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Insider News Article: Current Hunger State 

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Insider News Article: Current Hunger State 

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This article from Insider talks about the world hunger situation, and talks about the organization Compassion International.

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COLORADO SPRINGS, Colo. , /PRNewswire/ -- This Sunday is World Hunger Day, when we take time to reflect on the global crisis of hunger and highlight sustainable solutions. The world is hungrier than ever in 2023, with children in poverty among the most vulnerable. According to World Food Program, as many as 828 million people will go to bed hungry each night, and extreme weather, rising costs, and conflict continue to worsen the global food crisis.

That's why Compassion International is leading a local-first response in nine of the world's hunger hotspots in partnership with 1,600 frontline churches to provide both immediate and long-term support. Compassion provides food packs and cash transfers to stop hunger in its tracks and empowers families with seeds, fertilizer, livestock, and training so they'll have sustainable food supplies over time. Over the past year alone, Compassion supported more than 1.4 million people through its distribution of food packs.

Palamanga Ouali, Compassion's regional vice president for Africa, explains, "To thrive, children and youth must first have access to the basics of life. There is nothing more basic than food. The worry for most of us is about the ability of donors to commit and raise funds for the necessary interventions - short-term and medium to long-term sustainable interventions - to address the root cause of this problem."

The statistics are alarming, and the impact on children is severe. One UNICEF study looked at 15 developing countries and found that every minute, another child will suffer from severe malnutrition. The World Food Program reported that more than 345 million people are facing high levels of food insecurity in 2023. With numbers like these, children are more vulnerable to death, life-threatening illnesses, poor academic performance and intellectual development, gender-based violence and abuse, child marriage (as girls are offered in marriage for dowries that will feed their families), and child labor (as children leave school to support their families).

As hunger soars, how can the rest of the world make a difference for these hungry children and families? As a child development organization committed to caring for more than two million babies, children, and young adults, Compassion shares five ways:

Get the facts on the global food crisis. Learn how hunger affects children and their families. Explore how conflict creates chronic hunger. Watch this urgent video message from Compassion's church partners. Educate yourself on the link between poverty and hunger. Read up on topics like food security or malnutrition.

Use your voice. Share what you learned about hunger on social media or with those in your sphere of influence this May 28 on World Hunger Day. Raise awareness about the worsening global food crisis and spread the word about the needs of families and children in poverty.

Become part of the solution through support. Find humanitarian organizations that work with developing nations and support them. You can donate to Compassion to provide both immediate and long-term support to malnourished children and families. A $50 food pack will provide a family of five with a one-month supply of essentials, like rice, eggs, meat, milk, and corn; and sustainable solutions, such as livestock (chickens, goats, or pigs), mitigation (seeds, basic tools, and training), or agriculture (vegetable seeds or fruit trees), will help families find hope and build resilience over time.

Sponsor a child. Sponsoring a child in a hunger-affected country helps provide food security and gives children the opportunity to learn, play, grow, and reach their potential.

Pray. Compassion works with more than 8,500 frontline church partners all over the globe, and each church partner is trained to identify malnutrition and hunger and take immediate action to address it. Pray that God would equip these churches and staff members with wisdom, protection, endurance, and the resources to fight hunger and provide food security to children and families in their communities. And pray for God's comfort and provision to families struggling with food insecurity.

To learn more about poverty, hunger, and Compassion's solutions in the midst of a global food crisis, visit compassion.com/worldhungerday or compassion.com/globalfight.

About Compassion International
Compassion International is a Christian child development organization working to release children from poverty in Jesus' name. Founded in 1952, Compassion partners with more than 8,500 local churches in 29 program countries to deliver spiritual, economic, social, and physical care to over two million babies, children, and young adults in poverty. Ranked No. 12 in Forbes' America's Top Charities List in 2022, Compassion is a founding member of the Evangelical Council for Financial Accountability and an accredited charity with the Better Business Bureau's Wise Giving Alliance. For more information, visit compassion.com or follow us on Facebook, Instagram, and Twitter.

MEDIA CONTACT:219-384-8177
Allison Wilburn

awilburn@compassion.com

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SOURCE Compassion International

Markets Insider and Business Insider Editorial Teams were not involved in the creation of this post.

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On World Hunger Day in 2023, the world is hungrier than ever

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COLORADO SPRINGS, Colo. , /PRNewswire/ -- This Sunday is World Hunger Day, when we take time to reflect on the global crisis of hunger and highlight sustainable solutions. The world is hungrier than ever in 2023, with children in poverty among the most vulnerable.

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Nutrition, and therefor malnutrition, cna affect your mental health along with your physical health. This article highlights the effect nutrition has on mental health.

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INTRODUCTION

Few people are aware of the connection between nutrition and depression while they easily understand the connection between nutritional deficiencies and physical illness. Depression is more typically thought of as strictly biochemical-based or emotionally-rooted. On the contrary, nutrition can play a key role in the onset as well as severity and duration of depression. Many of the easily noticeable food patterns that precede depression are the same as those that occur during depression. These may include poor appetite, skipping meals, and a dominant desire for sweet foods.[ 1] Nutritional neuroscience is an emerging discipline shedding light on the fact that nutritional factors are intertwined with human cognition, behavior, and emotions.

The most common mental disorders that are currently prevalent in numerous countries are depression, bipolar disorder, schizophrenia, and obsessive-compulsive disorder (OCD).[ 2] The dietary intake pattern of the general population in many Asian and American countries reflects that they are often deficient in many nutrients, especially essential vitamins, minerals, and omega-3 fatty acids.[ 3] A notable feature of the diets of patients suffering from mental disorders is the severity of deficiency in these nutrients.[ 3] Studies have indicated that daily supplements of vital nutrients are often effective in reducing patients' symptoms.[ 4] Supplements containing amino acids have also been found to reduce symptoms, as they are converted to neurotransmitters which in turn alleviate depression and other mental health problems.[ 4] On the basis of accumulating scientific evidence, an effective therapeutic intervention is emerging, namely nutritional supplement/treatment. These may be appropriate for controlling and to some extent, preventing depression, bipolar disorder, schizophrenia, eating disorders and anxiety disorders, attention deficit disorder/attention deficit hyperactivity disorder (ADD/ADHD), autism, and addiction.[ 4] Most prescription drugs, including the common antidepressants lead to side effects.[ 4] This usually causes the patients to skip taking their medications. Such noncompliance is a common occurrence encountered by psychiatrists. An important point to remember here is that, such noncompliant patients who have mental disorders are at a higher risk for committing suicide or being institutionalized. In some cases, chronic use or higher doses may lead to drug toxicity, which may become life threatening to the patient.[ 4] An alternate and effective way for psychiatrists to overcome this noncompliance is to familiarize themselves about alternative or complementary nutritional therapies. Although further research needs to be carried out to determine the best recommended doses of most nutritional supplements in the cases of certain nutrients, psychiatrists can recommend doses of dietary supplements based on previous and current efficacious studies and then adjust the doses based on the results obtained by closely observing the changes in the patient.[ 4]

When we take a close look at the diet of depressed people, an interesting observation is that their nutrition is far from adequate. They make poor food choices and selecting foods that might actually contribute to depression. Recent evidence suggests a link between low levels of serotonin and suicide.[ 5] It is implicated that lower levels of this neurotransmitter can, in part, lead to an overall insensitivity to future consequences, triggering risky, impulsive and aggressive behaviors which may culminate in suicide, the ultimate act of inwardly directed impulsive aggression.

Depression is a disorder associated with major symptoms such as increased sadness and anxiety, loss of appetite, depressed mood, and a loss of interest in pleasurable activities. If there is no timely therapeutic intervention, this disorder can lead to varied consequences. Patients who are suffering from depression exhibit suicidal tendency to a larger degree and hence are usually treated with antidepressants and/or psychotherapy.[ 6] Deficiencies in neurotransmitters such as serotonin, dopamine, noradrenaline, and γ-aminobutyric acid (GABA) are often associated with depression.[ 6- 11] As reported in several studies, the amino acids tryptophan, tyrosine, phenylalanine, and methionine are often helpful in treating many mood disorders including depression.[ 12- 17] When consumed alone on an empty stomach, tryptophan, a precursor of serotonin, is usually converted to serotonin. Hence, tryptophan can induce sleep and tranquility. This implies restoring serotonin levels lead to diminished depression precipitated by serotonin deficiencies.[ 8] Tyrosine and sometimes its precursor phenylalanine are converted into dopamine and norepinephrine.[ 18]

Dietary supplements containing phenyl alanine and/or tyrosine cause alertness and arousal. Methionine combines with adenosine triphosphate (ATP) to produce S-adenosylmethionine (SAM), which facilitates the production of neurotransmitters in the brain.[ 19- 22] The need of the present paradigm is, more studies shedding light on the daily supplemental doses of these neurochemicals that should be consumed to achieve antidepressant effects. Researchers attribute the decline in the consumption of omega-3 fatty acids from fish and other sources in most populations to an increasing trend in the incidence of major depression.[ 23] The two omega-3 fatty acids, eicosapentaenoic acid (EPA) which the body converts into docosahexanoic acid (DHA), found in fish oil, have been found to elicit antidepressant effects in human. Many of the proposed mechanisms of this conversion involve neurotransmitters. For instance, antidepressant effects may be due to bioconversion of EPA to leukotrienes, prostaglandins, and other chemicals required by the brain. Others hypothesize that both EPA and DHA influence neuronal signal transduction by activating peroxisomal proliferator-activated receptors (PPARs), inhibiting G-proteins and protein kinase C, in addition to calcium, sodium, and potassium ion channels. Whichever may be the case, epidemiological data and clinical studies have clearly shown that omega-3 fatty acids can effectively treat depression.[ 24] In depressed patients, daily consumption of dietary supplements of omega-3 fatty acid that contain 1.5-2 g of EPA has been shown to stimulate mood elevation. Nevertheless, doses of omega-3 higher than 3 g do not show better effects than placebos and may be contraindicative in cases, such as those taking anticlotting drugs.[ 25] In addition to omega-3 fatty acids, vitamin B (e.g., folate) and magnesium deficiencies have been linked to depression.[ 26- 28]

Randomized, controlled trials that involve folate and vitamin B12 suggest that patients treated with 0.8 mg of folic acid/day or 0.4 mg of vitamin B12/day will exhibit decreased depression symptoms.[ 27] In addition, the results of several case studies where patients were treated with 125-300 mg of magnesium (as glycinate or taurinate) with each meal and at bedtime led to rapid recovery from major depression in < 7 days for most of the patients. Previous research has revealed the link between nutritional deficiencies and some mental disorders.[ 23, 25, 29- 32]

The most common nutritional deficiencies seen in patients with mental disorders are of omega-3 fatty acids, B vitamins, minerals, and amino acids that are precursors to neurotransmitters.[ 20, 23, 24, 27, 28, 30, 33] Accumulating evidence from demographic studies indicates a link between high fish consumption and low incidence of mental disorders; this lower incidence rate being the direct result of omega-3 fatty acid intake.[ 23, 31, 32] One to two grams of omega-3 fatty acids taken daily is the generally accepted dose for healthy individuals, but for patients with mental disorders, up to 9.6 g has been shown to be safe and effective.[ 34- 36] Majority of Asian diets are usually also lacking in fruits and vegetables, which further lead to mineral and vitamin deficiencies. The significance of various nutrients in mental health, with special relevance to depression has been discussed below.

CARBOHYDRATES

Carbohydrates are naturally occurring polysaccharides and play an important role in structure and function of an organism. In higher organisms (human), they have been found to affect mood and behavior. Eating a meal which is rich in carbohydrates triggers the release of insulin in the body. Insulin helps let blood sugar into cells where it can be used for energy and simultaneously it triggers the entry of tryptophan to brain. Tryptophan in the brain affects the neurotransmitters levels.

Consumption of diets low in carbohydrate tends to precipitate depression, since the production of brain chemicals serotonin and tryptophan that promote the feeling of well being, is triggered by carbohydrate rich foods. It is suggested that low glycemic index (GI) foods such as some fruits and vegetables, whole grains, pasta, etc. are more likely to provide a moderate but lasting effect on brain chemistry, mood, and energy level than the high GI foods - primarily sweets - that tend to provide immediate but temporary relief.

PROTEINS

Proteins are made up of amino acids and are important building blocks of life. As many as 12 amino acids are manufactured in the body itself and remaining 8 (essential amino acids) have to be supplied through diet. A high quality protein diet contains all essential amino acids. Foods rich in high quality protein include meats, milk and other dairy products, and eggs. Plant proteins such as beans, peas, and grains may be low in one or two essential amino acids. Protein intake and in turn the individual amino acids can affect the brain functioning and mental health. Many of the neurotransmitters in the brain are made from amino acids. The neurotransmitter dopamine is made from the amino acid tyrosine and the neurotransmitter serotonin is made from the tryptophan.[ 5] If there is a lack of any of these two amino acids, there will not be enough synthesis of the respective neurotransmitters, which is associated with low mood and aggression in the patients. The excessive buildup of amino acids may also lead to brain damage and mental retardation. For example, excessive buildup of phenylalanine in the individuals with disease called phenylketonuria can cause brain damage and mental retardation.

ESSENTIAL FATTY ACIDS

Omega-3 fatty acids

The brain is one of the organs with the highest level of lipids (fats). Brain lipids, composed of fatty acids, are structural constituents of membranes. It has been estimated that gray matter contains 50% fatty acids that are polyunsaturated in nature (about 33% belong to the omega-3 family), and hence are supplied through diet. In one of the first experimental demonstrations of the effect of dietary substances (nutrients) on the structure and function of the brain, the omega-3 fatty acids (specially alpha-linolenic acid, ALA) were the member to take part. An important trend has been observed from the findings of some recent studies that lowering plasma cholesterol by diet and medications increases depression. Among the significant factors involved are the quantity and ratio of omega-6 and omega-3 polyunsaturated fatty acids (PUFA) that affect serum lipids and alter the biochemical and biophysical properties of cell membranes. It has been hypothesized that sufficient long chain PUFAs, especially DHA, may decrease the development of depression.[ 37] The structural and functional components of membrane in cells of brain which is a lipid-rich organ, include polar phospholipids, spingolipids, and cholesterol. The glycerophospholipids in brain consist of high proportion of PUFA derived from the essential fatty acids (EFAs), linoleic acid and α-linolenic acid. The main PUFA in the brain are DHA, derived from the omega-3 fatty acid α-linolenic acid, arachidonic acid (AA) and docosa tetraenoic acid, both derived from omega-6 fatty acid linoleic acid. Experimental studies have revealed that diets lacking omega-3 PUFA lead to considerable disturbance in neural function.[ 38] Studies by Marszalek and Lodish indicate that despite their abundance in the nervous system, DHA and AA cannot be synthesized by mammals de novo and hence they or their precursors have to be supplied through the diet and transported to the brain. During late gestation and the early postnatal period, neurodevelopment occurs at significantly rapid rates which make the supply of adequate quantity of PUFAs, particularly DHA, imperative to ensure neurite outgrowth in addition to appropriate development of brain and retina.[ 39]

Bruinsma and Taren of University of Arizona College of Public Health, Tucson, USA explored the involvement of dieting-related psychological factors as potential confounders.[ 40] They discussed studies that have both supported and contested the proposition that lowering plasma cholesterol by diet and medications contributes to depression. Research findings point out that an imbalance in the ratio of the EFAs, namely the omega-6 and omega-3 fatty acids, and/or a deficiency in omega-3 fatty acids, may be responsible for the heightened depressive symptoms associated with low plasma cholesterol. These relationships may explain the inconsistency in the results of trials on cholesterol-lowering interventions and depression. On similar lines, dieting behaviors have been associated with alterations in moods.[ 41] Dietary omega-3 fatty acids play a role in the prevention of some disorders including depression. Their deficiency can accelerate cerebral aging by preventing the renewal of membranes. However, the respective roles of the vascular component on one hand (where the omega-3s are active) and the cerebral parenchyma itself on the other, have not yet been clearly resolved. The role of omega-3 in certain diseases such as dyslexia and autism is suggested. It was omega-3 fatty acids that participated in the first coherent experimental demonstration of the effect of dietary substances (nutrients) on the structure and function of the brain. Experiments were first of all carried out on x-vivo cultured brain cells (1), then on in vivo brain cells (2), finally on physicochemical, biochemical, physiological, neurosensory, and behavioral parameters (3). These findings indicated that the nature of polyunsaturated fatty acids (in particular omega-3) present in formula milks for infants (both premature and term) determines the visual, cerebral, and intellectual abilities.[ 16]

VITAMINS

B-complex vitamins

Nutrition and depression are intricately and undeniably linked, as suggested by the mounting evidence by researchers in neuropsychiatry. According to a study reported in Neuropsychobiology,[ 42] supplementation of nine vitamins, 10 times in excess of normal recommended dietary allowance (RDA) for 1 year improved mood in both men and women. The interesting part was that these changes in mood after a year occurred even though the blood status of nine vitamins reached a plateau after 3 months. This mood improvement was particularly associated with improved vitamin B2 and B6 status. In women, baseline vitamin B1 status was linked with poor mood and an improvement in the same after 3 months was associated with improved mood.

