Description
Nutritional Deficiencies
-
Did you know: Malnutrition presents itself in three ways: stunting (shorter-than-average height), wasting (having a low weight for one’s height) and being underweight (having a low weight for one’s age.) borgenproject.org
Common Types
Kwashiorkor
Kwashiorkor is a form of severe protein malnutrition characterized by edema and an enlarged liver with fatty infiltrates. It is caused by sufficient calorie intake, but with insufficient protein consumption, which distinguishes it from marasmus. Kwashiorkor cases occur in areas of famine or poor food supply. Cases in the developed world are rare.
Anemia
Anemia (also spelled anaemia) is a decrease in the total amount of red blood cells (RBCs) or hemoglobin in the blood, or a lowered ability of the blood to carry oxygen. When anemia comes on slowly, the symptoms are often vague and may include feeling tired, weakness, shortness of breath, and a poor ability to exercise. When the anemia comes on quickly, symptoms may include confusion, feeling like one is going to pass out, loss of consciousness, and increased thirst. Anemia must be significant before a person becomes noticeably pale. Additional symptoms may occur depending on the underlying cause.
Vitamin D Deficiency
Vitamin D deficiency, or hypovitaminosis D, most commonly results from inadequate sunlight exposure (in particular sunlight with adequate ultraviolet B rays). Vitamin D deficiency can also be caused by inadequate nutritional intake of vitamin D, disorders limiting vitamin D absorption, and conditions impairing vitamin D conversion into active metabolites—including certain liver, kidney, and hereditary disorders. Deficiency impairs bone mineralization, leading to bone softening diseases such as rickets in children. It can also worsen osteomalacia and osteoporosis in adults, leading to an increased risk of bone fractures. Muscle weakness is also a common symptom of vitamin D deficiency, further increasing the risk of fall and bone fractures in adults.
Scurvy
Scurvy is a disease resulting from a lack of vitamin C (ascorbic acid). Early symptoms of deficiency include weakness, feeling tired and sore arms and legs. Without treatment, decreased red blood cells, gum disease, changes to hair, and bleeding from the skin may occur. As scurvy worsens there can be poor wound healing, personality changes, and finally death from infection or bleeding.
Thiamine Deficiency
Thiamine deficiency is a medical condition of low levels of thiamine (vitamin B₁). A severe and chronic form is known as beriberi. There are two main types in adults: wet beriberi, and dry beriberi. Wet beriberi affects the cardiovascular system resulting in a fast heart rate, shortness of breath, and leg swelling. Dry beriberi affects the nervous system resulting in numbness of the hands and feet, confusion, trouble moving the legs, and pain. A form with loss of appetite and constipation may also occur. Another type, acute beriberi, is found mostly in babies and presents with loss of appetite, vomiting, lactic acidosis, changes in heart rate, and enlargement of the heart.
Folate Deficiency
Folate deficiency, also known as vitamin B₉ deficiency, is a low level of folate and derivatives in the body. Signs of folate deficiency are often subtle. A low number of red blood cells (anemia) is a late finding in folate deficiency and folate deficiency anemia is the term given for this medical condition. It is characterized by the appearance of large-sized, abnormal red blood cells (megaloblasts), which form when there are inadequate stores of folic acid within the body.
Iron Deficiency
Iron deficiency, or sideropaenia, is the state in which a body lacks enough iron to supply its needs. Iron is present in all cells in the human body and has several vital functions, such as carrying oxygen to the tissues from the lungs as a key component of the hemoglobin protein, acting as a transport medium for electrons within the cells in the form of cytochromes, and facilitating oxygen enzyme reactions in various tissues. Too little iron can interfere with these vital functions and lead to morbidity and death.
