MT, et al. Associations between hyponatraemia, volume depletion and the risk of falls in US hospitalised patients: a case‐control study. BMJ Open. 2017; 7(8):e017045.
31 31. Rittenhouse KJ, To T, Rogers A, et al. Hyponatremia as a fall predictor in a geriatric trauma population. Injury. 2015; 46(1):119–123.
32 32. Chung MC, Yu TM, Shu KH, et al. Hyponatremia and increased risk of dementia: A population‐based retrospective cohort study. PLoS One. 2017; 12(6):e0178977.
33 33. Gankam Kengne F, Andres C, Sattar L, Melot C, Decaux G. Mild hyponatremia and risk of fracture in the ambulatory elderly. QJM. 2008; 101(7):583–588.
34 34. Usala RL, Fernandez SJ, Mete M, et al. Hyponatremia is associated with increased osteoporosis and bone fractures in a large US health system population. J Clin Endocrinol Metab. 2015; 100(8):3021–3031.
35 35. Murthy K, Ondrey GJ, Malkani N, et al. The effects of hyponatremia on bone density and fractures: a systematic review and meta‐analysis. Endocr Pract. 2019; 25(4):366–378.
36 36. Corona G, Norello D, Parenti G, Sforza A, Maggi M, Peri A. Hyponatremia, falls and bone fractures: A systematic review and meta‐analysis. Clin Endocrinol (Oxf). 2018; 89(4):505–513.
37 37. Upala S, Sanguankeo A. Association between hyponatremia, osteoporosis, and fracture: a systematic review and meta‐analysis. J Clin Endocrinol Metab. 2016; 101(4):1880–1886.
38 38. Verbalis JG, Barsony J, Sugimura Y, et al. Hyponatremia‐induced osteoporosis. J Bone Miner Res. 2010; 25(3):554–563.
39 39. Abraham WT, Decaux G, Josiassen RC, et al. Oral lixivaptan effectively increases serum sodium concentrations in outpatients with euvolemic hyponatremia. Kidney Int. 2012; 82(11):1215–1222.
40 40. Verbalis JG, Ellison H, Hobart M, Krasa H, Ouyang J, Czerwiec FS. Tolvaptan and neurocognitive function in mild to moderate chronic hyponatremia: a randomized trial (INSIGHT). Am J Kidney Dis. 2016; 67(6):893–901.
41 41. Bhandari S, Peri A, Cranston I, et al. A systematic review of known interventions for the treatment of chronic nonhypovolaemic hypotonic hyponatraemia and a meta‐analysis of the vaptans. Clin Endocrinol (Oxf). 2017; 86(6):761–771.
42 42. Hannon MJ, Behan LA, O'Brien MM, et al. Hyponatremia following mild/moderate subarachnoid hemorrhage is due to SIAD and glucocorticoid deficiency and not cerebral salt wasting. J Clin Endocrinol Metab. 2014; 99(1):291–298.
43 43. Fenske W, Stork S, Blechschmidt A, Maier SG, Morgenthaler NG, Allolio B. Copeptin in the differential diagnosis of hyponatremia. J Clin Endocrinol Metab. 2009; 94(1):123–129.
44 44. Koenig MA, Bryan M, Lewin JL, 3rd, Mirski MA, Geocadin RG, Stevens RD. Reversal of transtentorial herniation with hypertonic saline. Neurology. 2008; 70(13):1023–1029.
45 45. Garrahy A, Dineen R, Hannon AM, et al. Continuous versus bolus infusion of hypertonic saline in the treatment of symptomatic hyponatremia due to SIAD. J Clin Endocrinol Metab. 2019.
46 46. Peri A. Clinical review: the use of vaptans in clinical endocrinology. J Clin Endocrinol Metab. 2013; 98(4):1321–1332.
47 47. Gheorghiade M, Konstam MA, Burnett JC, Jr., et al. Short‐term clinical effects of tolvaptan, an oral vasopressin antagonist, in patients hospitalized for heart failure: the EVEREST Clinical Status Trials. Jama. 2007; 297(12):1332–1343.
