Factors affecting nutritional status

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Appendix 5 Factors affecting nutritional status

Niikee Schoendorfer, ND, MHSc

A variety of factors other than dietary insufficiency may influence nutritional status and therefore should be taken into account if a particular deficiency is suspected or if a specific condition present. Some conditions may increase the need for a particular nutrient, while others may interfere with its absorption or excretion.

Vitamin A

• Levels are affected by preexisting conditions such as abetalipoproteinaemia, carcinoid syndrome, chronic infections, cystic fibrosis, disseminated tuberculosis, hypothyroidism,1 liver disease or a systemic inflammatory response,2 as well as diseases that cause fat malabsorption, including impaired pancreatic and/or biliary secretions such as Crohn’s and coeliac disease, radiation enteritis, ileal resection or damage.3
• Zinc deficiency impairs the absorption, transport and metabolism of vitamin A.4
• Protein deficiency can markedly affect vitamin A nutriture and in turn vitamin A deficiency can also influence protein metabolism.5
• Preterm infants are generally considered to be at risk because their plasma retinol concentrations are usually low.6

Vitamin B1

• Levels are affected by chronic alcoholism, gastric bypass surgery and gastrointestinal disorders.7
• Thiaminases that degrade thiamine are present in raw fish, fish paste and betel nut.7
• Antithiamine factors are also found in caffeic acid, tannic acid and salicylic acid, as well as blueberries, black currants, red cabbage, beetroot and brussels sprouts.8

Vitamin B2

• Levels are affected by alcoholism,9 diabetes mellitus, thyroid and adrenal insufficiency, liver disease, and gastrointestinal or biliary obstruction.10
• Several metals form chelates or complexes that may affect their bioavailability, such as copper, zinc, iron, tryptophan and vitamins B3 and C, as well as caffeine and saccharin.11
• Protein–energy malnutrition leads to increased urinary losses.12
• Exercise increases requirements.12

Vitamin B3

• Alcoholism, Crohn’s disease and anorexia12

Vitamin B6

• Levels are affected by alcoholism, asthma, carpal tunnel syndrome, gestational diabetes, lactation, malabsorption, malnutrition, neonatal seizures, normal pregnancies, occupational exposure to hydrazine compounds, pellagra, preeclamptic oedema, renal dialysis, uraemia,1 liver disease, oestrogen therapy, rheumatoid arthritis and HIV.13
• Vitamin B6 antagonists exist in foods such as some varieties of mushrooms, flaxseed meal, jack beans and mimosa, possibly via a systemic effect rather than interfering with its absorption.14
• Levels are affected by vitamin B2 deficiency.15

Vitamin B12

• Inadequate peptic digestion and gastric acid,16 pancreatic insufficiency3 and alcoholism may result in deficiency due to inadequate ingestion and absorption, as well as enhanced utilisation and excretion.17
• Bacterial overgrowth,18 tropical or non-tropical sprue, Crohn’s disease and inflammatory bowel disease may cause decreased levels.1
• Absorption through receptor sites in the ileum occurs in alkaline pH in the presence of calcium.10
• Diabetes, leukocytosis, hepatitis, cirrhosis, obesity and protein–energy malnutrition may cause increased levels.1

Folate

• Hyperthyroidism, pregnancy, haemolytic anaemia, the need for intensive care or any other sustained metabolic drain may increase folate need up to six- to eightfold.19
• Malabsorption of folate occurs secondary to an infection with Giardia lamblia and bacterial overgrowth.10
• Achlorhydria, oral contraceptive agents,14 oral oestrogen and antacids affect folate levels.20
• Conditions of increased cellular turnover such as cancer affect folate levels.10
• Vitamin B12 deficiency may induce a secondary folate deficiency by reducing the activity of the enzyme methionine synthase, which activates folate.10

Biotin

• Achlorhydria and alcoholism affect biotin levels.21
• Biotinases that degrade biotin are found in the protein avidin in raw egg white.21

Vitamin C

• Levels are affected by alcoholism, anaemia, cancer, haemodialysis, hyperthyroidism, malabsorption, rheumatoid disease1 and oral contraceptive pills, while acute infection and stress may increase urinary excretion.10
• Deficiency can occur secondary to some disease states such as liver disease, cancer, gastrointestinal disorders, cigarette smoking and environmental exposure.10
• Aspirin usage affects levels.22
• Excess iron and copper affect levels.14
• Pregnancy also lowers serum levels due to haemodilution and active transfer to the fetus, especially during the last trimester.10

