactor for Sulfit
Mapping Methylation™
vitamin
Pyridoxine (B6)
L
Supplemental form
Mapping Methylation™
Chemical
Sulfite
H
Used in increasing
Mapping Methylation™
Protein
MTR
H
Part of 5-methyl fol
Mapping Methylation™
Protein
MTR
H
aka - 5-methyltetra
Technician Notes: Possible Urea Cycle Disorder/ Hyperammonemia
The urea cycle involves a series of biochemical steps in which nitrogen, a waste product of protein metabolism, is removed from the blood and converted to a compound called urea in the blood. Normally, the urea is transferred into the urine and removed from the body. In urea cycle disorders, the nitrogen accumulates in the form of ammonia, a highly toxic substance, resulting in hyperammonemia (elevated blood ammonia). Most ammonia in the body forms when protein is broken down by bacteria in the intestines. The liver normally converts ammonia into urea, which is then eliminated in urine. Ammonia levels in the blood rise when the liver is not able to convert ammonia to urea. http://www.nucdf.org/ucd.htm https://www.ncbi.nlm.nih.gov/books/NBK1217/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3488504/ Possible Citrin Deficiency / Vitamin P One of the most common characteristics of citrin deficiency is a fondness for protein-rich and/or lipid-rich foods and aversion to carbohydrate-rich foods. May cause fatty liver and parenchymal cellular infiltration associated with hepatic fibrosis, variable liver dysfunction, hypoproteinemia, decreased coagulation factors, hemolytic anemia, and/or hypoglycemia. Citrin deficiency is a rare metabolic condition in which a chemical called citrin does not work correctly in your body. This can cause ammonia to build up in your blood over time. When ammonia builds up too much, it can cause serious health problems. http://themedicalbiochemistrypage.org/ureacycledisorders.php Citrullinemia A lack of functional citrin blocks the malate-aspartate shuttle, including the transport of aspartate out of mitochondria. This loss of citrin inhibits the normal production of proteins and nucleotides. It also reduces the amount of aspartate available to take part in the urea cycle. As a result, the liver cannot effectively process excess nitrogen into urea. A disruption in the urea cycle allows nitrogen (in the form of ammonia) and other byproducts of the urea cycle (such as citrulline) to build up in the bloodstream. Ammonia is toxic, especially to the nervous system, which helps explain the development of abnormal behaviors and other neurologic problems in people with adult-onset type II citrullinemia. https://ghr.nlm.nih.gov/gene/SLC25A13#conditions
TEMPLATE
CATEGORY NAME
TAG USE
OCCURS: 8 Disturbing Liver™
Herb
Olive Leaf
L
may help prevent fatty liv
Insulin-like Growth Factor-1 (IGF-1)
L
hormone of the liver
OCCURS: 7 Disturbing Liver™ Protein OCCURS: 6 Disturbing Liver™
Lipids
Eicosapentaenoic Acid (EPA)
L
may help prevent fatty liv
Disturbing Liver™
Activator
Lipoprotein Lipase
L
insulin stimulates activity
Disturbing Liver™
Activator
Lipoprotein Lipase
L
expressed in heart, musc
Disturbing Liver™ Toxin
Mercury
H
detrimental to liver func
Disturbing Liver™ Toxin
Mercury
H
dental amalgam
Insulin-like Growth Factor-1 (IGF-1)
L
hormone of the liver
OCCURS: 5 Disturbing Liver™
Activator
Disturbing Liver™
Biochemical S CoA
L
supports cholesterol meta
Disturbing Liver™
Protein
Low density lipoprotein receptor adaptor protein 1
L
mutations associated with
Disturbing Liver™
Amino Acid
Glutathione
L
Natural liver antioxidant
Disturbing Liver™
Activator
glycogen synthase, Liver
L
converts excess glucose
Disturbing Liver™ Sugar
Fructose
L
excessive may cause fa
Disturbing Liver™
Vitamin
Inositol
L
may help prevent fatty liv
Protein
Aspartate Aminotransferase, cystolic
H
assoc w glutamate Krebs
Disturbing Liver™
Protein
Thrombopoietin
H
hormone of the liver
Disturbing Liver™
Enzyme
HMG - Co A
H
statins inhibit this enzyme
Disturbing Liver™
Enzyme
HMG - Co A
H
directs body to create cho
OCCURS: 4
OCCURS: 3 Disturbing Liver™ OCCURS: 2
Technician Notes: Insulin-like growth factor 1 Low insulin-like growth factor-1 levels are associated with anaemia in adult non-diabetic subjects. Anaemia is a risk factor for cardiovascular morbidity and mortality. Among factors responsible for anaemia, insulin-like growth factor-1 (IGF-1) is a plausible candidate. We evaluated the association of IGF-1 with haemoglobin (Hb) concentration and anaemia in a cohort of 1,039 Caucasians subjects. Subjects with anaemia exhibited lower IGF-1 (p=0.006), and higher hsCRP levels (p=0.003). https://www.ncbi.nlm.nih.gov/pubmed/21057699 Low-density lipoprotein receptor adapter protein 1 (LDL) Mutations in this gene lead to LDL receptor malfunction and cause the disorder autosomal recessive hypercholesterolaemia. There are specialized receptors on cell surfaces that bind LDL-C, these are called LDL-receptors. A lack of LDL-receptors may reduce the uptake of cholesterol by the cells, forcing it to remain in the circulation thereby raising blood levels.