48 48. Dasta JF, Sundar S, Chase S, Lingohr‐Smith M, Lin J. Economic impact of tolvaptan treatment vs. fluid restriction based on real‐world data among hospitalized patients with heart failure and hyponatremia. Hospital practice (1995). 2018; 46(4):197–202.
49 49. Liber M, Sonnenblick M, Munter G. Hypernatremia and copeptin levels in the elderly hospitalized patient. Endocr Pract. 2016; 22(12):1429–1435.
50 50. Nigro N, Winzeler B, Suter‐Widmer I, et al. Copeptin levels and commonly used laboratory parameters in hospitalised patients with severe hypernatraemia – the ‘Co‐MED study’. Crit Care. 2018; 22(1):33.
51 51. Davies I, O'Neill PA, McLean KA, Catania J, Bennett D. Age‐associated alterations in thirst and arginine vasopressin in response to a water or sodium load. Age Ageing. 1995; 24(2):151–159.
CHAPTER 16 Vitamins and minerals
Mary Ann Johnson1s and Connie W. Bales2
1 Department of Nutrition and Health Sciences, University of Nebraska Lincoln, Lincoln, Nebraska, USA
2 Geriatric Research, Education and Clinical Center, Durham VA Medical Center, Department of Medicine, Duke University School of Medicine, Durham, North, Carolina, USA
Introduction
Essential vitamins and minerals are also known as micronutrients. While required in minute quantities, these nutrients are essential for life. They are uniquely required for essential biological and structural functions in the body, including as hormones, antioxidants, and enzyme cofactors and for one‐carbon metabolism and DNA synthesis. Because they cannot be synthesized in adequate quantities in the human body, they must be consumed from external sources such as foods, fortified or enriched foods, and/or dietary supplements. Vitamins are characterized as water‐soluble (e.g. B vitamins and vitamin C) or fat‐soluble (vitamins A, D, E, and K).
The shortfall in calorie and protein intake in many older adults is well recognized and the focus of considerable attention (see Chapters 12–14). Less appreciated is the concomitant risk of multiple micronutrient deficiencies. The same age‐associated changes in food intake that contribute to protein‐calorie inadequacies can also contribute to deficiencies of multiple micronutrients and are related to many different factors. These include age, psychological factors, physiological decrements, chronic disease, and medical factors.1 Inadequate micronutrient intake can lead to suboptimal cellular and physiological functions even before developing a ‘classic’ and symptomatic deficiency syndrome.2
Age‐related causes of suboptimal diet intake include anorexia of ageing, decreased olfaction, and decreased taste ability. Social factors include poverty, isolation, lack of knowledge, low health literacy, difficulties with meal preparation, inability to shop, and lack of culturally appropriate foods in the community, hospital, assisted living, or long‐term care. Psychological factors related to low nutrient and energy intake include depression, bereavement, addiction (alcoholism), dementia, paranoia, mania, anorexia tardive, and sociopathy. Physiological and chronic health problems include difficulties chewing and/or swallowing, gastrointestinal disease, hepatic disease, renal disease, and some drug‐nutrient interactions. Gastrointestinal disorders may decrease absorption of nutrients, while renal disease may alter excretion of nutrients, and renal and/or liver disease may alter metabolism to active forms (e.g. conversion of vitamin D to an active form, 1,25‐dihydroxyvitamin D). Several medical factors of concern for insufficient nutrient and energy intake and/or status are summarized in Table 16.1.1
Recommended intakes of vitamins and minerals
Recommendations for macronutrient intake (carbohydrate, fat, and protein) are typically stipulated by groups of experts in specific countries or geographic regions. National governments play a critical role in setting policies that promote adequate nutrient intake and improve public health, and there is global recognition of this approach for setting intake recommendations.2,3 In the US (National Academies of Sciences, Engineering, and Medicine [NASEM]) and Canada (Health Canada), recommendations for nutrient intakes, including vitamins and minerals, are based on life stage and gender for healthy individuals and include the following:
Estimated average requirement (EAR): The average intake level estimated