Micronutrient Deficiencies in Older Adults in Latin America: A Narrative Review

Commonly Measured Micronutrient Biomarkers

A total of 28 studies reported one or more MDs in OA in Latin America in 8 Latin American countries (Table 1). National health surveys and aging surveys conducted in Chile, Ecuador, Brazil, Costa Rica, and Mexico reported MD in their OA populations. In addition, MD prevalence was reported through local (community-based) studies in the same countries, with the addition of Argentina, Peru, and Venezuela.

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Table 1.

Summary of Studies Documenting the Prevalence of Micronutrient Deficiencies in Older Latin Adults.

Micronutrienta	Country	Year of study	Definition	Age group	Prevalence %	Study setting	Ref
Vitamin B12	Brazil	2011	B12 (<140 pg/mL)	≥60 y	17.4	Community	12
	Chile	2000b	B12 (<74 pmol/L)	Women ≥60 y	2.8	Urban community	13
				Men ≥60 y	6.5
			B12 (<148 pmol/L)	Women ≥60 y	30.9
				Men ≥60 y	51.1
		2005-2008	B12 (<148 pmol/L)	≥65 y	12.0	Community	14
				Women ≥65 y	9.0
				Men ≥65 y	18.2
			B12 (148-221 pmol/L)	≥65 y	13.4
				Women ≥65 y	10.9
				Men ≥65 y	18.8
		2009-2010	B12 (≤200 pg/mL)	≥60 y	8.1	Population based	15
				Women ≥60 y	9.2
				Men ≥60 y	6.6
		2020	B12 (≤200 pg/mL)	≥60 y	16.1	Hospital based	16
	Costa Rica	2008-2009	B12 (<193pg/mL)	≥65 y	5.3	Population based	17
	Ecuador	2003-2004	B12 (<185 pmol/L)	Women ≥65 y	19.6	Peri-urban Community	18
				Men ≥65 y	20.5
		2009-2010	B12 (≤350 pg/mL)	Women ≥60 y	30.6	Population based	19
				Men ≥60 y	47.8
	Mexico	2003-2004	B12 (<150 pmol/L)	≥60 y	30.0	Urban Community	20
		2015	B12 (<−0.5 SD)	≥60 y	9.0	Urban-Community	21
	Peru	2014-2020	B12 (<80 pg/mL)	≥60 y	21.0	Hospital based	22
Folate	Chile	1999-2000	Folate (<6.8 nmol/L)	≥70 y	1.8	Community	23
		2000	Folate (<7 nmol/L)	Women ≥60 y	33.1	Community	13
				Men ≥60 y	50.5
		2009-2010	Folate (≤4.4 µg/L)	≥60 y	0.3	Population based	15
				Women ≥60 y	0.4
				Men ≥60 y	0.1
	Costa Rica	2008-2009	Folate (≤6.0 ng/mL)	≥65 y	1.4	Population based	17
	Ecuador	2003-2004	Folate (<11.3 nmol/L)	Women ≥65 y	27.4	Peri-urban Community	18
				Men ≥65 y	37.0
	Mexico	2003-2004	Folate (<3 ng/mL)	≥60 y	0.0	Community	20
		2015	Folate (<4 ng/mL)	≥60 y	0.0	Community	21
	Peru	2014-2020	Folate (<3 ng/dL)	≥60 y	1.7	Hospital based	22
	Venezuela	2007	Folate (<3 ng/mL)	≥60 y	12.5	Community	24
Vitamin D (25(OH)D)	Argentina	2004	Deficiency < 10 ng/mL	≥65 y	North = 2	Urban community	25
					Center = 11
					South = 14
			Insufficiency 10-20 ng/mL		North = 52
					Center = 64
					South = 87
			Hypovitaminosis 20-40 ng/mL		North = 46
					Center = 35
					South = 13
	Brazil	2000-2001	Deficiency <25 nmol/L	>65 y	15.4	Urban community	26
			Insufficiency 25-50 ng/mL		41.9
		2000-2017	Deficiency <20 ng/mL	≥60 y	41.53	Meta-analysis	27
			Insufficiency 20-30 ng/mL		45.85