Vitamin E

• Fat malabsorption syndromes such as coeliac disease, cystic fibrosis and chronic cholestatic liver disease23, chronic pancreatitis, pancreatic carcinoma, chronic cholestasis,1 gastric surgery and alcoholism affect levels.12
• Levels are affected by abetalipoproteinaemia (which involves a defect in chylomicron synthesis), hyperthyroidism, cirrhosis of the liver, hereditary spherocytosis and β-thalassaemia, as well as associated with conditions such as bronchopulmonary dysplasia and retrolental fibroplasia.24
• Those with protein energy malnutrition25 and premature26 and low birth weight infants27 and children with cystic fibrosis are often found to have a vitamin E deficiency, which may also occur in children with chronic cholestasis.28
• Obstructive liver disease may increase levels.1

Vitamin D

• Nephrotic syndrome, advanced renal failure, chronic liver diseases, severe small-bowel disease, Fanconi’s syndrome, vitamin D-dependent rickets type I, neonatal hypocalcaemia, osteomalacia, osteoporosis, renal osteodystrophy affect levels.24
• Bowel resection, coeliac disease, inflammatory bowel disease, malabsorption, pancreatic insufficiency and thyrotoxicosis affect levels.1
• Magnesium deficiency, which may be due to both the decrease in parathyroid (PTH) secretion and a renal resistance to PTH, affects levels.29
• Lack of exposure to UV light combined with a bad diet affects levels.24
• Increased levels occur in primary hyperparathyroidism associated with hypophosphataemia, vitamin D-dependent rickets type II or sarcoidosis.24

Vitamin K

• Chronic fat malabsorption, liver disease, primary biliary cirrhosis, cancer, surgery and chronic alcoholism,6 Crohn’s disease, ulcerative colitis, chronic gastrointestinal diseases or resection,30 obstructive jaundice, pancreatic disease, diarrhoea in infants, haemorrhagic disease of the newborn and hypoprothrombinaemia affect levels.1
• Levels drop in subjects treated with antibiotics for extended periods, as approximately half of vitamin K intake is provided by bacterial synthesis in the jejunum and ileum.6
• Ingestion of supraphysiological doses of vitamins A and E31 may be inhibited by competitive mechanisms.

Magnesium

• Levels are affected by cardiovascular disease, myocardial infarction, toxaemia of pregnancy, hypertension or postsurgical complications, excessive vomiting and/or diarrhoea, burns, protein malnutrition, malabsorption syndromes, endocrine disorders such as diabetes mellitus, parathyroid disease, hyperparathyroidism with hypercalcaemia, hyperthyroidism and hyperaldosteronism,32,33 as well as alcoholism, chronic glomerulonephritis, haemodialysis, pancreatitis, severe loss of body fluids as in diarrhoea, sweating and laxative abuse.1
• Pregnancy and lactation affect levels.1
• High levels of carbohydrates and ethanol affect levels.34
• Diets high in caffeine, calcium, protein,35 although intakes of protein < 30 g/day may reduce magnesium absorption.10
• High dietary fibre, phytate, oxalate and phosphate intakes reduce magnesium absorption by binding cations.36
• Potassium depletion3 and hypophosphataemia stimulate magnesium excretion.37
• Magnesium also shares a common renal reabsorption pathway with sodium and increased sodium results in magnesuria.32
• Levels may be increased in Addison’s disease, adrenocortical insufficiency, severe diabetic acidosis, multiple myeloma, overuse of antacids, renal insufficiency, systemic lupus erythematosus, tissue trauma,3, increased parathyroid hormone,33 hypocalcaemia, fluid depletion and hypothyroidism inhibit magnesium excretion.34