Vitamin B12 Deficiency
Vitamin B₁₂ deficiency, also known as cobalamin deficiency, is the medical condition of low blood and tissue levels of vitamin B₁₂. In mild deficiency, a person may feel tired and have a reduced number of red blood cells (anemia). In moderate deficiency, soreness of the tongue may occur, and the beginning of neurological symptoms, including abnormal sensations such as pins and needles. Severe deficiency may include symptoms of reduced heart function as well as more severe neurological symptoms, including changes in reflexes, poor muscle function, memory problems, decreased taste, and psychosis. Infertility may occur. In young children, symptoms include poor growth, poor development, and difficulties with movement. Without early treatment, some of the changes may be permanent.
Our Nutritional Deficiencies Test Panel provides insight into how each patient metabolizes key vitamins and nutrients. Dietary vitamins and minerals are critical for nourishment and healing. Deficiencies in essential nutrients can contribute to many health ailments such as vision loss, osteoporosis, anemia, depression and more. Studies indicate that genetics play a large role in nutritional deficiencies. The information provided in the Nutritional report allows for patients and providers to make informed dietary and supplement choices.
Nutritional Health Panel Genetic Markers Include
TEST CATEGORIES | EFFECTS ON NUTRITIONAL HEALTH |
---|---|
Vitamin A | Impacts vision, immune function, and reproductive health |
Vitamin B12 | Deficiencies of this vitamin may lead to fatigue, weakness, megaloblastic anemia, and depression |
Vitamin D | Critical to sustaining healthy bones, prevention of depression, and support of the immune system |
Folate | Required for proper cellular function and the prevention of neural tube defects in utero |
Iron | Maintaining adequate bodily levels of this important mineral prevents iron deficiency anemia |
Ideal Candidates Have The Following Symptoms Or Conditions
- Anemia as evidenced by mucosal or nail bed pallor
- Abnormalities in CBC labs (High or low MCV, low MCH, low HgB, hypersegmented neutrophils)
- Chronic Fatigue
- Frequent illness
- Night blindness
- Rickets or osteomalacia
- Atrophic glossitis
- Poor response to nutritional therapies
- Poor growth in children
Scientific References
- Ferrucci L et al. “Common Variation in the B-Carotene 15, 15’-Monooxygenase 1 Gene Affects Circulating Levels of Carotenoids: A Genome-wide Association Study.” The American Journal of Human Genetics. 2009; 84, 123-133.
- Borel P et al. “Genetic Variations Involved in Interindividual Variability in Carotenoid Status.” Mol Nutr Food Res. 2012; 56(2): 228-40.
- Wyss A et al. Expression pattern and localization of β,β-carotene 15,15′-dioxygenase in different tissues. Biochem. J. 2001; 354:521–529.
- Lietz G et al. “Single Nucleotide Polymorphisms Upstream from the B-Carotene 15, 15’-Monoxygenase Gene Influence Provitamin A Conversion Efficiency in Female Volunteers.” J. Nutr. 2012; 142(1):161S-165S.
- Cheng JB et al. Genetic evidence that the human CYP2R1 enzyme is a key vitamin D 25-hydroxylase. Proc Natl Acad Sci U S A. 2004; 101:7711–7715.
- Ahn J et al. Genome-wide association study of circulating vitamin D levels. Human Molecular Genetics. 2010; 19(13): 2739-2745.
- Nissen J et al. Vitamin D Concentrations in Healthy Danish Children and Adults. PLOS One. 2014; 9(2):e89907.
- Harris HW et al. Supplementation might help patients with depression, seasonal mood disturbances. Current Psych. 2013; 12(4):19-25.
- Houssein-Nezhad A et al. Vitamin D for Health: A Global Perspective. Mayo Clin. Proc. 2013; 88(7):720-755.
- Holick MF and M Garabedian. Vitamin D: photobiology, metabolism, mechanism of action, and clinical applications. In: Favus MJ, ed. Primer on the metabolic bone diseases and disorders of mineral metabolism. 6th ed. Washington, DC: American Society for Bone and Mineral Research. 2006; 129-137.
- Lips P and NM van Schoor. The effect of vitamin D on bone and osteoporosis. Best Pract Res Clin Endocrinol Metab. 2011; 25:585–591.