		2015-2016	insufficiency and deficiency <50 nmol/L	Women ≥60 y	60	Population based cohort study	28
	Chile	2006	Deficiency <20 ng/mL	≥60 y	70.2	Community	29
				Women ≥60 y	82.5
				Men ≥60 y	55.3
			Insufficiency 20-29.9 ng/mL	≥60 y	24
				Women ≥60 y	14
				Men ≥60 y	36.2
		2016-2017	Deficiency <20 ng/mL	≥65 y	59.5	Population based	30
			Insufficiency ≥20 ng/mL		40.5
	Ecuador	2003-2004	Deficiency <20 ng/mL	Women ≥65 y	9.4	Community	18
				Men ≥65 y	18.8
		2009	Deficiency <20 ng/mL	≥60 y	21.6	Population based	31
				Women ≥60 y	29.6
				Men ≥60 y	11.5
			Insufficiency < 30 ng/mL	≥60 y	67.8
				Women ≥60 y	77.4
				Men ≥60 y	55.9
	Guatemala	2010	Deficiency <50 nmol/L	≥60 y	50.0	Community	32
			Insufficiency 50-80 nmol/L		46.3
	México	2012	Deficiency ≤20 ng/mL	≥60 y	36.9	Population based cohort study	33
				Women ≥60 y	46.8
				Men ≥60 y	26.3
		2015	Deficiency <50 nmol/L	≥60 y	9.7	Urban Community	21
		2020	Deficiency <20 ng/mL	≥60 y	34.2	Community	34
			Insufficiency 20-30 ng/mL		41.1
		2021	Deficiency <40 nmol/L	Women ≥60 y	49.1	Community	35
	Puerto Rico	2011	Deficiency <20 ng/mL	≥ 60 y	19.5	Community	36
			Insufficiency 20-30 ng/mL		43.4
	Tobago	1997-2003	Deficiency <20 ng/mL	≥60 y	2.8	Population-based cohort study	37
			Insufficiency 20-29 ng/mL	≥60 y	24.1
Iron	Brazil	2015	Depleted iron stores = s-ferritin <15 μg/L adjusted by CRP	≥60 y	1.9	Population-based	38
				Women ≥60 y	1.8
				Men ≥60 y	2
	Ecuador	2003-2004	s-Iron < 8.95 μmol/L women	Women ≥65 y	5	Urban community	18
			s-Iron < 11.6 μmol/L men	Men ≥65 y	4
	Mexico	2012	S-ferritin < 15 μg/L adjusted by CRP	≥60 y	4.2	Population based	39
				Women ≥60 y	1.3
				Men ≥60 y	4
		2015	S-ferritin < 15 adjusted by CRP and AGP & sTfR > 28 nmol/L	≥60 y	5.1	Urban community	21
		2018	S-ferritin <15 μg/L adjusted by CRP	≥60 y	5	Population-based	40
				Men ≥60 y	4.4
				Women ≥60 y	5.4
Vitamin A	Chile	2000	Retinol (<0.35 µ mol/L)	Women ≥60 y	15.9	Community	13
				Men ≥60 y	13.7
	Ecuador	2003-2004	Retinol (<1.05 µmol/L)	Women ≥65 y	4.1	Peri-urban Community	18
				Men ≥65 y	0.8
	Mexico	2015	Retinol (≤20 µg/dL)	≥60 y	3.4	Urban-Community	41
Copper	Chile	2000	Copper (<11.0 µ mol/L)	Women ≥60 y	5.1	Community	13
				Men ≥60 y	6.5
	Ecuador	2003-2004	Copper (<13.2 µmol/L)	Women ≥65 y	12.4	Peri-urban Community	18
				Men ≥65 y	16.7
Vitamin E	Ecuador	2003-2004	Vitamin E (<11.6 µmol/L)	Women ≥65 y	9.4	Peri-urban Community	18
				Men ≥65 y	18.8
Vitamin C	Ecuador	2003-2004	Vitamin C (<11.4 µmol/L)	Women ≥65 y	32.6	Peri-urban Community	18
				Men ≥65 y	59.8
Selenium	Costa Rica	2008-2009	Selenio (<60 µ/L)	≥65 y	29.0	Population based	17
Zinc	Brazil	2018-2019	Zinc (<70 µg/dL)	≥60 y	3.9	Community	42
	Ecuador	2003-2004	Zinc (<10.7 µmol/L)	Women ≥65 y	45.4	Peri-urban Community	18
				Men ≥65 y	41.3

Abbreviation: CRP, C-reactive protein; AGP, Alpha(1)-Acid glycoprotein; sTfR: serum soluble transferrin receptor.