Calcium

• Hypoparathyroidism,6 hypomagnesaemia,29 phosphate supplementation and impaired vitamin D synthesis are also associated with depression of serum calcium levels.38
• Malabsorption is associated with acute pancreatitis and gastrointestinal diseases such as Crohn’s and coeliac diseases, intestinal resection or bypass, and patients with renal failure caused by the reduced synthesis of 1,25-dihydroxyvitamin D.33
• Calcium absorption may be decreased with age, diabetes, chronic renal failure, non-tropical sprue and primary biliary cirrhosis.6 Low protein diets can also affect calcium absorption39 and cause decreased in bone mineral density.40
• Diets high in protein increase the urinary excretion of calcium, which is not compensated by increased calcium absorption.41 Caffeine and sodium also increase urinary losses, while high phosphorus intakes reduce urinary losses although increased faecal losses, which may negate any effects on calcium balance.33
• Calcium absorption in the intestine may be inhibited by the presence of oxalate, which is found in a variety of vegetables such as spinach, beets, celery, eggplant, greens, okra and squash, as well as fruits such as strawberries, blackberries, blueberries, gooseberries and currants, nuts such as pecans and peanuts, and beverages such as tea, Ovaltine and cocoa. Oxalate chelates calcium and increases faecal excretion of the complex.33
• Divalent cations such as magnesium and calcium compete for intestinal absorption whenever an excess of either is in the gastrointestinal tract, while diets high in phosphorus relative to calcium have also been shown to impair calcium balance.33
• Hyperparathyroidism is the most common cause of hypercalcaemia.6
• Elevated serum levels occur in association with hyperthyroidism, sarcoidosis and when large parts of the body are immobilised, as well as in vitamin D intoxication and in patients with kidney stones, usually due to excessive absorption.10

Zinc

• Malabsorption syndromes such as Crohn’s disease, short bowel syndrome and cystic fibrosis affect levels.42 Increased urinary losses occur in alcohol, cirrhosis, infections, diabetes mellitus, renal tubular diseases, anorexia, starvation, catabolism such as burns, dialysis, pregnancy, oral contraceptives and hypoalbuminaemia.12
• Disease processes such as infection, surgery, pancreatic insufficiency and alcoholism may sometimes alter zinc absorption in humans.43
• Gastric acid secretion inhibition, phytate such as in soy protein, fibre in wheat and corn flour, tea, coffee, cheeses and cow’s milk, calcium supplements and pregnancy affect levels.43
• As albumin appears to be the main portal carrier for newly absorbed zinc. Changes in the systemic level of albumin, such as inflammation or protein deficiency, may also alter zinc balance,43 while high levels of protein intake enhance urinary excretion.41
• Inorganic iron in pharmacological doses may increase zinc uptake, and other studies suggest haem iron has the same effect.43

Iron

• Lead poisoning may be associated with iron deficiency, as lead and iron share a common absorptive mechanism the activity of which is enhanced in iron deficiency.44
• Copper and vitamin A deficiencies can diminish iron status,45 while intermediate to high levels of manganese interfere with iron metabolism as shown by decreased haemoglobin concentrations and reversal by dietary iron supplementation.46
• High levels of zinc also decrease iron bioavailability, but it is not entirely clear whether this is a direct effect or is mediated indirectly through the copper effect on iron metabolism.46 A ratio of 3:1 iron to zinc is desirable to prevent competitive interference.47
• Ascorbic acid enhances the absorption of non-haem iron from foods consumed at the same meal, while absorption of haem iron is not affected by vitamin C intake.45

Selenium

• Catabolic states and deficiency over time may occur with increased oxidative stress and a concurrent inadequate dietary intake.38
• Premature infants are found to have lower plasma concentrations of selenium and glutathione peroxidase than full-term infants. To compound this problem, other commonly used supplements such as iron, calcium and phosphate may impair selenium absorption. These infants also have an increased need because of the high risk of oxidative diseases such as bronchopulmonary dysplasia and retinopathy.48
• Other groups prone to a low status include low birth-weight neonates, alcoholics, patients with Down’s syndrome or acquired immune deficiency disease, and those with malabsorption syndromes such as coeliac disease and cystic fibrosis.10
• Iron deficiency may affect selenium absorption or increasing selenium use in the body. Another possibility is that iron or an iron-containing protein may be needed for glutathione peroxidase activity.33

Iodine

• Secondary iodine deficiency may develop in the presence of a number of diseases of the thyroid gland, pituitary or hypothalamus.10
• Goitrogens that inhibit iodine activity occur naturally in foods such as cabbage, broccoli, turnips and cauliflower, as well as in soybeans and bacterial products of Escherichia coli in drinking water.49
• In populations with a high intake of cassava, the thiocyanate present may act as a goitrogen and impair the uptake of iodine by the thyroid gland.6
• Iodide in large doses has the potential to block the synthesis of thyroid hormone, usually temporarily, after which hormone synthesis resumes.50

EFAs

• Malabsorption, obesity-related bypass surgery, alcoholism, malignancy, biliary disease and multiple sclerosis affect levels, while surgery and trauma patients need increases up to fivefold.12

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