https://en.wikipedia.org/wiki/Low-density_lipoprotein_receptor_adapter_protein_1 http://www.docsopinion.com/health-and-nutrition/lipids/ldl-c/ Glycogen synthase Mutations in the GYS1 gene are associated with glycogen storage disease type. In humans, defects in the tight control of glucose uptake and utilization are also associated with diabetes and hyperglycemia. Patients with type 2 diabetes normally exhibit low glycogen storage levels because of impairments in insulin-stimulated glycogen synthesis and suppression of glycogenolysis. https://en.wikipedia.org/wiki/Glycogen_synthase#Clinical_significance Possible Fructose Malabsorption Fructose Malabsorption – Causes, Symptoms, and Diagnosis Since fructose causes diarrhea, it may flush some micronutrients (iron, vitamins) out from small intestine, before they are absorbed, resulting in anemia and various nutrient deficiences over the time. http://www.healthhype.com/fructose-malabsorption-cause-symptoms-and-diagnosis.html Aspartate Aminotransferase Cystic Possible Celiac/ Gluten Mild Elevation of Liver Transaminases Extra intestinal Manifestations of Celiac Disease Patients with celiac disease can present with various extraintestinal manifestations, including hematologic (iron-deficiency anemia and megaloblastic anemia secondary to nutritional deficiencies, abnormal coagulation due to vitamin K deficiency), neurologic (ataxia, depression, seizures, autistic-like behavior, headaches, peripheral neuropathy), rheumatologic (arthritis or arthralgias sometimes associated with systemic lupus erythematosus or rheumatoid arthritis), hepatic (hepatitis), cardiac (pericarditis), dental/oral (dental enamel hypoplasia, aphthous lesions), endocrine (short stature, delayed puberty), infertility and miscarriage, bone (decrease in bone density), and skin (dermatitis herpetiformis) complications. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2270871/ Thrombopoietin Increased Levels of Thrombopoietin and IPF in Patients with Iron Deficiency Anemia Thrombocytosis has been reported in about 50% of patients with iron deficiency anemia (IDA). The etiology of iron deficiency was gastrointestinal (GI) blood loss, menometrorrhagia, previous GI surgery, and low dietary iron intake. Menometrorrhagia is a condition in which prolonged or excessive uterine bleeding occurs irregularly and more frequently than normal. It is thus a combination of metrorrhagia and menorrhagia. http://www.bloodjournal.org/content/124/21/5018?sso-checked=true
https://en.wikipedia.org/wiki/Menometrorrhagia HMG-CoA HMG-CoA (or 3-hydroxy-3-methylglutaryl-coenzyme A) is an intermediate in the mevalonate and ketogenesis pathways. It is formed from acetyl CoA. High fat diet induced HMGCoA reductase activation and increased cholesterol biosynthesis. This may play a role in liver cholesterol accumulation and hypercholesterolemia. https://www.ncbi.nlm.nih.gov/pubmed/23651731
CATEGORY
NAME
TAG
USE
Krebs Cycle™
Enzyme
Succinic thiokinase
L
Catalyzes CoA to succinic acid and libe
Krebs Cycle™
Enzyme
L
AKA succinyl coenzyme A synthetase
Krebs Cycle™
Biochemical
L
Nicotinamide adenine dinucleotide -- es
Krebs Cycle™
Biochemical
Krebs Cycle™
Biochemical
Krebs Cycle™
Biochemical
Krebs Cycle™
Enzyme
Succinic thiokinase Nicotinamide adenine dinucleotide (NAD) Nicotinamide adenine dinucleotide (NAD) Nicotinamide adenine dinucleotide (NAD) Nicotinamide adenine dinucleotide (NAD) Succinic thiokinase
Krebs Cycle™
Enzyme
Krebs Cycle™
Biochemical
Krebs Cycle™
TEMPLATE OCCURS: 6
L L
Isocitrate dehydrogenase and malate de coenzyme Accepts two hydrogen atoms from form into NADH
L
Required for the E3, dihydrolipoyl dehyd
L