^a Data on micronutrient are ordered according to its description in the manuscript.

^b Not specified. Year of publication.

Vitamin B12 and Folate Deficiency

Ecuador, ¹⁹ Chile, ¹⁵ and Costa Rica ¹⁷ reported the prevalence of low vitamin B12 levels in OA from representative surveys (Table 1), with a large heterogeneity in the prevalence of Vitamin B12 deficiency (B12D) by sex, and when data was gathered from local studies.

The active forms of Vitamin B12 are methylcobalamine and adenosylcobalamin, they act as cofactors in 2 separate metabolic reactions, with cytosolic methionine synthase and mitochondrial methymalonyl CoA mutase. The disruption of either of these reactions can lead to B12 deficiency. In B12D, decreased levels of adenosylcobalamin lead to an increase in methylmalonyl-CoA, which affects synthesis of neuronal myelin in the developing central nervous system; while decreased levels of methylcobalamine leads to the functional deficiency of folate and accumulation of homocysteine. ^43,44 B12 metabolism is linked with folate-mediated one-carbon metabolism due to the utilization of 5-methyltetrahydrofolate as a methyl donor. ⁴⁴ Both, B12 and folate deficiency (FD), affect DNA synthesis with resulting macrocytic anemia. B12D increases cellular inflammation (hypersegmented neutrophils) and the synthesis of intermediate metabolites such as homocysteine and methylmalonic acid (MMA). ⁴⁴ Increased levels of homocysteine and MMA can result in severe damage to the brain and spinal cord, particularly in the corticospinal and spinocerebellar tracts, resulting in ataxia, neuropathy and in later life, cognitive decline. ⁴⁵ There are numerous studies exploring B12D in older populations due to the association with cognitive decline, impaired executive function, and the risk of dementia. The OA population is at higher risk of B12D due to malabsorption secondary to gastric atrophy, diminished intrinsic factor and hydrochloric acid. ⁴⁶ In Latin America, B12D has been widely studied in the Chilean population, with the Government responding with public health initiatives to address deficiencies. ⁴⁷ Along with Chile, ⁴⁸ Ecuador, ¹⁹ and Peru ²² have also documented the role of subclinical B12 deficiency on cognitive function in OA, with contradictory findings. In a cross-sectional study of older Cuban adults, higher homocysteine levels and FD but not B12D were associated with mild cognitive impairment. ⁴⁹ Daily fluctuations of B12 levels in serum may not properly reflect the true B12 status. What might be useful are combinatory approaches for measuring multiple, related indicators of VB12 levels in OA. For example, measuring the intermediate metabolites homocysteine and MMA, or others involved in the transport of B12 such as holotranscobalamin, which when combined, might improve sensitivity in the diagnosis of B12D. ⁵⁰

Since the introduction of the mandatory folate fortification in wheat and corn flour in some Latin American countries, ⁵¹ FD has dropped below 1% prevalence in OA. As such, FD is no longer considered an ongoing public health challenge in those countries. ⁵¹ Only a few studies have documented FD in OA. However, supraphysiological levels of folate have been reported in older Chilean and Mexican populations (Table 2). Elevated folate levels have been implicated in exacerbating B12D. ⁵² The mechanism of folate-VB12 interaction is not well understood; however, there is some evidence that high folate levels (HFL) decrease the effectivity of vitamin B12 treatment in B12D. ⁵³ In some studies, HFL and low vitamin B12 has been linked to impaired cognition in OA, ^54,55 but in other studies, authors have documented high folate levels associated with higher score in cognitive function, independent of B12 levels. ^56,57 More research is needed to better understand how low levels of vitamin B12 (subclinical deficiency) interact with high levels of folate in the progression of cognitive decline.

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Table 2.

Supraphysiological Levels of Folate and Iron in Older Population From Selected Studies in the Latin American Region.