Thiamine is known to modulate cognitive performance particularly in the geriatric population.[ 43]

Vitamin B12 (Cynocobalamin)

Clinical trials have indicated that Vitamin B12 delays the onset of signs of dementia (and blood abnormalities), if it is administered in a precise clinical timing window, before the onset of the first symptoms. Supplementation with cobalamin enhances cerebral and cognitive functions in the elderly; it frequently promotes the functioning of factors related to the frontal lobe, in addition to the language function of people with cognitive disorders. Adolescents who have a borderline level of vitamin B12 deficiency develop signs of cognitive changes.[ 43]

Folate

It has been observed that patients with depression have blood folate levels, which are, on an average, 25% lower than healthy controls.[ 44] Low levels of folate have also been identified as a strong predisposing factor of poor outcome with antidepressant therapy. A controlled study has been reported to have shown that 500 mcg of folic acid enhanced the effectiveness of antidepressant medication.[ 45] Folate's critical role in brain metabolic pathways has been well recognized by various researchers who have noted that depressive symptoms are the most common neuropsychiatric manifestation of folate deficiency.[ 46] It is not clear yet whether poor nutrition, as a symptom of depression, causes folate deficiency or primary folate deficiency produces depression and its symptoms.

MINERALS

Calcium

A recent study showed that selective serotonin uptake inhibitors (SSRIs) inhibit absorption of calcium into bones. In addition to this, the SSRIs can also lower blood pressure in people, resulting in falls which may lead to broken bones. Indiscriminate prescription of SSRIs by doctors and ingestion by patients at risk of depression or other mental health problems may put them at increased risk of fractures. Compounded by the fact that they may be aging and already taking other medications, may also predispose them to osteoporosis.[ 47]

Chromium

Many studies on the association of chromium in humans depression have been recorded[ 48, 49] which indicate the significance of this micronutrient in mental health.

Iodine

Iodine plays an important role in mental health. The iodine provided by the thyroid hormone ensures the energy metabolism of the cerebral cells. During pregnancy, the dietary reduction of iodine induces severe cerebral dysfunction, eventually leading to cretinism.

Iron

Iron is necessary for oxygenation and to produce energy in the cerebral parenchyma (through cytochrome oxidase), and for the synthesis of neurotransmitters and myelin. Iron deficiency is found in children with attention-deficit/hyperactivity disorder. Iron concentrations in the umbilical artery are critical during the development of the foetus, and in relation with the IQ in the child; Infantile anemia with its associated iron deficiency is associated with disturbance in the development of cognitive functions.[ 43] Research findings pointed out that twice as many women as men are clinically depressed. This gender difference starts in adolescence and becomes more pronounced among married women aged 25-45, with children. Furthermore, women of childbearing age experience more depression than during other times in their lives. These indicate the possible importance of iron in the etiology of depression since its deficiency is known to cause fatigue and depression. Iron deficiency anemia is associated, for instance, with apathy, depression, and rapid fatigue when exercising.[ 43]

Lithium

Lithium, a monovalent cation, was first discovered and defined by Johan August in 1817 while he did an analysis of the mineral petalite. The role of lithium has been well known in psychiatry. Half a century into its use, its choice for bipolar disorder with antimanic, antidepressant, and antisuicidal property. The therapeutic use of lithium also includes its usage as an augmenting agent in depression, scizoaffective disorder, aggression, impulse control disorder, eating disorders, ADDs, and in certain subsets of alcoholism.[ 50] But adequate care has to be taken while using lithium, the gold standard mood stabilizer, in the mentally ill. Lithium can be used in patients with cardiovascular, renal, endocrine, pulmonary, and dermatological comorbidity. The use of lithium during pregnancy and lactation, in pediatric and geriatric population needs careful observation about its toxicity.

Selenium

In a large review, Dr. David Benton of the university of Wales identified at least five studies, which indicate that low selenium intake is associated with lowered mood status.[ 51] Intervention studies with selenium with other patient populations reveal that selenium improves mood and diminishes anxiety.[ 52, 53]

Zinc

Zinc participates among others in the process of gustation (taste perception). At least five studies have shown that zinc levels are lower in those with clinical depression.[ 54] Furthermore, intervention research shows that oral zinc can influence the effectiveness of antidepressant therapy.[ 55] Zinc also protects the brain cells against the potential damage caused by free radicals.

Several studies have revealed the full genetic potential of the child for physical development and mental development may be compromised due to deficiency (even subclinical) of micronutrients. When children and adolescents with poor nutritional status are exposed to alterations of mental and behavioral functions, they can be corrected by dietary measures, but only to certain extent. It has been observed that, nutrient composition of diet and meal pattern can have beneficial or adverse, immediate or long-term effects. Dietary deficiencies of antioxidants and nutrients (trace elements, vitamins, and nonessential micronutrients such as polyphenols) during aging may precipitate brain diseases, which may be due to failure for protective mechanism against free radicals.

OTHER PHYSIOLOGICAL AND PSYCHOSOCIAL FACTORS

Another angle of viewing diet and depression involves old age, which is a time of vulnerability to unintentional weight loss, a factor that is often linked to increased morbidity and premature death. Anorexia of aging may play an important role in precipitating this, by either reducing food intake directly or reducing food intake in response to such adverse factors as age-associated reductions in sensory perception (taste and smell), poor dentition, use of multiple prescription drugs, and depression.[ 56] Marcus and Berry[ 57] reviewed malnutrition occurring in the elderly, in both institutional and community settings, due to refusal to eat. They suggest physiologic changes associated with aging, mental disorders such as dementia and depression, and medical, social, and environmental as causative factors. Currently to tackle the problem of depression, people are following the alternative and complementary medicine (CAM) interventions. CAM therapies are defined by the National Center for Complementary and Alternative Medicine as a group of diverse medical and health systems, practices, and products that are not currently considered to be a part of conventional medicine.[ 58] Mental health professionals need to be aware that it is likely that a fair number of their patients with bipolar disorder might use CAM interventions. Some clinicians judge these interventions to be attractive and safe alternatives, or adjuncts to conventional psychotropic medications.[ 59]

Current research in psychoneuroimmunology and brain biochemistry indicates the possibility of communication pathways that can provide a clearer understanding of the association between nutritional intake, central nervous system, and immune function thereby influencing an individual's psychological health status. These findings may lead to greater acceptance of the therapeutic value of dietary intervention among health practitioners and health care providers addressing depression and other psychological disorders.

REFERENCES

2. Murray CJL, Lopez AD. The global burden of disease. World Health Organization. 1996:270. [ Google Scholar]

3. American psychiatric A: Diagnostic and statistical manual of mental disorders. 4th ed. Washington DC: 2000. [ Google Scholar]

8. National Institute of Mental Health: Depression. National Institute of Mental Health. 2000. (US Department of Health and Human Services, Bethesda (MD) [reprinted September 2002]

18. Hoes MJ. L-tryptophan in depression. J Orthomolecular Psychiatry. 1982;4:231. [ Google Scholar]

19. Buist R. The therapeutic predictability of tryptophan and tyrosine in the treatment of depression. Int J Clin Nutr Rev. 1983;3:1-3. [ Google Scholar]

22. DeLeo D. S-adenosylmethionines an antidepressant: A double blind trial versus placebo. Cut Ther Res. 1987;41:865-70. [ Google Scholar]

42. Benton D, Haller J, Fordy J. Vitamin supplementation for one year improves mood. 1995;32:98-105. [[ PubMed] Google Scholar]

58. National Center for Complementary and Alternative Medicine - National Institutes of Health. 2002.

59. Andreescu C, Mulsant BH, Emanuel JE. Complementary and alternative medicine in the treatment of bipolar disorder: A review of the evidence. J Affecrt Disord. 2008 May 2; [Epub ahead of print] [[ PubMed] Google Scholar]

Articles from Indian Journal of Psychiatry are provided here courtesy of Wolters Kluwer -- Medknow Publications

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Understanding nutrition, depression and mental illnesses

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Few people are aware of the connection between nutrition and depression while they easily understand the connection between nutritional deficiencies and physical illness. Depression is more typically thought of as strictly biochemical-based or emotionally-rooted. On the contrary, nutrition can play a key role in the onset as well as severity and duration of depression.

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This article discusses malnutrition in the US, and a proposed solution to it.

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According to the latest estimates, as many as 9 million children in the United States live in "food insecure" homes. That phrase may sound mild, but it means that those households don't have enough food for every family member to lead a healthy life. That's one in eight children, or 12.5%. Feeding America 2021 data reports that 42,260 people are food insecure in St. Louis city and county.

In Haiti, it's about 50%, or 2.5 million children, who have been pushed into crisis-levels of hunger this year, with almost half the country's population not knowing where their next meal will come from, according to Save the Children.

Around the world starvation is stealing the next generation with 60 million acutely malnourished children at imminent risk of death, illness and longterm developmental impairments. We know how to stop the scourge of hunger - if we have the will.

The miracle answer for starving children is ready-to-use therapeutic food. It can be used anywhere and is highly effective with simple daily dosing that can be administered at home by any caretaker. It's portable, has a long shelf life even in the tropics and doesn't require refrigeration or clean water.

For more than 20 years, the St. Louis based Meds & Food for Kids has produced ready to-use therapeutic food that can cure 92% of malnourished children in a matter of weeks. Using this miracle treatment, Meds & Food for Kids already has saved more than 700,000 children in Haiti and 17 other countries in partnership with Unicef.

These results prove that there are simple solutions that work to end hunger. But decision-makers must have the will to prioritize, mobilize and invest on the same scale as the response to the HIV/AIDS epidemic.

For the first time ever, there are more severely malnourished children in need of therapeutic food than can be produced with current infrastructure. We have the knowledge and ability to produce this life-saving treatment. Hunger is intergenerational. Unless we break this deadly cycle, the world will face lost opportunities and lost capabilities of malnourished children for decades to come. We can and must break this cycle.

What we need is investment to scale-up production through the worldwide network of producers. An international network of producers and researchers are deeply engaged in solutions that work. Along with advocates from a wide range of practices - medicine, agriculture, education and research - these voices represent more than three decades of experience reporting on the politics and impacts of hunger, and options to help save generations of children from starvation, one child at a time.

As we learned from the pandemic, what happens in one part of our world impacts all of us. "A malnourished, stunted child anywhere is a stunted, malnourished child that we should collectively care about. A lost chance of greatness for any one child becomes a lost chance of greatness for us all," stated journalist Roger Thurow, who reported on the global cause of famine, hunger and starvation for more than 30 years for The Wall Street Journal.

David Miliband, president and chief executive of the International Rescue Committee, has called for an international response for curing the global hunger crisis. He said: "An act of U.S. leadership, similar to the 2003 HIV/AIDS emergency response, is needed to tackle the humanitarian crisis already causing millions of preventable deaths in severely malnourished children."

The difference between that emergency and malnutrition is that we already have a solution that saves starving children.

Once you hold a starving baby in your arms, your life is changed forever. We know how to save this generation of starving children. They deserve to be saved and have a chance for a life.

There's no time to waste. Join the voices calling for a presidential emergency nutrition plan that would scale-up practical, proven solutions. Americans should lead the global effort to end hunger by doing what works now. Patricia B. Wolff of St. Louis is founder of Meds & Food for Kids.

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Solution exists for child hunger and malnourishment

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According to the latest estimates, as many as 9 million children in the United States live in "food insecure" homes. That phrase may sound mild, but it means that those households don't have enough food for every family member to lead a healthy life. That's one in eight children, or 12.5%.

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Food Security in Niger: How We Are Working to End Hunger in Niger | Concern Worldwide

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The World Food Programme and its Mission 

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The World Food Programme and its Mission 

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The WFP does great work and this video gives an understanding of what they do and what their mission is.

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What is the best way to end World Hunger?

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Video: Types and Causes of Malnutrition 

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Video: Types and Causes of Malnutrition 

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This is a good video to give a basic understanding of the different types of and causes of malnutrition.

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Peer Reviewed Article: Adult Malnutrition 

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Peer Reviewed Article: Adult Malnutrition 

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In this article, the detrimental effect of malnutrition on older individuals and how it happens is discussed.

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Ina Bergheim, Academic Editor

Abstract

Malnutrition in older adults has been recognised as a challenging health concern associated with not only increased mortality and morbidity, but also with physical decline, which has wide ranging acute implications for activities of daily living and quality of life in general. Malnutrition is common and may also contribute to the development of the geriatric syndromes in older adults. Malnutrition in the old is reflected by either involuntary weight loss or low body mass index, but hidden deficiencies such as micronutrient deficiencies are more difficult to assess and therefore frequently overlooked in the community-dwelling old. In developed countries, the most cited cause of malnutrition is disease, as both acute and chronic disorders have the potential to result in or aggravate malnutrition. Therefore, as higher age is one risk factor for developing disease, older adults have the highest risk of being at nutritional risk or becoming malnourished. However, the aetiology of malnutrition is complex and multifactorial, and the development of malnutrition in the old is most likely also facilitated by ageing processes. This comprehensive narrative review summarizes current evidence on the prevalence and determinants of malnutrition in old adults spanning from age-related changes to disease-associated risk factors, and outlines remaining challenges in the understanding, identification as well as treatment of malnutrition, which in some cases may include targeted supplementation of macro- and/or micronutrients, when diet alone is not sufficient to meet age-specific requirements.