Catalyzes CoA to succinic acid and libe
L
AKA succinyl coenzyme A synthetase
L
Nicotinamide adenine dinucleotide -- es
Biochemical
Succinic thiokinase Nicotinamide adenine dinucleotide (NAD) NADPH
L
Enzyme cofactor
Krebs Cycle™
Biochemical
3-phosphoglycerate
L
Krebs Cycle™
Biochemical
3-phosphoglycerate
L
Krebs Cycle™
Biochemical
2-phosphoglycerate
L
Krebs Cycle™
Biochemical
2-phosphoglycerate
L
Metabolic intermediate in glycolysis Precursor for serine, which can, in turn, homoscysteine cycle Metabolic intermediate of glycolysis Catalyzed by enolase into PEP, the nex glucose to pyruvate
OCCURS: 5
Krebs Cycle™
Biochemical
Isocitrate
L
Krebs Cycle™
Biochemical
Isocitrate
L
Krebs Cycle™
Biochemical
Citrate
L
Krebs Cycle™
Biochemical
Citrate
L
Krebs Cycle™
Biochemical
Citrate
L
Krebs Cycle™
Element
Carbon
L
Krebs Cycle™
Enzyme
Malate dehydrogenase
L
Catalyzes the regeneration of oxaloace NAD
Krebs Cycle™
Protein
Malate dehydrogenase, soluble
L
Involved with energy metabolism
Krebs Cycle™
Biochemical
Cis-Aconitate
L
Krebs Cycle™
Biochemical
cis-Aconitic Acid
L
Krebs Cycle™
Biochemical
AMP
L
Krebs Cycle™
Biochemical
Coenzyme A
L
Krebs Cycle™
Biochemical
CoASH
L
Intermediate in the isomerization of citra Hydrated in the Krebs cycle to form isoc enzyme aconitase Stimulates pyruvate dehydrogenase The Krebs cycle consumes Acetyl-CoA 1 part HS-CoA Also known as Coenzyme A
Krebs Cycle™
Enzyme
Co-enzyme A
L
Coenzyme that plays a major role in the
Krebs Cycle™
Enzyme
Co-enzyme A
L
The biosynthesis of Coenzyme A requir
Krebs Cycle™
Biochemical
Glyceraldehyde 3-phosphate L
Serves as an intermediate for metabolic
Krebs Cycle™
Biochemical
Dihydroxyacetone phosphate L
Involved in metabolism of glycolysis me
Krebs Cycle™
Biochemical
Fructose 1,6-bisphosphate L
Krebs Cycle™
Biochemical
Fructose 1,6-bisphosphate L
Krebs Cycle™
Biochemical
Glyceraldehyde 3-phosphate L
Phosphorylated fructose sugar found At some point, the vast majority of gl be converted to this Serves as an intermediate for metabolic
Krebs Cycle™
Biochemical
Dihydroxyacetone phosphate L
Involved in metabolism of glycolysis me
Krebs Cycle™
Biochemical
GDP
L
AKA Guanosine Diphosphate
Krebs Cycle™
Biochemical
L
Serves as long term energy storage (
Krebs Cycle™
Enzyme
L
Inhibited by its own products, succinyl C
Krebs Cycle™
Enzyme
Glycogen alpha-Ketoglutarate dehydrogenase alpha-Ketoglutarate dehydrogenase
L
Catalyzes alpha ketoglutaric acid into su
AKA Isocitric Acid Oxidatively decarboxylated to alpha-ket enzyme Also known as Citric Acid
This is isomerized (same atoms, differe Undergoes dehydration in Krebs cycle a by aconitase The carbon atoms of acetyl CoA are ox
OCCURS: 4
OCCURS: 3
OCCURS: 2
Technician Notes: Possible Mitochondria Dysfunction / Krebs Cycle
TEMPLATE
CATEGORY
NAME
TAG
USE
Nutrition Provider™
Enzyme
Chymopapain
L
fiber - digests
Nutrition Provider™
Enzyme
Chymopapain
L
digestive - digests fiber
Nutrition Provider™
Enzyme
Maltase
L
digestion - digests carbohydrates
Nutrition Provider™
Enzyme
Lactase
L
digestion - digests sugar
Nutrition Provider™
Enzyme
Lactase
L
digestion - digests milk
Nutrition Provider™
Vitamin - co-zyme
Thiamine monophosphate
L
Vitamin coenzyme factor
Nutrition Provider™
Vitamin D3
Vitamin D3
H
AKA - Cholecalciferol
Nutrition Provider™
Vitamin
Citric Acid
H
Krebs (Energy) Cycle component
Nutrition Provider™
Flavonoid
Vitamin P
L
protects and enhances the action of
Nutrition Provider™
Flavonoid
Quercetin
L
capillary protectant
Nutrition Provider™
Flavonoid
Hesperetin
L
varicose veins - may help to treat/preve
Nutrition Provider™
Flavonoid
Bioflavonoids
L
pain - helps in relieving
Nutrition Provider™
Flavonoid
Bioflavonoids
L
Vitamin C and E - essential for the stab