Micronutrient	Country	Year of study	Definition	Age group	Prevalence %	Study setting	Ref
Folate	Chile	2009-2010	>20 µg/L	≥65 y	48.6	Population based	15
				Women ≥65 y	48.5
				Men ≥65 y	48.7
	Mexico	2003-2004	Folate >17 ng/mL	≥60 y	62	Urban-Community	20
		2015	Folate >17 ng/mL	≥60 y	5.1	Urban-Community	21
Iron	Brazil	2015	s-ferritin>150 μg/L	Women ≥60 y	NOa	Population based	38
			s-ferritin>200 μg/L	Men ≥60 y	35.8
	Mexico	2015	s-ferritin>150 μg/L women and >200 μg/L in men	≥60 y	29.8	Urban-Community	21
			s-ferritin>350 μg/L adjusted by CRP	≥60 y	7.35

Abbreviation: CRP, C-reactive protein.

^a NO: no observations.

Vitamin D Deficiency

Brazil, ²⁸ Chile, ³⁰ Ecuador, ⁵⁸ and Mexico ³³ reported the prevalence of low vitamin D levels in OA from representative surveys (Table 1). Vitamin D (VD) status is the most reported micronutrient in the LAC region. Both, VD insufficiency and deficiency (VDD) are highly prevalent in OA, reaching a prevalence (25[OH]D <20 ng/mL) higher than 50% in Brazil ²⁸ and Chile, ³⁰ which is comparable with other LMIC. ⁵⁹ Most studies have used 25[OH]D levels for classifying VDD in OA populations. ⁶⁰

At the community level, the VDD prevalence in OA varied, probably due to sample characteristics, seasonality (more prevalent in winter), and latitude (Table 1). Two metanalyses ^27,61 have been conducted to estimate VDD in the region, showing a prevalence of 41.5% (95%CI: 27.6, 55.4) in older Brazilian adults, and 34.8% (95%CI: 29.7, 40.2) in all age groups in the South-American Region.

Sun exposure is the primary source of vitamin D for the human body ⁶⁰ with dietary intake of VD making a smaller contribution to VD status. ^62,63 Advanced age has been associated with a lower capacity for the body to synthesize vitamin. ^64,65 In addition, OA with chronic comorbidities (such as obesity, diabetes, kidney disease) ⁶⁶ have impaired absorption and metabolism of vitamin D. ^67,68 Therefore, supplements of VD are often required to reach the daily intake recommendation.

Vitamin D (along with vitamin A) regulates gene expression and acts as transcription factor for multiple genes that modulate the immune response. ^69,70 VD is essential for maintaining bone, muscle health, and erythropoiesis, therefore, its deficiency can have a significant impact on quality of life for OA. ^71,72

Vitamin D deficiency increases the risk of osteoporosis, bone fractures, type 2 diabetes, respiratory diseases, sleep disorders, depression, impaired cognition, cardiovascular disease, autoimmune diseases, and some types of cancer. ^69,72,73 Older adults with VDD have a higher risk of falls, sarcopenia, and decreased functional capacity, which can in turn lead to increased frailty, dependence, and disability. ^71,73

Recent systematic reviews and meta-analysis has suggested a correlation between low Vitamin D and impaired cognitive function. ^72,74,75 Evidence from a number of observational studies is contradictory, possibly due to residual confounding. For instance, in one study, VDD was not associated with cognitive function in OA from Ecuador. ¹⁹ In other studies, metanalysis exploring supplementation of VD did not show any effect on cognition or depression. ^76,77

During the COVID-19 pandemic, VD was studied in several populations due its role in strengthening the immune system by modulating the inflammatory response during infection. For all age groups, including OA, VDD was associated with COVID-19 severity and mortality ^78,79 Supplementation with VD may contribute to the prevention and management of COVID-19 infection. ⁷⁹ Nonetheless, a causal relationship between vitamin D status, VD supplementation, and COVID-19 (incidence, severity and progression) has not been established due to methodological differences in those studies.