Keywords: malnutrition, ageing, inflammaging, sarcopenia, anorexia of aging, micronutrients, DoMAP, GLIM criteria

1. Introduction

The World Health Organization (WHO) has declared Healthy Ageing a priority of its work on ageing between 2016 and 2030 and developed a policy framework which emphasizes the need for action across multiple sectors [ 1]. The aim of the program is to enable older persons to develop and maintain functional ability which permits wellbeing and allows them to partake in society [ 1]. Older adults (individuals aged 65 or over) are the fastest growing age group and projections from the United Nations predict that by 2050, the number of adults aged 65 or over will be twice as big as the amount of children under the age of five and also surpass the number of adolescents aged between 15 and 24 years. In 2050, improvements in survival are expected to add approximately 5 years to the life expectancy at birth for the world's population which was 72.6 years in 2019 [ 2].

Biology of ageing is understood as the time related decline of physiological functions, leading to changes in functional performance of different organ systems as well as with reduced resilience to physical, cognitive and mental stressors, however, there are great individual differences in these changes. Advanced age is associated with reduced adaptive and regenerative capacity which is leading to higher rates of morbidity [ 3]. On the other hand, the presence of age-associated diseases in middle-aged individuals has been interpreted as a sign of accelerated ageing [ 4]. Maintaining an adequate nutritional status as well as a sufficient nutrient intake is key to health and quality of life and as such is one prerequisite for wellbeing in higher age and modulator of healthy ageing as defined by the WHO. However, older adults are susceptible to nutritional problems and ultimately also to malnutrition through a variety of mechanisms [ 5]. As age is one main risk factor for the development of chronic disease, older persons are particularly susceptible to disease-related weight loss, loss of muscle mass and strength (i.e., sarcopenia) and ultimately, the frailty syndrome, all of which can fundamentally impact recovery from disease and clinical outcome in general [ 6, 7, 8]. Weight loss, a marker of macronutrient deficiency and/or catabolism, is a common key initial phenomenon in old patients, which sets off a catabolic cascade of unfavourable events resulting in higher morbidity and mortality. The causes for weight loss in higher age are multifactorial, but can in part be attributed to both disease processes such as catabolic events, disease or age-related anorexia ("anorexia of aging") and subsequent insufficient dietary intake, but also to increased inflammatory status, depressive or cognitive disorders [ 9] as well as a decreased socio-economic status [ 10]. But even outside the context of disease or manifest disorders, both ageing processes and age-associated changes can slowly impact physiology and metabolism and thus effect a gradual change in the nutritional status of older adults [ 11].

The treatment of malnutrition requires early identification and multimodal intervention, in hospitalized patients as well as community dwelling older adults. However, treatment modality still poses a challenge for nutritional therapy with yet open questions [ 12, 13]. This review summarizes the current state of evidence on the complex aetiology of malnutrition in old adults, considering both effects of ageing processes and disease-related factors. Also remaining challenges in the identification and treatment of malnutrition in the old are outlined.

2. Impact of Malnutrition in the Old

Although clinical malnutrition predominantly occurs in patients in hospitals, care situations or nursing homes, malnutrition, nutritional risk and specific nutrient deficiencies in particular, are a common albeit frequently overlooked occurrence in community-dwelling old people [ 14, 15].

Consequences of malnutrition are deleterious and far reaching and have been described in detail [ 6]. While disease-related malnutrition is not limited to older adults, it is more frequent in higher age, and the consequences appear to be more severe in older persons due to their impaired regenerative capacity.

Malnutrition in general has serious implications for clinical outcome, for recovery from disease, trauma and surgery and is associated with increased morbidity and mortality both in acute and chronic disease [ 6] and has thus been acknowledged as serious burden for the health care system [ 16].

Depending on the type of malnutrition, protein catabolism can be pronounced. Disease-related malnutrition therefore leads to rapid skeletal muscle wasting, whereas age-related malnutrition is associated with a slower but progressive loss of muscle mass. The effects of protein catabolism are prominently reflected by lower muscle mass, muscle strength and function with severe implications for physical performance [ 17]. At the same time, malnutrition [ 18] but also reduced dietary protein intake per se [ 19] are associated with a decrease in bone mineral mass in higher age. Together with poor physical performance and coordination resulting in higher fall risk, these factors accelerate the age-related risk of osteoporosis and osteoporotic fractures [ 20]. Taken together, the risk of falling and the subsequent loss of independence and disability are greatly increased.

Malnutrition-related protein catabolism and micronutrient deficiency have been prominently linked to the impairment of immune function [ 21], which is already affected in higher age. In older malnourished adults, this manifests as the loss of cell-mediated immunity in particular [ 22], increasing the risk for infection and delaying recovery from disease [ 23]. Several studies have thus shown a close relationship between malnutrition and risk for infection, such as healthcare-associated infections [ 24], infectious complications and subsequent longer stays in intensive care units (ICU) and increased ICU mortality in older malnourished patients [ 25].

Wound healing as well as tissue recovery are also impaired in malnutrition, which in part can be attributed to micronutrient deficiency [ 26]. This clearly predisposes older adults to wound healing disorders and chronic wounds which are a great burden to patients as well as associated with decreased quality of life and furthermore with higher expenditure in the health care setting [ 27].

One particularity of malnutrition in older adults is that the impact appears to be more severe than in younger adults. Studies have not only shown that changes in body composition in malnutrition occur to a greater extent in older compared to younger adults [ 28], but also that recovery of low body cell mass or muscle mass is impaired in higher age following weight loss [ 17]. This predisposes malnourished older adults to the risk of developing the so-called geriatric syndromes which have been described as multifactorial syndromes typical in higher age [ 29]. Geriatric syndromes greatly compromise health status, cognitive functioning, functional ability, and compensatory capacity [ 29] and result in higher mortality, albeit predominantly in the younger old [ 30].

2.1. Role of Malnutrition in the Geriatric Syndromes Frailty, Fatigue, Sarcopenia

Malnutrition plays an important role in the development of certain geriatric syndromes. Geriatric syndromes are complex multifactorial conditions occurring in higher age with serious implications for health [ 29] and have been described as "phonotypical presentations of accumulated and underlying ageing-related dysfunctions spanning over different organ systems" [ 31]. They include (but are not limited to) dementia and delirium, depression, incontinence, fall risk, visual as well as hearing impairment, wound healing disorders, frailty, and sarcopenia [ 32].

Involuntary weight loss, a hallmark of malnutrition, is inevitably associated with loss of skeletal muscle mass, which appears to occur at a greater extent in higher age. This increases the risk of developing sarcopenia, a phenomenon which is characterized by the loss of both muscle mass as well as muscle strength and function. As these two entities frequently occur together, this has led to the new term "sarcopenia malnutrition syndrome" [ 33] and a need for new screening tools which reliably identify both conditions has been voiced [ 34].

A phenomenon, which is often overseen in this content but nonetheless is important in an increasingly obese society, is sarcopenic obesity [ 35], which describes a condition with reduced lean mass and increased fat mass, resulting in a high-risk body composition phenotype. This underlines the importance of evaluating muscle mass independently from weight loss, since age-related changes in body composition such as increases in (visceral) fat mass may well mask low lean mass. Furthermore, ectopic fat infiltration in the muscle lowers the quality of skeletal muscle and thereby impairs muscle functionality [ 35].

As sarcopenia has been called the biological substrate of frailty, the close relationship between malnutrition and sarcopenia suggests a link between malnutrition and frailty as well. Not surprisingly, involuntary weight loss, which is an indicator of catabolism, is a major risk factor for developing physical frailty [ 36]. Weight loss is therefore not only one of five factors such as fatigue, weakness, slow gait speed and low physical activity which constitute frailty as defined by the frailty phenotype [ 37], but is also linked causally to the other four factors [ 36]. As such, there is a close relationship between malnutrition and frailty which has been well documented [ 38], although they are considered conceptually distinct conditions. Numerous studies have shown a significant overlap of both entities in hospital patients [ 39] and community dwelling old [ 40, 41]. There is even evidence that the consequences frequently attributed to malnutrition might in reality be due to the effects of frailty. An evaluation in 2804 community-dwelling older adults from the Singapore Longitudinal Aging Study II revealed that functional decline measured by decreased (instrumental) activities of daily living, disability, impaired quality of life and long-term mortality in particular was more apparent in older adults with physical frailty with or without malnutrition [ 42].

2.2. Prognostic Impact of Malnutrition in the Old on Mortality

It is well established that malnutrition is associated with increased mortality in both acute and chronic disease, and this effect is still observed in older adults. The risk for both short-term mortality in acute conditions [ 54] as well as for long-term mortality in chronic disease is significantly increased [ 55]. One large cohort study included 1767 older individuals with a variety of disease ranging from cancer to diseases of the circulatory or respiratory system and revealed that the increased risk of mortality due to malnutrition existed irrespective of the cause of death [ 56].

3. Malnutrition: Definition and Types and How to Screen for Them

Despite an ongoing debate, there is still no universally accepted definition of malnutrition [ 57]. Therefore, in 2016, the world's four leading Clinical Nutrition Societies (ESPEN, ASPEN, FELANPE, and PENSA) representing more than 70 national scientific societies started a consensus process in order to develop criteria for malnutrition which could be used in all clinical settings on a global scale. The resulting concept of the Global Leadership Initiative on Malnutrition (GLIM) [ 58, 59] was published in 2019 and considers three phenotypic criteria for the diagnosis of malnutrition: weight loss (>5% within past 6 months, or >10% beyond 6 months), low body mass index (BMI) (<20 kg/m ² if <70 years, or <22 kg/m ² if >70 years), reduced muscle mass (according to validated body composition techniques), and two etiologic criteria: reduced food intake or assimilation (≤50% of energy requirements >1 week, or any reduction for >2 weeks, or any chronic gastro-intestinal condition that adversely impacts food assimilation or absorption), and inflammation (acute disease/injury or chronic disease-related). It is proposed that the diagnosis of malnutrition is based upon the presence of at least one phenotypic and one etiologic criterion, and in a second step different thresholds of the criteria can be used for severity grading of malnutrition. The GLIM criteria are subject of numerous ongoing validation studies. A recently published study on community-dwelling older adults participating in a long-term osteoporosis trial in Hongkong demonstrated that the GLIM criteria were associated with a higher risk for sarcopenia, frailty, and mortality during a 14-year follow-up period [ 60]. While the GLIM criteria are not age-specific, they do include age as a risk factor among the components. For geriatric patients, the guidelines on Enteral Nutrition in Geriatrics by the European Society of Clinical Nutrition and Metabolism (ESPEN), have defined clinical malnutrition as the presence of either weight loss which reflects a catabolic state (>5% in six months) and/or low BMI (i.e., BMI below 20 kg/m²) which represents depleted physiological stores [ 61].

Nutritional risk is less well defined but commonly understood to be a condition in which the present nutritional status is at imminent risk of impairment due to a range of factors such as medical history, comorbidities or drugs which might increase dietary requirements or interfere with nutrient absorption or metabolism. Further factors may include physical, mental or cognitive status which might prevent the older person to properly care for themselves as well as socio-economic factors which hinder access to a varied high-quality diet [ 61].

Screening tools which are suitable for the use in older adults need to focus on the most important risk factors for malnutrition in high age, in order not only to diagnose manifest malnutrition but also to capture the risk to develop malnutrition as described above. That way, screening tools can be used to identify patients early in order to initiate nutritional treatment. Several screening tools have been established for the specific use in older adults, but the most widely used and most studied instrument is the Mini Nutritional Assessment (MNA) in its long or short form. However, due to its broad range of covered topics, the specificity of the MNA has been questioned, as it is associated with a high risk of "over-diagnosing" malnutrition in the old [ 62]. This problem might be countered by complementing the MNA with the GLIM criteria as suggested [ 59].

Screening for and treating malnutrition has also been acknowledged as one of the first necessary steps in the identification and treatment of sarcopenia [ 63]. Recent studies have compared the ability of screening tools for malnutrition such as the MNA short or long form to predict the development of sarcopenia to newer diagnostic tools such as the GLIM criteria [ 58, 59]. In the SarcoPhAge cohort, the GLIM criteria did predict incident sarcopenia, whereas neither of the MNA forms did [ 17].

3.1. Macronutrient Deficiencies

Also, depending on the type of malnutrition and underlying disease, protein catabolism can be pronounced. Protein requirements are therefore further increased in older adults with malnutrition or disease (1.2-1.5 g/kg body weight) [ 65, 66].

3.2. Micronutrient Deficiencies

One specific form of malnutrition frequent in older adults are micronutrient deficiencies [ 10, 69]. In contrast to quantitative malnutrition, which is reflected by weight loss, micronutrient deficiencies are much harder to screen for and identify, in part also due to methodological issues such as missing suitable markers of stored or available micronutrients. The majority of dietary intake surveys have, however, identified an inadequate intake of a broad range of micronutrients in older adults [ 70]. Since micronutrient deficiency such as iron (Fe), vitamins C and D, vitamins B6 and B12, as well as folic acid and the trace element zinc (Zn), have been prominently linked to the impairment of immune function [ 71], the following chapter focusses on recent findings regarding these nutrients in particular.

Moreover, it is known that inflammation, which is common in older adults, affects trace element status and their biomarkers, resulting in depleted plasma stores of Fe, Zn, and manganese, a phenomenon which is partly known as nutritional immunity and serves as a defence against invading pathogens [ 77].

Due to the multifactorial role of micronutrients in various metabolic processes as well as immune functioning, cell proliferation and growth, signalling processes and genomic stability, micronutrient deficiencies are in turn involved in the pathogenesis of a variety of conditions and age-related diseases [ 78]. One of the most well studied trace elements in higher age is Zn, and dietary Zn intake has also been reported to be frequently insufficient in older adults [ 78]. Age-associated alterations of intestinal absorption, problems regarding chewing and swallowing, drug-interactions, and impaired subcellular processes in Zn metabolism can further contribute to low Zn absorption and availability. In turn, low dietary Zn intake with subsequent Zn deficiency has been linked to depressive disorders [ 79], loss of appetite and cachexia in age-advanced old [ 80], and to increased muscle catabolism via inflammatory cytokine activation [ 81] as well as to immunosenescence [ 82] and frailty [ 83]. Moreover, in older adults, an inadequate intake of antioxidant micronutrients such as vitamin E, carotenoids, and vitamin C has also been linked to the development of impaired muscle strength and physical performance [ 84, 85, 86, 87].

4. Prevalence of Malnutrition

Despite the body of evidence describing the personal and clinical consequences of malnutrition and its economic impact on the health care system, malnutrition in the old remains a considerable problem with reported high frequencies, especially in situations of dependency [ 88]. This has been attributed to poor awareness and lack of time or education in medical as well as nursing staff, but recognition and treatment of malnutrition in older adults is undeniably a challenge even when identified early. All in all, it is estimated that roughly a quarter of European adults over the age of 65 are at high risk of malnutrition across various settings [ 89, 90].