- Wang T et al. Common genetic determinants of vitamin D insufficiency: a genome-wide association study. Lancet. 2010; 376(9736):180-188.
- Bischoff-Ferrari HA et al. A pooled analysis of vitamin D dose requirements for fracture prevention. N Engl J Med. 2012; 367:40–9.
- Grober U et al. Vitamin D: Update 2013: From rickets prophylaxis to general preventive healthcare. Dermato-Endocrinology. 2013; 5(3):331-47.
- Kelly RJ et al. Sequence and expression of a candidate for the human Secretor blood group alpha (1,2)fucosyltransferase gene (FUT2). Homozygosity for an enzyme-inactivating nonsense mutation commonly correlates with the non-secretor phenotype. J Biol Chem. 1995; 270:4640–4649.
- Hazra A et al. Genome-wide significant predictors of metabolites in the one-carbon metabolism pathway. Hum Mol Gen. 2009; 18(23):4677-4687.
- Semmes BJ. Depression: a role for omega-3 fish oils and B vitamins? Evid. Based Integr. Med. 2005; 2:229–237.
- Tiemeier H et al. Vitamin B12, Folate, and Homocysteine in Depression: The Rotterdam Study. Am J Psychiatry. 2002; 159:2099-2101.
- Frankenburg, FR. The role of one-carbon metabolism in schizophrenia and depression. Harv. Rev. Psychiatry. 2007; 15:146–160.
- Seppälä et al. Association between vitamin b12 levels and melancholic depressive symptoms: a Finnish population-based study. BMC Psychiatry 2013; 13:145.
- Tanaka T et al. Genome-wide Association Study of Vitamin B6, Vitamin B12, Folate, and Homocysteine Blood Concentrations. The American Journal of Human Genetics. 2009; 84:477-482.
- Hazra A et al. Common variants of FUT2 are associated with plasma vitamin B12 levels. Nat. Genet. 2008; 40:1160–1162.
- http://lpi.oregonstate.edu/infocenter/vitamins/vitaminB12/.
- Gozdzik A et al. Association of vitamin D binding protein (VDBP) polymorphisms and serum 25(OH)D concentrations in a sample of young Canadian adults of different ancestry. J Steroid Biochem Mol Biol. 2011; 127:405–412.
- Ahn J et al. Genome-wide association study of circulating vitamin D levels. Human Molecular Genetics. 2010; 19(13) 2739-2745.
- Nissen J et al. Vitamin D Concentrations in Healthy Danish Children and Adults. PLoS One. 2014; 9(2):e89907.
- Foucan L et al. Polymorphisms in GC and NADSYN1 Genes are associated with vitamin D status and metabolic profile in non-diabetic adults. BMC Endocrine Disorders. 2013; 13:36.
- Wang T et al. Common genetic determinants of vitamin D insufficiency: a genome-wide association study. Lancet. 2010; 376(9736):180-188.
- Grober U et al. Vitamin D: Update 2013: From rickets prophylaxis to general preventive healthcare. Dermato-Endocrinology. 2013; 5(3):331-47.
- Bischoff-Ferrari HA et al. A pooled analysis of vitamin D dose requirements for fracture prevention. N Engl J Med. 2012; 367:40–9.
- Wagner C. Biochemical role of folate in cellular metabolism. In: Bailey LB, editor. Folate in health and disease. New York, NY: Marcel Dekker Inc.; 1995. p. 23–42.
- Bailey LB and JF Gregory III. Polymorphisms of Methylenetetrahydrofolate Reductase and Other Enzymes: Metabolic Significance, Risks and Impact on Folate Requirement. J Nutr. 1999; 129(5):919-22.
- Stover PJ. Polymorphisms in 1-Carbon Metabolism, Epigenetics and Folate-Related Pathologies. J. Nutrigenet Nutrigenomics. 2012; 4(5):293-305.
- Refsum H et al. The Hordaland Homocysteine Study: A Community-Based Study of Homocysteine, Its Determinants, and Associations with Disease. J Nutr. 2006; 136:1731S-1740S.