Iron Deficiency

Information about iron deficiency (ID) in OA is scant. In those studies that report it (Mexico and Brazil), the prevalence of ID was around 5% or less. ^38,40 Low iron stores, and ID, are typically defined by measuring s-ferritin levels (an acute phase protein). However, established thresholds for defining ID are based on adult populations that do not take into account any normative changes that might occur in OA. ⁸⁰ The diagnosis of ID is challenging in OA since low grade inflammation secondary to the aging process (inflammaging), infection and chronic comorbidities may all increase ferritin levels. Functional ID can be the result of inflammation (for example caused by infection, cancer, rheumatoid arthritis, autoimmune disease or, chronic disease), ⁸¹ as a result of increased hepcidin, a protein that blocks iron export from ferroportin in the epithelial cells thereby limiting iron availability in the bone marrow. In the presence of infection, the body reduces circulating iron in an attempt to combat pathogens. ⁸² Consequently, prolonged iron deprivation (referred to as functional iron deficiency) can lead to anemia of chronic diseases or anemia of inflammation. ⁸³ To improve diagnosis specificity for ID, the use of s-ferritin as an indicator should be used in conjunction with inflammatory biomarkers to generate a more reliable indicator of overall iron status. ⁸⁴ Iron deficiency and anemia are detrimental to health. Iron deficiency is the main cause of anemia in younger populations in LMIC ⁸⁵ and it is estimated to be the second leading cause in OA. ⁸⁶ Few studies have documented the causes of anemia in OA in Latin America. ^21,87,88

Iron deficiency leads to poor quality of life and disability. ⁸⁹ It has also been established that ID anemia (IDA) increases the risk of morbidity and mortality in OA. ^90,91 The causes of ID in OA are usually associated with gastrointestinal blood loss (caused by varices in portal hypertension, gastritis, ulcers, inflammatory bowel diseases, among others) which can lead to IDA. In addition, alcohol abuse, malnutrition, and chronic diseases as chronic renal failure and inflammatory diseases can also result in ID and lead to IDA.

Iron is a trace mineral essential for maintaining normal physiological processes involved in the electron transport chain, mitochondrial respiration, DNA synthesis, and synthesis of heme, myelin, and neurotransmitters. Due to its role in redox activity, iron is tightly regulated in the body. Excessive iron results in catalyzed oxidative reactions that generate reactive oxygen species (ROS). ROS (oxidative stress) causes DNA damage, lipid peroxidation, and aberrant posttranslational modification of proteins. ⁹² In mitochondria, energy production generates ROS. Iron utilization in the mitochondria requires proteins to regulate iron homeostasis (frataxin, mitoferrin) since it is vulnerable to iron-induced oxidative stress. The loss of mitochondrial iron homeostasis in combination with iron accumulation, may contribute to mitochondrial decay, which is characteristic of aging. ⁹³ These mitochondrial changes may be involved in the pathogenesis of age-related neuro-muscular degeneration (muscle atrophy, sarcopenia). ⁹³ As part of normal aging, the central nervous system shifts into a pro-inflammatory state, with increases in glial cells numbers and increased permeability of the blood–brain barrier. These ageing-related changes can lead to regional increases in brain iron ⁹⁴ which in turn has been correlated with the presence of neurodegeneration. ^95,96 To date, this correlation has not been shown to be causal. ^95,97 Evidence from observational studies linked high ferritin levels and neurodegeneration has been inconclusive. High ferritin levels have been linked to cardiovascular disease, diabetes, and increased mortality in the older adult population. ^98,99 Two studies in the Latin American region (Brazil and Mexico) reported a higher prevalence of increased ferritin levels in OA. To better understand the nature of the relationship (correlation, cause, or consequence) between increased iron levels and aging, more research in the LAC region is needed.

Vitamin A Deficiency

Few countries (Chile, Mexico, and Ecuador) have reported the prevalence of Vitamin A (VA, also known as retinol) deficiency in older Latin America population, with estimates of less than 5% prevalence (Table 1).

Vitamin A is a liposoluble vitamin that plays an important role in gene expression, transcription, stem cell differentiation, cell proliferation, vision, growth, maintenance of epithelial cellular integrity, and immune function. ¹⁰⁰ Vitamin A deficiency leads to a depleted immune system, night blindness, altered bone metabolism, ¹⁰¹ and increased risk of respiratory infections. ¹⁰² Retinoic acid (the main metabolite of VA) has been reported to have neuroprotective effects in the amyloid signaling cascade, as well a role in synaptic plasticity, associated with memory. ^103,104 We previously reported a cross-sectional association of low serum retinol with lower verbal fluency in older Mexican adults. ⁴¹ In older Cuban adults, vitamin A deficiency was cross-sectionally associated with increased risk for mild cognitive impairment. ⁴⁹ Moreover, higher retinol levels have been associated with higher adverse events in other OA populations (lower bone density, cardiovascular risk, and mortality). ^101,102