Prevalence of malnutrition, however, strongly depends on the setting, on underlying or accompanying diseases as well as on screening and assessment methods. Numerous studies have investigated prevalence of malnutrition in hospital and nursing home settings; but recently, several meta-analyses have been published which also use meta-regression to further explore determinants. Although the specific number of malnutrition prevalence differs between meta-analyses, the main findings are comparable, showing the lowest percentage of malnourished individuals in the community setting and the highest percentage in acute and subacute care settings, higher prevalence rates in higher age as well as sex-specific differences, as women had the highest risk. Also, region and instrument used to identify malnutrition had a significant impact on prevalence. One systematic review and meta-analysis of prevalence data of malnutrition and nutritional risk in older adults across different healthcare settings showed a wide range of malnutrition from 3% in the community setting to approximately 30% in rehabilitation and subacute care, even though the review only included studies using the MNA [ 91]. This study was recently complemented by two systematic reviews and meta-analyses [ 89, 90]. Leji-Halfwerk et al. included further studies using 22 malnutrition screening tools validated for use in adults aged 65 years or more. They reported pooled prevalence rates of high malnutrition risk across all countries and screening tools which ranged from 8.5% in the community setting to 28.0% for the hospital [ 89, 90]. The meta-analysis and systematic review by Crichton and colleagues focussed on studies carried out in community-dwelling older adults who had been assessed with Subjective Global Assessment (SGA), Patient-generated (PG)-SGA or MNA and found clear differences across countries with low prevalence in Northern Europe and highest in Southeast Asia. Using meta-regression, both meta-analyses reported higher prevalence rates in adults aged above the age of 80 [ 89, 90], in women, in patients with one or more comorbidities and a higher prevalence of malnutrition in rural rather than metropolitan regions [ 90].

Recent advances in prevalence research has also included re-evaluation of large pool datasets using harmonized definitions of malnutrition indicators such as low BMI, weight loss, low food intake and combinations of these. Wolters et al. were able to show varying prevalence of malnutrition according to the different criteria used and concluded that it might be more useful to consider the criteria separately as each may reflect a distinct nutritional problem [ 92].

5. Determinants of Malnutrition

Malnutrition in older adults is of complex and multifactorial origin. A variety of factors such as life-style factors, disease and ageing processes may be involved and interaction between these factors is common. Understanding risk factors is crucial in order to address malnutrition effectively, but the complex aetiology of malnutrition is still not perfectly understood.

In industrial countries, disease is one of the most common reasons for developing malnutrition and the onset of malnutrition can be both acute and slow. Age in itself is an established non-modifiable risk factor for malnutrition. Higher age is associated with physiological changes which can potentially slowly result in or further malnutrition such as impaired taste and smell, decreased gastric flexibility, reduced appetite, etc. As higher age clearly increases the risk for disease, there is considerable risk for potentiation of nutritional problems.

5.1. Modifiable Determinants of Malnutrition

Recent research has particularly focussed on the evidence of potentially modifiable risk factors of clinical malnutrition, as targeting these risk factors is a fundamental element in the prevention and treatment of malnutrition. A recent meta-analysis investigated which factors are associated with incident malnutrition and identified marital situation, hospitalisation and physical limitations as the most important predictors [ 93]. Another systematic review categorized the evidence grade of thirty potentially modifiable factors which have been associated with malnutrition; however, stating that robust evidence was lacking for most of the studied determinants and highlighting the need for high quality prospective studies [ 94].

In a modified Delphi process, an international expert group therefore developed a model for the theoretical framework on the aetiology of malnutrition termed DoMAP (Determinants of Malnutrition in Aged Persons) and specifically, potential causative mechanisms [ 95]. The model construct consists of three triangle-shaped levels illustrates the suggested direction of causality of the various risk factors for developing malnutrition. Malnutrition is at the inner core of the DoMAP model surrounded by different layers of risk factors. The immediate layer consists of the three principal conditions which result in malnutrition (low intake, increased requirements, and impaired nutrient bioavailability). The next layer consists of the factors which are believed to directly cause one of these conditions and the outermost level presents factors which impact the direct factors and indirectly cause one of the three main conditions. By illustrating the sequence of events which can cause malnutrition the DoMAP model offers a better understanding of the aetiology which can be used both in research as well as in clinical routine. By addressing factors, which can potentially impact the three principal components and thus cause malnutrition, the model also offers the possibility of early identification of patients at risk for malnutrition.

5.2. Age-Associated Changes as Risk Factors

Physiological factors which may precipitate malnutrition in higher age include sensory impairment such as diminished taste or olfactory dysfunction, delayed gastric emptying, and disturbed motility leading to a functional decline of the ageing gut [ 96]. Ageing is therefore also associated with an increase in colonic transit time, increased intestinal permeability, and, ultimately, altered intestinal microbiota [ 97], which includes loss of biodiversity, enrichment in opportunistic pathogens, and concomitant reduction of health-associated species, such as short chain fatty acid producing species [ 98]. The changes in the microbiome have recently been implicated in the development of loss of appetite and frailty and as such are also potentially promoting malnutrition [ 99, 100], but more studies are needed in this context.

Moreover, a decrease in gastrointestinal hormones (e.g., ghrelin), with concomitant adverse changes in anorectic signalling (e.g., neuropeptide Y, peptide YY (PYY), orexin A, leptin, cholecystokinin (CCK)) [ 101, 102, 103] leading to an altered appetite regulation in higher age have been described. While ghrelin is the only appetite-enhancing peptide, other hormones such as CCK and PYY for instance are recognized as relevant mediators in satiety. Those gut-derived peripheral hormones as well as systemic insulin, glucose and fatty acid levels regulate central appetite and hunger in the hypothalamic region in a feedback loop [ 104, 105, 106]. As has been shown in a postprandial setting with 14 frail and 20 non-frail old (>70 years) as well as 19 young adults (20-65 years), older persons have higher levels of fasting insulin and glucose as well as increased and prolonged postprandial insulin, glucose and CCK levels compared to younger adults [ 107]. Furthermore, frail older persons exhibited significantly less hunger in the fasting condition and impaired gastric emptying and gallbladder contraction in the postprandial period [ 107]. Similarly, in a small study, the suppressed postprandial hunger in the old was paradoxically accompanied by sustained ghrelin levels [ 108].

Last but not least, in the case of reduced smell and taste, the reward system in the central nervous system (CNS) is hampered in the perception of pleasure associated with palatable foods [ 109] which may in turn further decrease dietary intake.

Some of the pathway dysregulations can be attributed to the chronically elevated inflammation observed in higher age since enhanced cytokine levels (e.g., tumour necrosis factor alpha (TNF-α), interleukin (IL)-1β) are able to affect appetite regions in the CNS [ 103, 110]. The resulting loss of appetite and early satiety seen in older adults has been termed "anorexia of aging" and leads to an insufficient food intake with a higher risk for both quantitative and qualitative malnutrition [ 111, 112]. One risk factor for anorexia in healthy older adults is, not surprisingly, ageing itself [ 113]. Furthermore, body weight dissatisfaction, which might lead to avid dieting, weight loss and eating disorders, is frequent in older adults [ 114] and has been studied as possible precursor of appetite loss. Ultimately, anorexia of ageing has even been proposed to be a geriatric syndrome [ 115] as it significantly and independently affects nutritional und functional status in the old [ 116, 117].

Recent research has also focussed on postprandial regulation of metabolic parameters. Age-related changes in postprandial glucose and insulin have been well established [ 107, 124], but more recently, age-specific changes in the postprandial dynamics of fibroblast growth factor 21 (FGF21) have also been shown, resulting in considerably higher values in older compared to younger adults [ 125]. FGF21 is an important metabolic parameter which regulates glucose and lipid metabolism, but higher levels in older adults are paradoxically associated with higher mortality [ 126] and have been implicated in the loss of muscle [ 127, 128] and bone mass [ 129] as well as in the cachexia anorexia syndrome in old hospitalized patients [ 130]. Altered postprandial regulation of FGF21 might contribute to explain the higher values. Similarly, concentrations of adiponectin, a mediator of FGF21 functions increase with age [ 131] and are also associated with all-cause mortality in the old [ 132]. Again, alterations in postprandial adiponectin response have been shown in higher age which were positively associated with the FGF21 response [ 133].

Taken together, in contrast to disease-related mechanisms such as catabolism, which can result in acute weight loss and malnutrition, altered appetite regulation in higher age and changes in postprandial metabolism are associated with gradual changes that may not necessarily result in manifest malnutrition but contribute to or exacerbate existent nutritional problems and facilitate nutritional deficiencies.

5.3. Inflammaging as a Risk Factor for Malnutrition

Under physiological conditions, inflammatory processes represent a desired, strictly controlled and usually self-limiting reaction. However, chronic inflammation has long-term negative effects on the entire system. Increasing knowledge indicates that ageing is accompanied by slightly but chronically elevated inflammation levels. This sterile and silent inflammation in old adults has been termed "inflammaging" [ 134]. Inflammaging has since been investigate a whole range of age-related diseases within the so-called "network theory of aging". Recently, in the pandemic of coronavirus disease 2019 (COVID-19), inflammaging gained additional attention in view of the observed cytokine storm and autoimmunity during infection among older patients, which can result in multiple organ failure and is in general associated with a worse disease outcome [ 135, 136] and of course potentially increases the risk for malnutrition, though data are lacking [ 137]. This severe systemic inundation of cytokines might be further triggered by the dysregulated immune system in old age (immunosenescence), which is expressed in an imbalanced homeostasis of pro- and anti-inflammatory mediators [ 135].

Meanwhile, it is widely recognized that inflammaging is partly responsible for triggering many age-related diseases, e.g., Alzheimer's Disease ("neuroinflammation") [ 142], atherosclerosis and cardiovascular events [ 143, 144], type 2 diabetes mellitus ("metaflammation") [ 145], (osteo-) sarcopenia and frailty [ 146, 147] as well as cancer [ 148, 149, 150]. Therefore, there is considerable potential that inflammaging also contributes to an impaired nutritional status [ 151], but more studies are needed to explore the relationship. In the old, increased levels of pro-inflammatory cytokines have early on been associated with cachexia ("geriatric cachexia") [ 152]. Cachexia is a well described complex wasting syndrome which is driven by inflammation and reflected by a striking loss of skeletal muscle mass and function [ 153]. It is the most pronounced condition within the disease-related PEM spectrum and occurs in catabolic disease such as cancer, chronic kidney disease, HIV/AIDS, chronic obstructive pulmonary disease. Pro-inflammatory cytokines, such as TNF-α, initially called "cachectin" [ 154] and IL-6, also known as the "cytokine for gerontologists" [ 155, 156], play a dominant role in this phenomenon. The underlying inflammatory processes actively fuel the muscle protein breakdown via pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) which on the one hand stimulate the ubiquitin-proteasome signalling pathway, while on the other hand inhibiting anabolic pathways [ 157]. Although cachexia is generally associated with severe disease, there is definite overlap in the mechanisms that have been used to explain malnutrition in the old caused by inflammaging [ 158] and in geriatric cachexia [ 152]. Inflammatory and related immunological processes in older persons is clearly associated with a higher risk for malnutrition (as indicated by the MNA) [ 158].

Taken together, the aetiology of malnutrition is complex, and a multitude of risk factors can contribute to or aggravate the development of malnutrition as illustrated in Figure 1 . While it is important to further understand age-associated changes which impact nutritional intake, nutrient absorption, digestion and metabolism, many of these factors are not easily identified or modified. They, however, need to be accounted for when assessing the risk for malnutrition and in the concept of treatment.

6. Treatment of Malnutrition

Acknowledging the different and complex risk factors, which can result in or aggravate malnutrition or contribute to the risk of developing it, it becomes clear that treatment of malnutrition is as complicated and challenging. Dependent on both setting and the situation of the older adult, different therapy approaches are warranted.

Regarding the overwhelming evidence that protein requirements are higher in older age [ 65, 66], adequate protein with appropriate energy intake is crucial in order to prevent malnutrition and sarcopenia. Further, due to the frequent micronutrient deficiencies in higher age, targeted supplementation of micronutrients might be useful, when diet alone is not sufficient to meet the age-specific requirements. However, there are still considerable gaps concerning the evidence of non-pharmacological treatment of malnutrition.

Available studies so far have delivered conflicting evidence on the benefits of nutritional theory. Recently, an international panel of nutrition experts identified the shortcomings of these studies which include heterogeneous study populations and too short or varying treatment duration as well as issues relating study methodology such as inadequately described control group and no placebo, no blinding of study personnel, frequently no intention-to-treat-analyses as well as selective outcome presentation [ 13]. Therefore, it remains unresolved which interventions are most effective in which patient groups and whether specific approaches are needed depending on the aetiology of malnutrition [ 13].

A recent meta-analysis, which did not find convincing evidence of the use of oral nutritional supplements in the treatment of malnutrition in older patients, also highlighted the need for more and larger trials to identify suitable and effective interventions for treating malnutrition [ 159]. Pooling data from 9 randomized controlled trials from different care settings [ 160], Reinders and colleagues found evidence that dietary counselling with or without oral nutritional supplements was more effective across the settings than oral nutritional supplements alone, but the outcome parameters included merely energy intake and body weight, and no other relevant outcome parameters such as improved muscle strength or function were considered.

7. Remaining Challenges

Despite the overwhelming evidence regarding the negative outcome of malnourished older adults, there are still many remaining challenges in the understanding, identification and treatment of malnutrition in older adults. They concern both the prevention of slow onset age-associated malnutrition as well as the treatment of disease-related malnutrition. Figure 2 summarizes open questions and remaining challenges in this field.

One particular concern regarding the prevention of malnutrition is that some nutritional requirements are not well established in higher age. Micronutrient and trace element concentrations have been shown to change with age [ 74] and have even been implicated to play a role in the ageing processes [ 161]. Changes in body composition and physical activity may lower energy requirements, but not the requirements of nutrients in general. In order to ensure a sufficient supply of essential nutrients, this requires a high nutrient density in the diet. Therefore, requirements of micronutrients which are frequently deficient in older adults, clearly need elucidation given their multifactorial role in promoting health. Also, while the need for some nutrients may change in higher age, ageing processes themselves may impact the requirements of certain nutrients, in particular in the presence of inflammation. As inflammation alters the trace element profile (increasing copper, decreasing selenium and Zn among other trace elements), an inflammation adapted intake of these trace elements may be necessary. However, more research is needed to elucidate inflammation related needs of the older population and the possible benefit of a tailored supplementation. Furthermore, as higher age is frequently associated with disease, disease-specific nutrient requirements may further complicate the picture.

Taken together, a need to critically appraise current nutrient recommendations for the older age group has been identified, and the WHO has been challenged to issue guidelines [ 162]. There is also an increasing demand worldwide for WHO guidelines which competent national authorities can use to address the nutritional needs of their growing older populations [ 70].

Moreover, although recent research on determinants of malnutrition has added considerable new evidence, the impact of ageing-related changes on the long-term development of malnutrition, still needs further elucidation. One example is the ageing gut and its altered microbiome, which have gained attention in the last years. Emerging technologies, such as e.g., high-throughput culturing, will further the research on ageing microbiome, so its role in the development of malnutrition might soon be elucidated. Novel dietary approaches which modulate the ageing microbiome such as the Mediterranean diet [ 163] are of interest in the prevention of malnutrition, and more studies are warranted. Considering the importance of muscle mass maintenance [ 164], nutritional intervention needs to focus on muscle mass and also, needs to be combined with exercise. Therefore, more studies on nutritional therapy together with different kinds of exercise regimen are clearly needed.

Lastly, not only the prevention of malnutrition, but also the topic of treatment of malnutrition needs more research, in terms of well-designed and adequately powered clinical trials in order to ensure sufficient statistical power to identify true treatment effects. Moreover, relevant outcome parameters need to be included, and a careful selection of target populations with well-defined malnutrition is necessary. Also, more research is needed for treatment approaches which specifically target the underlying causes of malnutrition themselves [ 165] i.e., causative treatment. This, however, not only requires a longer time frame and a broader inter-disciplinary approach, but more research regarding the most relevant causes and their common pathophysiology which would allow a "causation-oriented" multimodal treatment [ 13].