Nutrition Provider™
Cell Salt
Magnesium Phosphate
L
leg cramps - helpful for
Nutrition Provider™
Cell Salt
Magnesium Phosphate
L
menstrual cramps - helpful for
Nutrition Provider™
Cell Salt
Magnesium Phosphate
L
chest cramps - helpful for
Nutrition Provider™
Cell Salt
Magnesium Phosphate
L
feet cramps - helpful for
Nutrition Provider™
Cell Salt
Magnesium Phosphate
L
cramp - helpful where cramping is a pro
Nutrition Provider™
Cell Salt
Silicon oxide
L
constipation - helpful for
Nutrition Provider™
Cell Salt
Silicon oxide
L
waste - may be helpful in purification
Nutrition Provider™
Amino Acid
Cystine
L
skin - aids in formation of
Nutrition Provider™
Amino Acid
Cystine
L
GTF - important part of (glucose toleran
Nutrition Provider™
Amino Acid
Cystine
L
blood - important role in white blood
Nutrition Provider™
Amino Acid
Cystine
L
bronchitis - helps
Nutrition Provider™
Amino Acid
Cystine
L
burns, healing - necessary for
Nutrition Provider™
Amino Acid
Cystine
L
copper - reduces absorption of
OCCURS: 3
OCCURS: 2
Nutrition Provider™
Amino Acid
Cystine
L
cysteine - converted from
Nutrition Provider™
Amino Acid
Cystine
L
sugar - helps in assimilation of
Nutrition Provider™
Amino Acid
Cystine
L
wounds, healing - helpful in, especially
Nutrition Provider™
Amino Acid
Cystine
L
healing, wounds - helpful for
Nutrition Provider™
Amino Acid
Cystine
L
insulin - assists in supply of
Nutrition Provider™
Amino Acid
Cystine
L
oxygen - prevents oxygen from destroyi
Nutrition Provider™
Amino Acid
Cystine
L
pancreas - assists in supply of insulin to
Nutrition Provider™
Amino Acid
Cystine
L
starches, assimilation - aids in
Nutrition Provider™
Amino Acid
Cystine
L
vitamin B6 - important for proper util
Nutrition Provider™
Amino Acid
Cystine
L
vitamin C - prevents oxygen from destro
Nutrition Provider™
Amino Acid
Cystine
L
found in eggs, dairy products, beans, br
Nutrition Provider™
Enzyme
Lipase
L
digestion - digests fats
Nutrition Provider™
Cell Salt
Calcium fluoride
L
ache, back - useful in aiding
Nutrition Provider™
Cell Salt
Calcium fluoride
L
hemorroids - may be helpful in treating
Nutrition Provider™
Cell Salt
Calcium fluoride
L
muscle, ligament, torn - helpful in healin
Nutrition Provider™
Cell Salt
Calcium fluoride
L
vein, varicose - may be helpful in treatin
Nutrition Provider™
Cell Salt
Calcium fluoride
L
skin, cracked - helpful for
Nutrition Provider™
Cell Salt
Calcium fluoride
L
muscle, strain - useful for
Nutrition Provider™
Cell Salt
Calcium fluoride
L
tissue - necessary for proper elastici
Nutrition Provider™
Vitamin B
Orotic Acid
L
AKA - Vitamin B13; used for metaboliza
Nutrition Provider™
Vitamin B
Orotic Acid
L
calcium and magnesium - assists the ab
Nutrition Provider™
Vitamin B
Orotic Acid
L
heart attack - beneficial to take after
Nutrition Provider™
Vitamin B
Orotic Acid
L
genetic material - helps the production o
Nutrition Provider™
Enzyme
Diastase
L
carbohydrates - digests
Nutrition Provider™
Enzyme
Diastase
L
digestion - digests carbohydrates
Technician Notes: http://umm.edu/health/medical/altmed/supplement/cysteine https://breakingmuscle.com/fuel/the-amazing-benefits-of-the-mysterious-vitamin-p
TEMPLATE
CATEGORY NAME
TAG
USE
Maintenance & Repair™
Amino Acid
Taurine
L
May reduce severity of diabetic n
Maintenance & Repair™
Activator
Osteomodulin
L
Induces ectopic bone formation u
Maintenance & Repair™
Activator
Keratocan
L
Scaffolding protein, cornea, inters
Maintenance & Repair™
Protein
Elastin
L
Vascular development
Maintenance & Repair™
Hormone
Luteinizing Hormone
L
Induces muscle growth by stimula
Maintenance & Repair™
Activator
Spectrin beta non-erythrocytic 5
H
Actin cytoskeleton
OCCURS: 2