Copper, Zinc, Vitamin E, Vitamin C Selenium, and Magnesium Deficiencies

There are very few reports of levels of copper, zinc, vitamin E, vitamin C, or selenium in Latin American populations. One study in a subset of OA Ecuadorians in a low-income peri-urban community in Quito, documented a cross-sectional association of low levels of vitamin C, E, copper, and zinc with anemia and respiratory infections via negative impacts on immune function. ¹⁸ Costa Rica is the only country in the region that has published evidence of low levels of s-selenium in OA. ¹⁷ Deficiency of all these micronutrients in OA from other populations has been associated with a deprived immune system, ¹⁰⁵ oxidative stress, ¹⁰⁶ anemia, ¹⁰⁷ cardiovascular disease, ¹⁰⁸ and impaired cognitive function, ¹⁰⁹ among others.

Zinc plays a pivotal role in maintaining health and well-being in OA. In the region, Brazil ⁴² and Ecuador ¹⁸ are the only countries that have reported serum zinc concentrations in OA. Low zinc levels affect T cells and cytokines activity, wich impairs the immune response. ¹¹⁰ Consequently, OA with zinc deficiency (ZD) might experience a higher incidence and longer duration of respiratory diseases, as shown in the study with Ecuadorian OA. ¹⁸ Intervention studies with zinc supplementation have shown that an increase in serum zinc levels boosts T cells, enhancing immune system function. ¹¹¹ Zinc is also involved in preserving bone integrity by controlling bone resorption and deposition, with low levels of zinc being a risk factor for osteoporosis. ¹¹² Furthermore, the brain contains the highest zinc concentration compared to other organs. Zinc acts as a modulator for neurotransmitters such as glutamate, and γ-aminobutyric acid (GABA), is involved in glycinergic synaptic transmission. ¹¹³ ZD can impair enzyme metabolism in the brain, leading to an accumulation of pathological proteins linked to Alzheimer’s disease. ¹¹⁴ In older Brazilian adults, ZD has been associated with cognitive decline. ⁴²

So far, no countries in the region have studied the role of Magnesium (Mg) and health in OA. Mg has a pivotal role in aging and longevity since it modulates both the innate and the acquired immune response acting as anti-ROS preserving genomic stability, ¹¹⁵ and as a cofactor for multiple proteins reactions (eg. muscle synthesis ATP, vitamin D synthesis among others). ¹¹⁶ In the brain, Mg preserves the integrity and stability of the cell membrane, reduces neuroinflammation, is involved in neural maturation and clearance the proteins and toxins from the brain. ¹¹⁷ Deficits of Mg have been associated with insulin resistance, diabetes, cardiovascular disease, cancer, hypertension, asthma, psychiatric disorders, osteoporosis, cognitive decline, and Alzheimer´s disease. ^{116,118 -120} Epidemiological studies in OA (from North America, Japan and Australia) have shown that low intakes of Mg are associated with a higher risk of cognitive decline and dementia of all types, including vascular dementia. ^{121 -123} Further research is needed to better understand the role of Zn, Mg, and others MD in health and disease, in order to design effective strategies to achieve a healthy aging in the region.

The Gaps and Challenges

To date, information on the micronutrient status in older populations is scarce in most Latin American countries. Information that is reported comes from representative surveys and local studies (which are not representative of the national population within each country). Most of the aging surveys used in Latin America do not collect enough information about nutritional biomarkers to accurately characterize the micronutrient status of the population, and these biomarkers are not routinely measured. The assessment of the micronutrient status at a population level in OA requires investment, a coordinated approach to data collection, as well the appropriate equipment and certified laboratories to process biological samples. Moreover, there are no universally agreed serum/plasma micronutrient thresholds to define deficiency in OA. ¹²⁴ A variety of cut-off points to define micronutrient deficiencies are used which makes comparison across the Latin American region difficult. Some existing thresholds used to define “deficiency” are based on data from younger adults and do not consider age-related changes. This brings challenges when interpretating the “deficiency status” in this age group, including in the identification of deficiencies in the subclinical range, which might represent the best opportunity for timely intervention. Malabsorption syndromes, polypharmacy, and chronic comorbidities are common conditions of OA, which in themselves can exacerbate micronutrient deficiencies. Additionally, the effect of low-grade inflammation during aging might mask underlying deficiencies in micronutrients such as retinol, iron, and zinc. With all of this in mind, it is likely that micronutrient deficiency is underestimated in OA in LAC. Micronutrient deficiencies tend to disproportionately affect underrepresented and vulnerable groups, such as black, indigenous, rural populations, and those with lower socioeconomic status, where health inequities persist. ¹²⁵ More research is needed to better understand the long-term risk of MD and the inherent inequities in the LA region, before it can be effectively addressed. ¹²⁵