8. Conclusions

Taken together, more research is needed to understand which ageing-related changes are early predictors/precursors of malnutrition that in turn can be addressed in order to prevent the development of nutritional deficiencies. For clinically manifest malnutrition, more studies need to be performed in older adults in order to identify the suitable treatment for the various settings.

Abbreviations

ASPEN

American Society for Parenteral and Enteral Nutrition

BMI

body mass index

CCK

cholecystokinin

CNS

central nervous system

COVID-19

coronavirus disease 2019

DoMAP

Determinants of Malnutrition in Aged Persons

DNA

deoxyribonucleic acid

ESPEN

European Society of Clinical Nutrition and Metabolism

Fe

iron

FELANPE

Federación Latinoamericana de Terapia Nutricional, Nutrición Clínica y Metabolismo

FGF21

fibroblast growth factor 21

GLIM

Global Leadership Initiative on Malnutrition

HIV/AIDS

human immunodeficiency virus/acquired immunodeficiency syndrome

ICU

intensive care unit

IL

interleukin

MNA

Mini Nutritional Assessment

PENSA

The Parenteral and Enteral Nutrition Society of Asia

PEM

protein-energy malnutrition

PEU

protein-energy undernutrition

(PG-) SGA

(Patient-Generated) Subjective Global Assessment

PYY

peptide YY

SASP

senescence-associated secretory phenotype

TNF-α

tumour necrosis factor alpha

WHO

World Health Organization

Zn

zinc

Author Contributions

Conceptualization, K.N.; writing-original draft preparation, K.N. and U.H.; writing-review and editing, K.N. and M.P.; visualization, U.H. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Conflicts of Interest

The authors declare no conflict of interest.

Footnotes

Publisher's Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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Malnutrition in Older Adults-Recent Advances and Remaining Challenges

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Ina Bergheim, Academic Editor Malnutrition in older adults has been recognised as a challenging health concern associated with not only increased mortality and morbidity, but also with physical decline, which has wide ranging acute implications for activities of daily living and quality of life in general.

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Peer Reviewed Article: Mother and Child Malnutrition

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Peer Reviewed Article: Mother and Child Malnutrition

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This article gives a great background and comprehension of how not only a child's malnutrition but also the mothers during pregnancy can affect the child's development.

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BMC Medicine 18, Article number: 135 (2020) Cite this article

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Abstract

Background

Early-life malnutrition may have long-lasting effects on microbe-host interactions that affect health and disease susceptibility later in life. Diet quality and quantity in conjunction with toxin and pathogen exposure are key contributors to microbe-host physiology and malnutrition. Consequently, it is important to consider both diet- and microbe-induced pathologies as well as their interactions underlying malnutrition.

Main Body

Gastrointestinal immunity and digestive function are vital to maintain a symbiotic relationship between the host and microbiota. Childhood malnutrition can be impacted by numerous factors including gestational malnutrition, early life antibiotic use, psychological stress, food allergy, hygiene, and exposure to other chemicals and pollutants. These factors can contribute to reoccurring environmental enteropathy, a condition characterized by the expansion of commensal pathobionts and environmental pathogens. Reoccurring intestinal dysfunction, particularly during the critical window of development, may be a consequence of diet-microbe interactions and may lead to life-long immune and metabolic programming and increased disease risk. We provide an overview of the some key factors implicated in the progression of malnutrition (protein, fat, carbohydrate, iron, vitamin D, and vitamin B12) and discuss the microbiota during early life that may contribute health risk later in life.

Conclusion

Identifying key microbe-host interactions, particularly those associated with diet and malnutrition requires well-controlled dietary studies. Furthering our understanding of diet-microbe-host interactions will help to provide better strategies during gestation and early life to promote health later in life.

Peer Review reports

Background

Microbes of the gastrointestinal tract are associated to health and disease. It is well established that their functional coexistence within the gut can be manipulated by altering their environment, of which host nutrition has the greatest impact [ 1]. Although disease causality has not been directly attributed to the microbiota, researchers hypothesized that early-life exposure and assembly of microbes in the gut influences host development [ 2, 3]. The developmental origins of health and disease (DOHaD) hypothesis proposes that an early-life window exists where environmental exposures, including the mode of birth, nutrition, breastfeeding, infection, and antibiotics, lead to programming effects that can affect long-term health [ 4]. During the first 1000 days of life, host immune, endocrine, metabolic, and other developmental pathways mature in tandem with the microbiome to achieve a mutualistic relationship [ 5]. Even transient disturbances to microbial communities ("dysbiosis") during this critical window of development have been associated with immune-mediated, metabolic, and neurodevelopmental disorders [ 6, 7, 8]. In this review, we discuss the potential implication of maternal and infant diet-induced microbial and host changes surrounding early-life protein, fat, carbohydrate, iron, vitamin D, and vitamin B12 malnutrition.

Contribution of microbes in health and disease

EE, also known as environmental enteric dysfunction, is a major contributor to early childhood stunting [ 14]. EE is a subclinical disorder associated with altered diet-microbe-host interactions and characterized by intestinal injury, nutrient malabsorption, and inflammation [ 15, 16]. EE can induce stunting and wasting through poor digestion and autoimmune dysfunction rather than food shortage [ 14]. Brown and colleagues show in a mouse model that specific bacteria are required for the development of EE [ 17]. Researchers were able to recreate the full effects of human EE by gavaging a defined mixture of Bacteroidales species and Escherichia coli to mice fed a protein-deficient diet (7% of the diet). However, when given an isocaloric protein-sufficient diet (20% of the diet), mice that were colonized with the same bacterial mixture did not develop EE symptoms. This suggests that both diet and microbes are necessary to induce EE.

Observations in mouse models reflect what has been observed in clinical studies, where EE symptoms are associated with both a malnourished diet and specific microbial signatures [ 18, 19, 20]. Metabolomic and proteomic analysis of blood plasma combined with metagenomic analyses of fecal samples revealed distinct microbe and host functions between healthy children and those with severe acute malnutrition when consuming the same therapeutic diet. As the children transitioned from severe to moderate acute malnutrition, their proteomic profiles became more similar to that of healthy children [ 19]. A microbiota-direct dietary intervention to these children had a greater impact than conventional therapy to restore microbiota structure and health [ 20]. Developmentally, a microbiota-direct dietary intervention increased biomarkers and mediators of growth, bone formation, neurodevelopment, and immune function towards a healthy phenotype [ 19]. Gnotobiotic mice and piglet models colonized with malnourished Malawian microbiota and fed a low caloric nutrient-deficient diet, resulted in weight loss and metabolic profiles distinctive of EE [ 18]. Kau et al. were able to show that a higher proportion of Enterobacteriaceae members relative to Akkermansia municiphila and Clostridium scindens in malnourished Malawian children was indicative of a pathogenic community related to malnutrition [ 21]. Using mouse models, researchers confirmed that a combination of diet and Enterobacteriaceae, Enterococcus, and Bacteroidetes members are required for EE pathogenesis.

Pathobionts

Gastrointestinal dysbiosis is characterized by the loss of beneficial commensal microbe-host interactions and expansion of some commensal organisms, known as pathobionts, that exert pro-inflammatory effects on the host [ 22]. Pathobionts are opportunistic bacteria that pose a unique challenge in malnutrition research because their pathogenicity is dictated by host diet and immune function [ 23]. Numerous microbes have been identified as major contributors of gut dysbiosis and inflammation linked to disease, including commensal Escherichia coli strains [ 24], Helicobacter hepaticus [ 25], Bilophila wadsworthia [ 26], Bacteroides fragilis [ 27], Fusobacterium nucleatum [ 28], Enterococcus faecalis [ 29], and Akkermansia muciniphila [ 30]. Although diet, antibiotic, infection, and intestinal inflammation are the primary triggers of dysbiosis, pathobionts can exacerbate gastrointestinal dysfunction [ 22]. The impact of pathobiont overgrowth in the gastrointestinal tract on health may also be context-dependent. For example, Akkermansia muciniphila has been shown to improve glucose control [ 31, 32], but has also been shown to exacerbate infections and colitis [ 33, 34]. Reoccurring EE may be a consequence of poor diet-microbe-host interactions that limit the capacity of the gut to maintain the functional network of microbes that keep pathobionts in check.

The critical window

The critical window of development is theorized to begin during the preconception period, lasting from conception to up to the first 1000 days of life [ 5]. It is considered the period during development characterized by greatest phenotypic plasticity, and during which exogenous factors such as diet, antibiotics, mode of birth, and pollutants may lead to long-term physiological and immunological programming [ 35, 36]. The "fetal programming hypothesis" suggest that maternal nutrition and exogenous factors have long-term metabolic, immune, cardiovascular, and central nervous system effects on their offspring [ 37, 38, 39]. Moreover, the "missing microbe hypothesis" that occurs over-generations is believed to increase disease susceptibility due to suboptimal microbe-host mediated immune development. For instance, the adoption of a low-fiber diet is considered a major player responsible for the intergenerational disappearances of microbes that may promote gut stability and resiliency [ 40, 41]. Exogenous factors that alter early colonization and succession of microbes in the gut may delay gut maturation and development. Disruptions to microbial networks during this critical window of development are associated with asthma, allergies, diabetes, inflammatory bowel disease, and obesity [ 35, 42]. It is during this time that the host forms a mutualistic or immune-tolerant relationship with microbes and is thought to alter disease susceptibility (Fig. 1).

The perinatal period represents a time in development when exogenous factors that affect the microbiome such as antibiotics, diet, hygiene, pathogens, mode of birth, and pollutants can alter immune and physiological programming. The effects of early-life programming may lead to increased disease susceptibility later in life. Created with BioRender.com

Hygiene

As stated in the UN Millennium Development Goals, the supply of potable water and proper sanitation to control gastroenteritis and malnutrition are important targets across the globe. Intervention trials in these areas, also referred to as WASH (water supply, sanitation, and hygiene), involve the provision of water quality at a public or household level, improved means of excreta disposal, health, and hygiene education, and promotion of handwashing. It has been suggested that EE is a contributor to malnutrition and growth delay in children living in areas with poor sanitation. A systematic review by Gera et al. of trials conducted over the past 10 years in developing countries [ 43] documented a modest effect of WASH interventions on most anthropometric parameters and studies were of low-quality evidence. Improvement in water quality was associated with a slightly higher weight-for-age Z-score ( p = 0.06). Combined water, sanitation, and hygiene intervention improved height-for-age Z-scores (MD 0.22; 95% CI 0.12, 0.32) and decreased the risk of stunting (RR 0.87; 95% CI 0.81, 0.94). Several ongoing trials on these interventions may improve the quality of evidence on infant malnutrition. In a more recent trial of WASH and de-worming in Timor-Leste [ 44], a trend was observed for a reduction in levels in young children of the fecal EE biomarker, myeloperoxidase; this finding was statistically significant when household water was stored in covered containers.

On the other hand, improved hygiene through regular use of household cleaning products in developed countries has had unintended consequences on infant growth. Despite their widespread use since the late 20th century, antimicrobial cleaning products have not always reduced infection rates of household members, and they release chemicals into the indoor environment [ 45]. Based on data from full-term infants in the Canadian Healthy Infant Longitudinal Development (CHILD) birth cohort, it was found that infant exposure to frequent cleaning with household disinfectants was associated with altered gut microbial composition at age 3-4 months and risk of being overweight by age 3 [ 46]. The main attribute of hygiene on malnutrition is immune and gut maturation, where excessive hygiene may hamper symbiont colonization and too little may increase pathogen load.

The diet-microbe link

As in many cases, there is a constant struggle between cause and effect with respect to microbial dysbiosis and disease outcome in the study of malnutrition and the microbiome. Although the debate to what effect the microbiota contributes to disease remains unclear, it is reasonable to conclude that both gut microbes and environment contribute to the pathogenesis of malnutrition and undernutrition (Fig. 2). Dietary components play a major role in maintaining microbe-host interactions that may promote intestinal health [ 47]. Therefore, nutrition is an important tool that can be manipulated to restore beneficial microbe-host interactions that enhance intestinal integrity and health.

Diet is a major contributor to the pathology of malnutrition and undernutrition. Nutrient quality and quantity can alter host immunity directly and through alteration of gut microbial communities. Dysbiosis adds to the cycle of malnutrition through dietary fermentation by-products, pathobiont overgrowth, and epithelial oxygenation. These conditions alter intestinal permeability, leading to increased pathogen susceptibility and endotoxemia that hampers host immunity and increases disease susceptibility. Created with BioRender.com

Protein

Beginning in the 1950s, protein-energy malnutrition (PEM) became a primary focus associated with stunting and disease susceptibility in children from developing countries [ 48]. Food shortage is the main culprit of PEM and is estimated to affect 1 in 4 children under the age of 5 worldwide [ 49, 50]. The prevalence of stunting and wasting, particularly in developing countries, is attributed to low protein-energy intake and increased exposure to enteric infections as a result of poor sanitation [ 51]. The "protein gap" was considered the primary reason for PEM; however, after much debate, children in developing countries were actually estimated to consume adequate protein, even above recommended levels [ 48, 52]. The prevalence of stunting could not be explained by protein intake alone and instead has been attributed to intestinal dysfunction and poor energy density from weaning food in developing countries [ 49, 52]. Unabsorbed proteins can alter intestinal dynamics directly by disrupting gastrointestinal enzymes, receptors, or other activities [ 53]. Indirectly, protein malabsorption in the small intestine can lead to microbial proteolytic fermentation by-products (H2, CO2, CH4, H2S, short-chain fatty acids (SCFAs), branched chain amino acids (BCAAs), nitrogenous compounds, phenols, and indoles) in the colon with poorly understood health outcomes [ 54, 55]. Using national level data collected from 180 countries, Ghosh and colleagues concluded that dietary utilizable protein provides a better index of protein inadequacies than total crude protein intake alone [ 56]. An individual's protein requirement should be based on protein quality and digestibility, along with the burden of infection and energy deficits of the individual [ 48, 56]. In addition, microbe-host interactions directed by dietary proteins can provide further insight to assess protein quality and requirements that optimize intestinal health, especially during early development.

Protein-insufficient diet models are used to study the effects of protein malnourishment on intestinal health [ 17, 57]. Reducing dietary protein in mice from 20 to 5% has drastic consequences on growth stunting, intestinal permeability, and immune function resulting in intestinal inflammation with features similar to EE in humans [ 17]. Dietary protein provides essential amino acids for protein synthesis, as well as is important for satiety, glucose, and lipid metabolism, blood pressure, bone metabolism, and immune function [ 53]. Studies show a unique microbial signature specific to protein-deficient diets, distinguished by an increase in Bacteroidetes and Proteobacteria species, and a decrease in Lactobacillaceae and Erysipelotrichaceae in the gastrointestinal tract [ 17, 57]. A decrease in Lactobacillaceae and Erysipelotrichaceae family members are associated with intestinal integrity dysfunction, inflammation, and increased susceptibility to enteric pathogens in mice [ 58, 59]. Similarly in humans, the population of Bacteroidetes and Proteobacteria species has been shown to be high, while Lactobacillaceae species stay low as assessed in a Malawian twin study that evaluated kwashiorkor disease [ 18]. Early-life protein restriction post-weaning in mice led to temporary glucose intolerance following nutritional recovery but did not increase susceptibility to diet-induced liver steatosis and insulin resistance later in life [ 60]. A critical window may exist during gestation and suckling prior to weaning that this study did not include and may explain the transient metabolic dysfunction associated from post-weaning dietary protein deficits.