- Frosst P et al. A candidate genetic risk factor for vascular disease: a common mutation in methylenetetrahydrofolate reductase. Nat Genet. 1995; 10:111–113.
- Van der Put NM et al. A second common mutation in the methylenetetrahydrofolate reductase gene: an additional risk factor for neural-tube defects? Am J Hum Genet. 1998; 62(5):1044–51.
- Weisberg I et al. A second genetic polymorphism in methylenetetrahydrofolate reductase (MTHFR) associated with decreased enzyme activity. Mol Genet Metab. 1998; 64:169–72.
- Teng Z. The 677C>T (rs1801133) polymorphism in the MTHFR gene contributes to colorectal cancer risk: a meta-analysis based on 71 research studies. PLoS One. 2013; 8(2):e55332.
- Hara N et al. Molecular identification of human glutamine- and ammonia-dependent NAD synthetases. Carbon-nitrogen hydrolase domain confers glutamine dependency. J. Biol. Chem. 2003; 278(13):10914-10921.
- Wassif CA et al. Mutations in the human sterol Δ7-reductase gene at 11q12–13 cause Smith–Lemli–Opitz syndrome. Am. J. Hum. Genet. 1998; 63:55–62.
- Wang T et al. Common genetic determinants of vitamin D insufficiency: a genome-wide association study. Lancet. 2010; 376(9736):180-188.
- Harris HW et al. Supplementation might help patients with depression, seasonal mood disturbances. Current Psych. 2013; 12(4):19-25.
- Houssein-Nezhad A et al. Vitamin D for Health: A Global Perspective. Mayo Clinic. Proc. 2013; 88(7):720-755.
- Bischoff-Ferrari HA et al. A pooled analysis of vitamin D dose requirements for fracture prevention. N Engl J Med. 2012; 367:40–9.
- Grober U et al. Vitamin D: Update 2013: From rickets prophylaxis to general preventive healthcare. Dermato-Endocrinology. 2013; 5(3):331-47.
- Stoltzfus RJ. Iron deficiency: global prevalence and consequences. Food Nutrition Bulletin. 2003; 24:S99–S103.
- Patel KV. “Variability and heritability of hemoglobin concentration: an opportunity to improve understanding of anemia in older adults.” Haematologica 2008; 93:1281-1283.
- Benyamin B et al. Common variants in TMPRSS6 are associated with iron status and erythrocyte volume. Nature Genetics 2009; 41:1173-1175.
- Chambers JC et al. Genome-wide association study identifies variants in TMPRSS6 associated with hemoglobin levels. Nature Genetics 2009; 41:1170-1172.
- Morris HA. Vitamin D Activities for Health Outcomes. Ann Lab Med 2014; 34:181-186.
- Turner AG. Vitamin D and bone health. Scand J Clin Lab Invest Suppl. 2012; 243:65-72.
- Palomba S et al. BsmI vitamin D receptor genotypes influence the efficacy of antiresorptive treatments in postmenopausal osteoporotic women. A 1-year multicenter, randomized and controlled trial. Osteoporosis Int. 2005; 16(8):943-52.
- Jia F et al. Vitamin D receptor BsmI polymorphism and osteoporosis risk: a meta-analysis from 26 studies. Genet Test Mol Biomarkers. 2013; 17(1):30-4.
- Ji GR. BsmI, TaqI, ApaI and FokI polymorphisms in the vitamin D receptor (VDR) gene and risk of fracture in Caucasians: a meta-analysis. Bone. 2010; 47(3):681-6.
- Bischoff-Ferrari HA et al. A pooled analysis of vitamin D dose requirements for fracture prevention. N Engl J Med. 2012; 367:40–9.
- Grober U et al. Vitamin D: Update 2013: From rickets prophylaxis to general preventive healthcare. Dermato-Endocrinology. 2013; 5(3):331-47.
Reviews
There are no reviews yet.