The lack of information about MD in most countries across the region make it challenging to respond adequately and comprehensively to the UN declaration of the decade of healthy aging. Regular data collection is crucial for surveillance of micronutrient levels in OA population. In addition, longitudinal studies in OA are needed to accurately describe trends in MD and to identify the window of opportunity where nutritional intervention would be most effective. Revising and agreeing on recommendations of micronutrient levels in OA, and including consensus criteria for diagnosing deficiencies, are both needed to allow comparison within and between countries as well as to evaluate the response to any interventions. Without this, the existing gaps in our understanding continue to limit opportunities to address inequities in nutrition to improve the nutritional status of the older population and achieve healthy aging.

Dietary deficiencies are considered to be the main causes of MD, which are intimately linked to food insecurity and poverty. ^7,126 Data exploring the link between dietary practices and geriatric syndromes are scarce, and where is does exist, is poorly documented across the region. In addition, national diet and food policies vary across Latin American countries, which may contribute to the prevalence of MD, where known. Fortification of staple foods such as wheat and maize, with critical micronutrients including iron, vitamin A, zinc, calcium, and vitamin D, is a strategy that has been successfully used to address MD at the population level. ¹²⁷ However, surveillance in the adherence to fortification guidelines is necessary in counties where fortification is not mandatory. For example, a study in 2018 conducted in Mexico City reported that only a low proportion of flours were adequately fortified, despite national policy recommending fortification. ^128,129

Most countries in the region have implemented food fortification programs, such as adding folic acid to wheat and corn flours which explains the decline in the prevalence of FD in the region. ⁵¹ What is perhaps missing is research into the effects of supraphysiological levels of some micronutrients, such as folic acid and vitamin A, and their effect on outcomes in OA, some of whom may also be participating in the supplementation programs.

Supplementation strategies have been effective when designed to target specific populations. For example, in Chile the program “Complementary Feeding for older adults” was designed to address VB12 deficiencies in the Chilean OA population. This program supplemented 58% of the daily recommended intake of B12 ¹³⁰ but previous reports had already shown that this dose would be insufficient. ⁴⁷ When safely implemented targeted population strategies are cost-effective approaches to improve micronutrient status, health, and aging-related outcomes. ¹³¹

Final Remarks

Micronutrient deficiency is detrimental for health across the whole lifespan. The risk of MD increases with age. A more comprehensive understanding of the main drivers of MD in LAC is needed in order to generate public health-level solutions that improve overall health, independence, and quality of life for OA. The OA population is projected to grow in Latin America which brings challenges to the health system unless early nutritional interventions are delivered to maximize healthy aging. Effective screening of MD will be a critical step to maintain biological function and preserve functionality for at-risk populations. Public health policies focusing on the prevention of malnutrition offer an economic alternative to costly treatment of potentially preventable chronic conditions.

Investment in research and capacity building in the region is crucial to identify equitable solutions to enable healthier populations. By investing in targeted research, we will gain valuable insights into factors contributing to micronutrient deficiencies in OA in LAC. Such insights will inform the development of targeted interventions, policy recommendations, and educational programs aimed at promoting healthy aging and improving the overall well-being of OA. Concurrently, building capacity among health care professionals, policymakers, and community stakeholders will foster a collaborative environment for effective implementation and sustainability of interventions.

Studies that adopt a life-course perspective will enable better understanding of early social determinants, nutritional interventions, long-term outcomes ^132,133 and identification of the most cost-effective strategies for the prevention and treatment of age-related diseases associated with MD.