Aside from the microbiota, there is evidence suggesting that maternal protein consumption can impact the metabolism and immune system of their offspring. A high-protein maternal diet was able to stimulate hypothalamic MAPK insulin signaling pathways that are involved in controlling energy and nutrient homeostasis [ 61]. A diet low in protein was determined to activate the liver and hypothalamus hedgehog-signaling pathway that is positively correlated with liver disease (e.g., NAFLD) and hepatic repair mechanisms [ 61]. A low-protein diet during pregnancy and lactation leads to increased inflammatory status as determined by the expression of microRNAs (miRNAs), and levels of inflammatory IL-6 and TNF-α markers in mice [ 37]. miRNAs are shown to be involved in the pathogenesis of metabolic disorders by regulating insulin signaling, immune-mediated inflammation, adipokine expression, adipogenesis, lipid metabolism, and food intake [ 62]. In pigs, a low-protein diet increased cortisol and decreased protein levels in sows, and led to high cortisol, low IgA, and increased mortality in suckling piglets [ 63]. The high-protein diet decreased systemic immunoglobulin (IgA, IgG, and IgM) and increased systemic CD4⁺ lymphocytes and CD4⁺/CD8⁺ ratio in weaned piglets indicating altered immune function. An optimal quantity of dietary protein may exist because both low- and high-protein diets increased IL-6 in the blood of piglets challenged with lipopolysaccharide (LPS) compared to normal protein feeding [ 63]. Maternal high-protein (40% of diet) diets during pregnancy, but not lactation, alter hepatic gene expression in adult mouse offspring, suggesting permanent imprinting on metabolic function [ 64]. A small number of genes persisted in adulthood, including those involved in liver regulation, damage, and metabolic dysfunction ( Hifla and Hnf4a), and genes that regulate liver DNA methylation ( Mecp2 and Sin3a) that explain the long-term imprinting effects of a prenatal high-protein diet [ 64]. Moreover, glucagon-like protein-1 (GLP1) was higher in high-protein offspring (protein induces satiety) and was associated with reduced insulin sensitivity as determined by high insulin serum levels and increased resistin and IL-6 expression in brown adipose tissue in rats [ 65]. Rat offspring from dams given a high-protein diet during gestation had a 41.2% increase in adiposity correlating with a significantly increased phosphoenolpyruvate carboxykinase (PEPCK; a gluconeogenesis enzyme) and altered insulin signaling compared to normal protein maternal diets [ 66]. A high-protein diet during gestation and lactation is shown to increase plasma insulin when rat pups are weaned on a normal protein diet; however, weight gain remained the same between groups [ 67]. This research indicates that maternal and infant protein consumption may contribute to metabolic programming lasting into adulthood. Yet, the discrepancy between some studies linking high-maternal-protein diets to offspring weight gain may indicate a role of the gut microbiota and requires further investigation.

The amount of protein consumed early in life may play an important role in programing metabolic function. Although the mechanism of programming is poorly defined, the effects of dietary protein may have a microbial component. The "early protein hypothesis" suggests that the consumption of a high-protein diet with sufficient energy, such as the typical infant formula, increases infant weight gain, adipogenic activity, and obesity risk later in life [ 68]. During the first 6 months of life, protein intake has been shown to be 66-70% higher in formula-fed (FF) than in breastfed (BF) infants leading to greater weight gains in infants from 3 to 9 months [ 69]. This is partly due to the fact that infant formula contains higher concentrations of protein than human breast milk. Protein content of human breast milk ranges from 1.4-1.6 g/100 mL to 0.8-1.0 g/100 mL after 4 months of lactation, whereas infant formula ranges from 2 to 3.5 g/100 mL, with a higher protein formula given to low birth weight or preterm infants [ 70]. In a multicenter, double-blind, randomized clinical trial, high-protein FF infants (6 years old) had a significantly higher body mass index (BMI) and were twice as likely to develop obesity compared to the low-protein FF infants [ 71]. Limiting protein intake may help reduce the effects of long-term metabolic programming; however, the events leading to this observation and cause are still poorly understood. A targeted serum metabolome analysis revealed BF infants demonstrated increased fat metabolism, whereas FF infants had a metabolite profile indicative of protein metabolism [ 72]. The greatest difference was determined at 2 months (baseline), 4 months, and 6 months of age, and remained different when "carbohydrate-rich" complementary foods were added to the diet. Fecal microbiome structure and metabolomic profile mirrored changes associated with serum metabolite profiles [ 72, 73]. As expected, protein-rich infant formula induced microbial end-products typical of peptide and amino acid fermentation such as branched chain fatty acids (BCFAs; isobutyrate and isovalerate) and phenylacetate [ 73]. The contribution of the microbiota to the relationship between early-life protein and long-term metabolic outcomes has not been explored in a controlled system; however, given the evidence linking early-life microbial disruptions with long-term disease risk supports a role of protein-microbe interactions.

Excessive protein intake can lead to protein fermentation products known to disrupt gastrointestinal tract function and contribute to the pathogenesis of irritable bowel syndrome and ulcerative colitis, with a distinguishing malodorous flatus [ 54]. Plant-based diets from developing countries such as bean and cowpea flour are primarily poor in protein quality and reduced linear growth compared to fish protein-rich diets [ 74]. Maize and cassava are other popular protein sources in developing countries that are poor sources of tryptophan and lysine [ 75]. Microbiota-derived tryptophan metabolites are instrumental in maintaining intestinal homeostasis [ 76]. In fact, tryptophan is considered the limiting amino acid in infant formula (~ 250 mg/L) due to low bioavailability from bovine milk protein. Formula would require twice as much tryptophan to reach the bioavailable levels similar to that of breast milk (~ 200-400 mg/L) [ 72]. Processes that disrupt microbial activity and reduce tryptophan metabolite capacity can lead to increased digestive dysfunction and pathogen susceptibility [ 77, 78]. In mice, dietary amino acid metabolism has been mechanistically linked to angiotensin I-converting enzyme 2 (Ace2) deficiency by altering microbial gut ecology and antimicrobial peptide expression, increasing infection susceptibility [ 79]. Bioavailability of certain amino acids may play an instrumental role in diet-induced dysfunctions leading to PEM. Protein source and digestibility can impact microbe-host interactions in the gut, perpetuating malnutrition by decreasing intestinal integrity and function [ 47]. More research is needed to determine to what extent the microbiota and host intestinal activities are programmed through maternal exposure to the amount and source of proteins.

Fats

A universal deficiency that occurs in malnutrition, both energy and PEM, is a less than sufficient intake of fat and/or essential polyunsaturated fatty acids. Although the gut microbiota is recognized as an important pathophysiologic factor in the development and sustainment of malnutrition, there are few studies that have specifically examined their impact in relation to dietary fat. It is, however, generally accepted that the bidirectional interactions between the microbiome, fat availability, and gastrointestinal function contribute to a vicious circle, further impairing health outcome in malnutrition [ 80].

Although gut microbes have been implicated in regulating fat absorption and metabolism [ 81], a comprehensive and mechanistic approach to understanding the pathways is still needed. In a healthy infant, > 95% of fats are absorbed before entering the large intestine. Malnutrition, especially in infants/children results in a generalized disturbance of the small intestine structure (shortened, blunted villi, and increased crypt depth) and function (disturbances in permeability and absorption) resulting in fat malabsorption [ 80]. This results in diarrhea, weight loss, other nutritional deficiencies, and gut dysbiosis [ 80]. The accompanying intestinal and systemic inflammation are suggested to contribute to these pathological changes [ 80, 82]. Additionally, the microbiota plays a major role in bile acid deconjugation [ 83]. Altered microbial deconjugation of bile acids would further impair absorption of fat, cause bile salt injury to the colon, and interfere with digestive enzymes and nutrient transporters [ 80].

In the colon, microbial perturbations can indirectly alter energy balance via changes in the levels of anorectic hormones (peptide YY (PYY) and GLP-1) and effects on energy (both lipid and glucose) metabolism [ 84]. The gut microbiota has been demonstrated to stimulate hepatic triglyceride production (lipogenesis) by activating the transcription factors, carbohydrate response element binding protein (ChREBP), and sterol response element binding protein (SREBP) [ 85]. Recently, a critical role of the, complex but less diverse, small intestine microbiota as a regulator of fat digestion and absorption has been identified [ 86, 87]. These microbes appear to be essential for host adaptation to dietary lipid changes by regulating gut epithelial processes involved in their digestion and absorption. It is hypothesized that this occurs via systemic control of enteroendocrine signaling and an effect on erythrocytes fatty acid transport [ 87]. As fat is the major energy source for infants and children, an inadequate supply can lead to long-term health consequences to the infant/child through the impact on inadequate energy reserve, epigenetic changes in cells critical for growth, long-term defects in the small intestine and immune maturation, and recurrent bouts of infection [ 82]. Changes to the microbiome early in life could also have lasting effects on the ability to adapt to changes in fat intake later in life, thereby contributing to metabolic disorders [ 87].

Studies have shown that different types of dietary fat, including saturated fatty acids (SFAs), monounsaturated fatty acids (MUFAs), and PUFAs, and their abundance in the diet, could change gut microbiota composition [ 91]. There is growing evidence for a potential role of a disrupted microbiota in metabolic disorders induced by n-3 PUFA deficiency. Studies have shown that dietary n-3 PUFAs can modify the intestinal microbiota composition by increasing the number of bifidobacteria that decrease gut permeability and decreasing the number of Enterobacteria that increase intestinal permeability [ 92]. Animal studies have reported that supplementation of n-3 PUFA in young rodents can restore the disturbed gut microbiota composition of maternally separated female rats [ 93] or the disrupted function of the microbiome in male pups [ 90]. The position of the DHA or ARA in milk triacylglycerols has also been demonstrated to modify the intestinal bacterial population of the suckling rodent [ 94]. The effect of these fats on the microbiota is best explained by indirect mechanisms. This is particularly evident in a study that demonstrated differences in microbial composition in response to changes in the parenteral fatty acid formulations [ 95].

The impact of PUFA on the gut microbiota is less well defined. The few studies completed in adults showed some common changes in the gut microbiota after n-3 PUFA supplementation. In particular, a decrease in Faecalibacterium, often associated with an increase in the Bacteroidetes and butyrate-producing bacteria [ 92]. Although the literature on this topic is discordant, n-3 PUFAs are generally associated with anti-inflammatory effects, in comparison with the omega-6 PUFAs that are linked to pro-inflammatory effects, due to the different downstream lipid metabolites [ 92]. Supplementation with n-3 PUFAs can exert a positive action by reverting the microbiota composition in adult inflammatory diseases and increase the production of anti-inflammatory compounds, like short-chain fatty acids [ 92]. In addition, accumulating evidence in animal model studies indicates that the interplay between gut microbiota, n-3 PUFA, and immunity helps to maintain intestinal integrity and influences the gut-brain axis, acting through shifts in the microbial gut network [ 92]. Infant trials have demonstrated that supplementation with PUFA results in greater bacterial diversity combined with lower abundance of some pathogenic bacteria, such as Streptococcus, Clostridium, and some genera of the Enterobacteriaceae family, such as Escherichia, Klebsiella, Serratia, and Citrobacter, suggesting that n-3 PUFAs favor the butyrate-producing bacterial genera [ 96]. Identifying direct and indirect attributes of dietary fats on microbial networks and immune function will help elucidate the contribution of dietary fat type and quantity on malnutrition status.

Carbohydrates

Unabsorbed carbohydrates are fermented by gut bacteria into lactic acid, succinate, SCFAs (acetate, propionate, and butyrate), and hydrogen, methane, and carbon dioxide gases [ 101]. SCFAs are associated with improved intestinal and metabolic health; however, it may also contribute to a variety of gastrointestinal symptoms including abdominal cramps, bloating, flatulence, and diarrhea [ 102]. Carbohydrate malabsorption is frequently reported in severely malnourished children; however, to what extent it contributes to the pathologies surrounding malnutrition remains unclear [ 103]. Population-based studies that followed the introduction of refined carbohydrates to the diet have shown an increased prevalence of atherosclerotic disease, coronary heart disease, and diabetes [ 104, 105]. The risks associated with diets high in simple sugars (e.g., sucrose, glucose, fructose) is considered a result of impaired intestinal permeability due increased LPS endotoxemia and loss of luminal SCFAs [ 106, 107]. Although a strong link exists between a high simple sugar diet and poor health outcomes, research suggests that dietary fiber and resistant starches may be more important than quantity and glycemic load of simple carbohydrates [ 108].

Dietary fiber and resistant starch are complex polysaccharides that support homeostasis through their effects on the intestinal mobility and microbiota. The recommended adequate intake of dietary fiber is 14 g/1000 kcal, equating to approximately 28-36 g/day in human adults, a number that many experts believe should be closer to 50 g/day [ 109, 110]. The bulking properties of dietary fiber are well known to positively influence gastric emptying, fecal frequency, and satiety [ 111]. The production of SCFAs, specially butyrate, provides direct energy to gut epithelial cells and promotes intestinal homeostasis by maintaining a hypoxic environment, mucus production, and antimicrobial peptide secretion [ 112, 113, 114, 115, 116]. Commonly known as prebiotics or microbial-accessible carbohydrates (MACs), fibers and starches that encourage SCFA production also promote microbial diversity and resiliency. In mouse models, these attributes have consistently supported the positive effect of MACs on intestinal integrity [ 117, 118]. A MAC-deficient diet is hypothesized to have contributed to gut microbe extinctions across generations, leading to reduced diversity and SCFA production, and dysbiosis associated to disease later in life [ 5, 41]. The type and quantity of MACs directly alters microbial gut networks and fermentation products, such as SCFAs, wherein effects on host physiology and health have been exhaustively reviewed [ 109, 118, 119]. To what extent dietary MACs shape early-life development and disease risk remains unknown and requires well-controlled studies comparing MAC type and introduction to the diet during the critical window of development.

Iron

Iron deficiency (ID) is the most common nutritional deficiency in the world and is highly prevalent in both developed and developing nations. The sub-populations most at risk of ID, irrespective of geographical location, are pregnant women and young children [ 120]. The world health organization (WHO) estimates that 38% of all pregnant women (~ 496 million worldwide) and 43% of children (~ 273 million worldwide) are anemic [ 121], of which more than half are attributed to ID [ 120]. Early childhood is characterized by increased demands for iron, which is needed to support tissue and organ development as well as blood volume expansion. Consequently, reduced iron availability (due to inadequate intake or absorption, chronic inflammation, or insufficient iron accretion and storage in gestation) during this critical period can lead to suboptimal growth, with potential consequences for long-term health. Indeed, epidemiological studies show ID in childhood is associated long-lasting deficits in cognitive ability, memory, and executive function [ 122, 123, 124, 125]. Studies in rats show that maternal iron restriction in pregnancy and consequent ID in offspring affects growth and developmental trajectories, with lasting effects on behavior and cognition [ 126], and cardiovascular and metabolic health [ 127, 128, 129, 130, 131].

The mechanisms by which ID impacts offspring development are complex and likely depend on the organ system in question, but pathophysiological processes including hypoxia [ 132], altered energy metabolism, reactive oxygen species generation [ 133], epigenetic changes [ 134, 135], and altered neurotransmitter and hormonal profiles [ 136, 137, 138] are implicated. More recently, the profound modulatory effects of iron availability on gut microbiome composition and function have been demonstrated [ 139, 140], with implications for metabolic substrate production [ 139, 140] and risk of infection by enteropathogens in young children with ID. Indeed, just as iron is essential for eukaryotic cell function, most bacterial species depend on iron for survival and pathogenicity [ 141, 142, 143], and as such, availability of iron may play an important role in microbiome niche selection.

In young children, ID anemia was associated with increased enterobacteria and Veillonellaceae, reduced Coriobacteriaceae, and reduced the bifidobacteria/enterobacteria ratio [ 144]. A study by McLorry et al. also showed that anemia in boys and girls was associated with lower levels of butyrate-producing bacteria ( Butyricicoccus in females, Coproroccus and Roseburia in males) [ 145]. In general, these reports are consistent with in vitro studies using a continuous gut fermentation model inoculated with child gut microbiota [ 139, 140]. In these experiments, Dostal et al. reported that low iron conditions reduced butyrate-producing bacteria (e.g., Roseburia spp., Eubacteria rectale, Clostridium cluster IV members, and Bacterioides spp.) and reduced butyrate concentrations and other SCFA (acetate and propionate) [ 139, 140], and these effects could be reversed with provision of iron [ 139]. The authors also recapitulated these trends in vivo in weaning rats [ 146].

However, the influence of iron status on microbial composition and function in children is complicated by several population factors, including enteropathogen exposure (e.g., high vs. low pathogen burden [ 147]), anemia identification with and without iron deficiency, dietary fortification regimens, and use of iron supplements. The latter is particularly notable, because iron supplementation is routinely implemented in populations at risk of ID, including young children [ 148]. In excess, unabsorbed iron remains in the gastrointestinal tract, where it may provide a labile iron pool for bacteria. Notably, several species of Proteobacteria (e.g., Enterobateriaceae such as Escherichia coli and Salmonella) and Firmicutes (Bacillus) require iron to colonize and persist in the intestine [ 149]. In an iron-rich colonic environment, such as that produced by excess iron supplementation, Proteobacteria may thrive at the expense of other gut bacteria [ 150, 151]. Consistent with this idea, studies show that supplementation with iron supplements and iron-rich micronutrient powders can increase diarrhea risk, which may be mediated by increased abundance of Enterobacteria (including E. coli) and reduced abundance of beneficial commensal bacteria (e.g., bifidobacteria, lactobacilli) [ 152, 153, 154]. The risks and benefits of iron supplements and micronutrient powders in children, particularly in low- and middle-income countries, is an active area of research, and several excellent reviews on the topic are currently available [ 148, 155].

It is interesting that ID anemia, which is presumably associated with reduced iron availability in the gut, is associated with increased abundance of Enterobacteria (as discussed above), given the iron requirements for colonization and virulence. However, many members of this group are known to use siderophores, high-affinity compounds that bind and sequester iron, and other specialized iron transport systems which enable these bacteria to effectively compete for iron when availability is scarce [ 141]. In their study, Dostal et al. showed that the abundance of Enterobacteriaceae increased with low iron, but decreased with provision of FeSO ₄ [ 146]; the latter finding may reflect a loss of this competitive advantage with increasing iron availability, and the reduced growth may be secondary to growth promotion of other bacterial groups (e.g., Allobaculum spp.). Notwithstanding, these studies highlight a complex but important interrelationship between the microbiota in childhood and iron status, and highlight a myriad of influences on this relationship, including use of iron supplements and their formulations, population characteristics, presence of other nutritional deficiencies, or excesses among others.

Vitamin D

A recent systematic review provides up-to-date information regarding vitamin D and the gut microbiota in animal, cell, and human studies [ 161]. In animal studies which typically use VDR KO (knock-out) mice, microbial "dysbiosis" has been reported, characterized by a greater abundance of Proteobacteria, Bacteroides spp. and Clostridium spp. [ 162, 163]. Few studies have been published in human adults. In a cross-sectional analysis of 150 healthy adults, Luthold and colleagues found higher levels of serum 25(OH)D to be associated with greater abundance of Bifidobacterium and Prevotella in gut microbiota but a depletion in Haemophilus and Veillonella [ 164]. Stool samples and biopsies obtained from the gastrointestinal tract of 15 healthy adults taken before and after supplementation with high doses of vitamin D3 showed higher microbial richness and enrichment with Proteobacteria in biopsies; no significant changes to the microbial composition in stool samples [ 165]. Finally, human adults who are deemed to have an "insufficient" serum vitamin D level have two times greater odds of acquiring Clostridium difficile infections at hospitalization, compared to patients who are vitamin D deficient [ 166].

The evidence in human infants is even more sparse. The KOALA birth cohort study examining both maternal and infant vitamin D supplementation found that infant direct supplementation (i.e., via liquid drops) did not alter gut microbial composition at 1 month after birth [ 167]. However, indirect vitamin D exposure, specifically maternal prenatal multivitamin supplementation, was correlated with greater abundance of Bacteroides fragilis and reduced presence of Bifidobacterium spp. and C. difficile. In the Vitamin D Antenatal Asthma Reduction (VDAART) Trial, mothers of infants received either 4000 IU vitamin D plus prenatal vitamins or 400 IU vitamin D plus prenatal vitamins during the first trimester of pregnancy [ 168]. There were no observed differences between the diversity of microbiota in the two exposure groups at 3-6 months of age. However, enrichment with Lachnospiraceae and Lachnobacterium and depletion of Lactococcus were observed in infants with higher vitamin D levels in cord blood.

Maintaining adequate vitamin D levels is crucial for vitamin D-dependent immunity and physiology, which is particularly important during growth and development. Increasing vitamin D status through nutrition, supplementation, or sun exposure will modulate the gastrointestinal microbiota by supporting the gut environment and normalizing autoimmune responses [ 169]. Although vitamin D can be treated with supplementation and increased sunlight exposure, genetic factors, malabsorption (i.e., EE), and underlying conditions, such as cystic fibrosis, celiac disease, and IBD, can lead to deficiencies [ 170]. Future studies should focus to delineate between host physiological and immune changes surrounding vitamin D status that may alter the gastrointestinal environment and the succession of microbes to children from vitamin D-deprived mothers at birth.

Vitamin B12

Vitamin B12, also known as cobalamin, is a water soluble cobalt-containing vitamin that is exclusively synthesized by bacteria and archaea [ 171]. In humans, it is essential for DNA synthesis, cellular energy production, red blood cell maturation, and myelin synthesis of neural networks. Inadequate absorption of cobalamin from diet leads to anemia and neurologic dysfunction [ 172]. In malnourished children, vitamin B12 deficiency is more common than folate and iron deficiency and can lead to long-term brain damage [ 173, 174]. Insufficient vitamin B12 status has been shown to lower cognitive development and performance [ 175], cause growth and motor retardation [ 176], and decrease bone mass in children [ 177].

Many gut bacteria encode for multiple vitamin B12 transporters, while less than 25% are predicted to synthesize it [ 178]. Because endogenous bacterial production of vitamin B12 occurs in the colon, it is unlikely to significantly contribute to host B12 status. Enterohepatic circulation and microbial remodeling contribute to a pool of at least eight distinct vitamin B12-derivatives (corrinoids) identified in human feces [ 179]. The presence of multiple corrinoids, corrinoid microbial transporters, and corrinoid-dependent enzymes suggest competition exists between gut bacteria. Research has focused to identify the ability of vitamin B12 to modulate gut microbial ecology and how these interactions influence disease status [ 180].

Vitamin B12 derivatives are involved in syntrophic microbe-microbe interactions in the gut that help maintain symbiosis and intestinal health [ 180]. For instance, in vitro co-culture studies suggest Akkermansia muciniphila, a mucus-degrading microbe associated with a lean phenotype and enhanced barrier function, may rely on Eubacterium hallii to provide them with corrinoids [ 181]. Competition between gut bacteria for corrinoids occurs when resources are limited or when an increased demand is required [ 182]. Research has shown that commensal Bacteroides thetaiotaomicron is able to outcompete enterohemorrhagic E. coli (EHEC) for vitamin B12 via cell surface-exposed lipoproteins [ 183]. Furthermore, mutant B. thetaiotaomicron lacking B12 transporters lose their ability to inhibit EHEC virulence factors [ 184]. In excess through supplementation, vitamin B12 availability may increase the risk of enteric pathogens in the gut. This is especially important in regions of poor socioeconomically status, where risk of enteric infection is high. Deficiencies treated with supplements in excess can help to restore vitamin B12 status but may also support enteric pathogen fitness contributing to EE and worsening malnutrition status. Future research should focus on the effects of dietary vitamin B12 on microbial gut ecology and intestinal health.

Conclusion

Controlling the microbiota with targeted dietary interventions, particularly in cases of malnutrition, may prove to be a vital therapeutic option in preventative healthcare. The mounting concerns over early-life nutrition have pointed towards the microbiota and disruptive gut function as a causal factor towards disease susceptibility later in life; however, the direct cause and effect are difficult to tease out. Future nutritional research will require well-controlled studies of a nutrient on its own and in combination with other components that stress and protect the gut. Using an omics and an extensive host phenotyping approach will help unravel the complex interactions between the gut microbiota and health of malnourished children.

Abbreviations

DOHaD:

Developmental origins of health and disease

IBD:

Irritable bowel disease

EE:

Environmental enteropathy

WASH:

Water supply, sanitation and hygiene

CHILD:

Canadian Healthy Infant Longitudinal Development

PEM:

Protein-energy malnutrition

SCFAs:

Short-chain fatty acids

BCAAs:

Branched chain amino acids

MAPK:

Mitogen-activated protein kinase

NAFLD:

Nonalcoholic fatty liver disease

miRNAs:

MicroRNAs

LPS:

Lipopolysaccharide

PYY:

Peptide YY

GLP1:

Glucagon-like protein-1

PEPCK:

Phosphoenolpyruvate carboxykinase

FF:

Formula-fed

BF:

Breastfed

BCFA:

Branched chain fatty acids

Ace2:

Angiotensin I converting enzyme 2

ChREBP:

Carbohydrate response element binding protein

SREBP:

Sterol response element binding protein

PUFA:

Polyunsaturated fatty acid

EPA:

Eicosapentaenoic acid

DHA:

Docosahexaenoic acid

SFAs:

Saturated fatty acids

MUFA:

Monounsaturated fatty acids

ARA:

Arachidonic acid

MACs:

Microbial-accessible carbohydrates

ID:

Iron deficiency

WHO:

World Health Organization

VDR:

Vitamin D receptor

KO:

Knock-out

EHEC:

Enterohemorrhagic Escherichia coli

References

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Authors and Affiliations

1. Department of Agricultural, Food and Nutritional Science, University of Alberta, Edmonton, Alberta, Canada

Andrew J. Forgie, Catherine J. Field & Benjamin P. Willing

2. Department of Pediatrics, University of Alberta, Edmonton, Alberta, Canada

Kelsea M. Drall & Anita L. Kozyrskyj

3. Department of Anesthesiology & Pain Medicine, University of Alberta, Edmonton, Alberta, Canada

Stephane L. Bourque

Contributions

AJF conceived, edited, and wrote the manuscript. BPW conceived and edited the manuscript. ALK and KMD wrote the hygiene and vitamin D section. CJF wrote the fat section. SLB wrote the iron section. All authors have read and approved the final manuscript.

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Correspondence to Benjamin P. Willing.

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Forgie, A.J., Drall, K.M., Bourque, S.L. et al. The impact of maternal and early life malnutrition on health: a diet-microbe perspective. BMC Med 18, 135 (2020). https://doi.org/10.1186/s12916-020-01584-z
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Keywords

Undernutrition

Malnutrition

Diet

Microbiome

Gastrointestinal

Disease

Health

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The impact of maternal and early life malnutrition on health: a diet-microbe perspective - BMC Medicine

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Background Early-life malnutrition may have long-lasting effects on microbe-host interactions that affect health and disease susceptibility later in life. Diet quality and quantity in conjunction with toxin and pathogen exposure are key contributors to microbe-host physiology and malnutrition. Consequently, it is important to consider both diet- and microbe-induced pathologies as well as their interactions underlying malnutrition.

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Peer Reviewed Article: Malnutrition and Poverty

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Peer Reviewed Article: Malnutrition and Poverty

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This is a great article that discusses the effects of poverty and how those suffering from it are all the more likely to suffer malnutrition.

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Division of Women and Child Health, Aga Khan University, Karachi, Pakistan

Robinson Research Institute, Adelaide Medical School, University of Adelaide, Adelaide, SA, Australia

Despite social and economic development, the burden of malnutrition across the globe remains unacceptably high. A vital relationship exists between nutritional status, human capital, and economic standing. Malnutrition adversely affects the physiological and mental capacity of individuals; which in turn hampers productivity levels, making them and their respective countries more susceptible to poverty. A two-way link exists between malnutrition and poverty, creating a vicious cycle with each fueling the other. Malnutrition produces conditions of poverty by reducing the economic potential of the population and likewise, poverty reinforces malnutrition by increasing the risk of food insecurity. The aim of the paper is to describe the interconnection between malnutrition and poverty, and to highlight how both serve as the cause and consequence of each other. The paper also discusses ways to move ahead to tackle these issues in a parallel manner rather than in separate silos.

Introduction

Malnutrition relates to a deficiency, excess, or imbalance of energy and other macro and micro-nutrients. It comprises of varying degrees of under- or over- nutrition, which leads to changes in body composition, body function, and clinical outcomes. In other words, malnutrition is an all-inclusive term that represents all manifestations of poor nutrition and ranges from extreme hunger and undernutrition to obesity ( 1, 2). Despite social and economic development, the burden of malnutrition across the globe remains unacceptably high ( 2), recent data suggests that ~800 million people are undernourished, out of which 780 million reside in low-to-middle income countries, especially in Sub-Saharan Africa and South Asia ( 2). In 2015, inadequate food intake and poor dietary quality were responsible directly or indirectly for causing ill-health with six of the top 11 global risk factors being associated with dietary imbalances ( 2) and in 2017, 11 million deaths and 255 million disability-adjusted life years (DALYs) were attributable to dietary risk factors ( 3). Children under the age of 5 years are highly vulnerable to malnutrition with estimates suggesting that in 2019, globally 144 million children under the age of five were stunted (short for his/her age), 47 million wasted (thin for his/her height) and 38 million overweight (abnormal or excess bodyweight) ( 4). In adults, obesity is becoming more prevalent worldwide with ~38.9% of the adult population being either overweight or obese ( 5). Paradoxically, even though women have a higher prevalence (15.1%) of obesity than men (11%) ( 5); millions of women around the world are still underweight and one-third of women of reproductive age are estimated to have anemia ( 5).

Malnutrition has long been linked to poverty as higher rates of malnutrition are found in areas with chronic poverty ( 6). The impact of poverty on individuals can be seen through multiple manifestations and includes poor nutritional status, food insecurity, vulnerability to disease, reduced productivity levels, and compromised physical and intellectual development. Additionally, people living in poverty are unable to access necessities including nutritious food, hygienic environment, appropriate shelter, and adequate health care ( 7). Therefore, it would not be incorrect to suggest that even though malnutrition is a global phenomenon, those living in poverty face a higher burden. The question that now arises is whether malnutrition is a cause or consequence of poverty. The relationship between the nutritional status and economic standing has been further explored through the course of this paper.

Poverty

The World Bank has set the International Poverty Line at $1.90 per person per day using 2011 Purchasing Power Parity (PPP) conversion factors ( 8). Therefore, households with a per capita income or expenditure less than the standard poverty line are defined as being poor ( 9). This makes income level the prime indicator for poverty, however with the passage of time, the need for re-conceptualizing poverty is becoming more evident as poverty is complex and multifaceted. Therefore, the conceptualization of poverty should not be limited to average income and wealth only but should encompass various other deprivations that are often experienced by people living in poverty. The global Multidimensional Poverty Index (MPI) is an international measure of acute poverty covering over 100 developing countries; created by the Oxford Poverty and Human Development Initiative (OPHI) and the United Nations Development Programme (UNDP) in 2010 ( 10). The global MPI steps away from the traditional view of poverty being solely limited to average income and wealth; to a more holistic view that highlights the need for using multiple indicators to account for various issues faced by people as a consequence of poverty ( 10). Through this index, poverty is portrayed to be a deprivation of basic amenities that restricts individuals from leading a good and healthy life ( 11) and takes into account the systemic disparities within a country and stretches the boundaries of poverty beyond the shortage of material assets to a concept that encompasses multiple deprivations, including but not limited to: assets, living standards, education, sanitation and hygiene, health and nutrition ( 10).

Since the 1990s, it is estimated that the proportion of the world's population living in extreme poverty has declined by more than a half ( 8). In 2015, 10% of the world's population lived under the poverty line; compared to nearly 36% in 1990 ( 8). Unfortunately, despite the overall decline in global poverty, progress has been uneven and disproportionate with the majority of the world's poor residing predominantly in Sub-Saharan Africa and South Asia ( 8). In 2015, 736 million people lived in extreme conditions of poverty with half of them i.e., 368 million residing only in five countries of India, Nigeria, Democratic Republic of Congo, Ethiopia, and Bangladesh ( 8). This illustrates that certain countries especially those afflicted by conflict, poor governance, and natural disasters continue to experience a skewed burden of poverty.

To analyze the vital linkages between poverty and malnutrition; it is important to highlight the growing evidence that health outcomes including malnutrition are driven by social determinants of health i.e., the conditions and circumstances in which people live, learn, work, and even play have a significant impact on their health ( 12). This interconnection between people's conditions and circumstances and their health can be displayed using the concept of poverty and food insecurity. The term "food insecurity" refers to a situation in which people do not have adequate physical, social or economic access to sufficient and nutritious food ( 13). Broadly, food insecurity is assessed using four dimensions i.e., food availability, access to food, stability of supply and safe, and healthy food utilization ( 14). Food insecurity may occur at various levels including regional, national, household, or individual. Poverty and food insecurity are deeply related, as poverty may adversely affect the social determinants of health and may create unfavorable conditions in which people might experience unreliable food supply ( 13). Food is a major household expenditure for the poor households ( 15). Data from African countries indicate that close to half of household income is spent on food: Nigeria (56.4%) ( 16); Kenya (46.7%), Cameroon (45.6%), Algeria (42.5%) ( 17). Similarly, within high-income countries, low-income households spend a significant proportion of their income on food: Ireland (14-33%), USA (28.8-42.6%) ( 17, 18). In comparison, the wealthiest households in the USA spend a much lower 6.5-9.2% of household income on food ( 17). Despite spending a large proportion of their household income on food, many poor households continue to remain food insecure because of their insufficient, irregular, and fluctuating incomes ( 2, 13).

Poverty, Food Insecurity and Double Burden of Malnutrition

A vital relationship exists between malnutrition and poverty. Poverty creates unstable and unfavorable conditions that may contribute to fueling the problem of malnutrition ( 7). People living in poverty often face financial limitations, which hinders their ability to access safe, sufficient, and nutritious food ( 7). Food insecurity compromises people's ability to acquire the amount of food needed to fulfill the bodily requirement of calories and without sufficient calorie intake, an individual may not be able to build up energy or strength to carry out everyday life activities and this also hampers the capacity and productivity to earn ( 19). While people living in poverty may require a greater quantity of food than they cursrently have, it is important to take into consideration that appropriate intake of nutrients and quality of food is equally important ( 19). Poverty can contribute to worsening malnutrition by compromising the quality of food intake and bolstering hidden hunger which is the deficiency of essential vitamins and minerals. The burden of obesity has extended beyond wealthier, developed nations and has now also become a feature of the developing world ( 16). Poverty leads to financial constraints that in turn lead to the consumption of cheap, high-energy staple foods, primarily carbohydrates, and fats rather than nutritionally dense food. Through the consumption of carbohydrates and fats, energy levels spike; but nutritional quality becomes compromised. The consequence of this is reduced nutritional quality and nutrient deficiencies. Poverty plays a significant role in regulating access and preference of foods ( 13, 16), and this is evident in studies that showcase that when people living in poverty get a chance to spend relatively more on food; they often prefer to buy better tasting food, rather than good quality food ( 19).

The deficiency of micronutrients or "hidden hunger" is an important component of malnutrition ( 13). Micronutrient deficiencies can exists in all age groups and in any socioeconomic bracket. Iron, folate, vitamin A, iodine, and zinc deficiencies are among the most common and widespread micronutrient deficiencies among women and children in low- and middle- income countries and many of these micronutrient deficiencies co-exist. Assessing the relationship between malnutrition and poverty, requires consideration of micronutrient deficiencies. While macro- and micro- nutrient deficiencies may cause suboptimal mental and physical development, recurrent infections and growth retardation ( 20, 21); micro-nutrient deficiencies may also result in adverse birth outcomes including low birth weight babies ( 22, 23). To date, ~20 million babies are born with low birth weight each year and there is growing evidence of the connections between slow growth in height early in life and impaired health and educational and economic performance later in life ( 5, 24). Low birth weight in babies can contribute to the vicious cycle of malnutrition since maternal nutrition status especially maternal stature has been reported to be inversely associated with offspring mortality, underweight, and stunting in infancy and childhood ( 22, 23). Moreover, the importance of adequate intake of micronutrients can be noted in children born to mothers with sufficient amounts of iodine during pregnancy ( 19), as these children tend to complete one-third or one-half a year more schooling than children born to mothers with inadequate amount of iodine during pregnancy ( 19). It has been suggested that if every mother took iodine capsules during pregnancy then this could improve educational attainment among children in Central and Southern Africa ( 19).

Briefly put, the double burden of malnutrition and the importance of micro-nutrients should be recognized when analyzing the malnutrition-poverty cycle. There is a growing need to reimagine the concept of malnutrition and development experts and policy makers should make strides to account for the inherent complexities of both concepts in order to develop successful and sustainable nutritional strategies ( 19).

Malnutrition: Cause or Consequence of Poverty?

The question that now arises is whether malnutrition is a cause or consequence of poverty and vice versa? To elaborate upon this, it is important to highlight the relationship of human capital with nutrition and poverty.

Human capital is an integral asset of any country and the process of developing human capital begins from infancy and continues throughout the course of an individual's life ( 25). Nutritional status has a profound impact on human capital. The reasoning is simple, improved nutritional status is vital for escaping poverty, as good health is needed to increase productivity levels, contribute to economic growth, and improve a country's overall welfare ( 6). Without adequate nutrition, human capital starts to decline. This is because malnutrition negatively impacts physical and mental development, intellectual capacity, productivity, and the economic potential of an individual ( 25). As a consequence, economic stability is threatened, making a country more vulnerable to poverty. Poverty contributes to the problem of food insecurity which is referred to as a "resourced-constrained" or "poverty related" condition. Although the populations affected by poverty and food insecurity overlap; it is important to note that not all people living in poverty are food insecure and that this problem also exists in people living above the poverty line. Moreover, poverty also contributes in creating conditions of micro-nutrient deficiencies and hidden hunger. These factors exacerbate the issue of malnutrition and makes individuals more vulnerable to other health concerns. Irregular and unstable food supply along with low quality of food due to insufficient or inadequate nutrient intake can compromise immunity and make individuals more susceptible to infections. Additionally, if infected, matters tend to become worse because infections may further reduce nutritional and health status, thereby aggravating malnutrition and reinforcing its cycle with poverty ( 25, 26).

A vicious cycle exists through which both poverty and malnutrition fuel and reinforce each other ( 25). Globally, the poorest countries are the countries bearing the highest burden of malnutrition. Nutritional imbalances reduce work capacity and human capital; and this makes countries more susceptible to poverty. Furthermore, malnutrition is also a consequence of poverty, as poverty increases food insecurity and hidden hunger; which contributes to the problem of malnutrition. This makes both these elements a cause and a consequence of each other. Establishing a linear relationship between the two would overlook the complexities and nuances that exist within the framework of this topic.

What Will be the Next Steps?

In order to progress socially and economically, there is an urgent need to recognize the burden of poverty and malnutrition and to take immediate steps to break the ongoing cycle. To achieve this target, it is important to understand what factors feed and reinforce it.

The cycle of poverty and malnutrition appears to be intergenerational. Evidence suggests that malnourished women are at a higher risk of having malnourished children and this creates an intergenerational effect ( 6). It is imperative to intervene early in life in order to maximize the effectiveness of interventions and break the cycle. The Lancet Nutrition Series ( 27) modeled the effect of 10 evidence based nutrition specific interventions on lives saved in the 34 countries that have 90% of the world's children with stunted growth. The series also examined the effect of various delivery platforms and delivery options using community health workers to engage poor populations and promote behavior change, access to and uptake of these interventions. Findings suggest that the current total of deaths in children younger than 5 years can be reduced by 15% if populations can access these 10 evidence-based nutrition interventions at 90% coverage. These nutrition specific interventions included salt iodization, multiple micronutrient supplementation in pregnancy (includes iron-folate), calcium supplementation in pregnancy, energy-protein supplementation in pregnancy, vitamin A supplementation in childhood, zinc supplementation in childhood, breastfeeding promotion, complementary feeding education, complementary food supplementation, and management of severe acute malnutrition in children. The findings also support the use of various community engagement and delivery strategies that can help reach poor segments of the population at greatest risk in order to make a difference ( 27). In other words, the interventions need to reach the poorest of the poor to break the cycle of malnutrition and poverty and should also incorporate disease and infection prevention as a part of their strategy ( 25).

Considering the inter-linkages described above between malnutrition and poverty, nutrition specific interventions need to be augmented with nutrition sensitive interventions in order to accelerate the progress of reducing malnutrition. Nutrition sensitive interventions are those that address intermediate and underlying causes of malnutrition and help to improve access to nutritious food, clean water and sanitation, education and employment, and health care etc. Large scale nutrition programs focusing on evidence based nutrition interventions should also target key underlying determinants of nutrition including poverty in order to enhance the coverage and effectiveness of nutrition-specific interventions. These include interventions in the sectors of agriculture, social safety nets, early child development, education, and women's empowerment. Women's empowerment is instrumental in not only improving malnutrition but general well-being ( 28). Hence, a parallel focus on nutrition sensitive and nutrition specific interventions has the potential to greatly accelerate progress in not only the areas of nutrition but also break the intergenerational cycle of malnutrition and poverty ( 29). More recently, bio-fortification and agricultural biodiversity are also considered to have the potential to cater to the issues of poverty and malnutrition in a parallel manner ( 30). In developing countries, bio-fortification could focus on improving quality of coarse cereals, as well as fodders along with community participatory approaches to enhance agricultural biodiversity. This approach not only could contribute to a reduction in malnutrition and poverty, but reduce food insecurity and improve sustainability ( 31, 32), though further research is needed in the domain ( 30, 31). Income disparity is also a factor that allows the malnutrition-poverty cycle to persist. In fact, a country may experience economic growth, but still have widespread poverty and high levels of malnutrition. This is because income inequality translates as health inequality; as the income gap grows, so does health disparity ( 7, 13, 25). Furthermore, gender inequities have also been associated with both poverty and malnutrition as a result of lower opportunities for women in the fields of education and employment. A recent analysis based on data from 49 low- and middle-income countries assessing the relationship between gender equity and malnutrition and health suggests that gender equity in education and employment decreases child malnutrition and is an important determinant in nutrition and access to health care ( 33). Therefore, any attempt to improve global nutritional status and to achieve the targets set by the "2030 Agenda for Sustainable Development" requires a focus on alleviating poverty and simultaneously focusing on agriculture, social safety nets, early child development, education, and strengthening women's position in society ( 34- 37).

Nutritional interventions should be designed in an all-rounded, holistic manner. It would be fruitful to involve multiple stakeholders including health, education, agriculture, water, sanitation and hygiene, gender and economics. To ensure sustainability, nutritional interventions should be context-specific and should also be cost-effective since these issues concern low and middle income countries.

Conclusion

Ending poverty in all its forms is the first of the 17 Sustainable Development Goals and ending hunger, reducing food insecurity and improved nutrition and agriculture is the second goal. Furthermore, at least 12 of the 17 goals contain indicators that are highly relevant to nutrition. Poverty and malnutrition are deeply interrelated, with each fuelling the other and hence it is imperative to tackle both issues simultaneously rather than in parallel silos. A two-way link exists, with both elements being the cause and consequence of each other. This vicious cycle remains a prime public health concern and immediate strides need to be made against it. For a sustainable improvement in nutritional outcomes, the battle against poverty and malnutrition has to be fought on all fronts, to achieve a healthier and more equitable society.

Author Contributions

All authors contributed to the study and the write-up.

Conflict of Interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

References

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Frontiers | The Intertwined Relationship Between Malnutrition and Poverty

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Despite social and economic development, the burden of malnutrition across the globe remains unacceptably high. A vital relationship exists between nutrition...

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This article talks about the urgent need for help regarding the crisis of malnutrition, particularly of children in Malawi.

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Lilongwe, 19 May 2023 - At least 573,000 children under five are at risk of suffering from malnutrition in Malawi, UNICEF warns. Despite recent progress in reducing chronic malnutrition, acute food insecurity-compounded by recurrent climate shocks, preventable disease outbreaks, economic instability, and chronic underfunding in the social sectors - threatens to reverse past gains.

Malawi is still grappling with the devastation caused by Tropical Cyclone Freddy in March, with 659,000 people currently internally displaced, including many children. Meanwhile, an ongoing cholera outbreak in the country has already claimed 1,759 lives.

"Children in Malawi are at the sharp end of the global polycrisis. Food insecurity, exasperated by a growing climate crisis, disease outbreaks, and the global economic downturn, is threatening to wreak havoc and disrupt the lives of millions of children," said UNICEF Country Representative Gianfranco Rotigliano. "The prospect of having over half a million children suffering from malnutrition is unacceptable. Without an immediate response, the impact on these vulnerable children will be deadly."

A new Humanitarian Action for Children (HAC) appeal, launched by UNICEF today, shows an increase in malnutrition cases among children in Malawi over the last five years, with the challenge accelerating significantly in recent months. In 2023 alone, it is estimated that over 62,000 children, aged between 6 to 59 months, are at risk of severe acute malnutrition (SAM), often called wasting.

To respond to the urgent needs of 6.5 million people, including 3.3 million children, UNICEF has increased its appeal for Malawi from US$52.4 to US$87.7 million. This funding will be used to meet priority needs, such as ready-to-use therapeutic food (RUTF) for treating severe acute malnutrition, access to safe drinking water, sanitation, hygiene items, health, nutrition, education, child protection services, and cash transfer schemes.

In the first quarter of 2023, with the support of donors and partners, UNICEF assisted the Government of Malawi in screening 140,307 children under the age of five for acute malnutrition. Among them, 522 children were identified as having SAM and were referred to health facilities for further care.

"Without increased support, poor and vulnerable households with children will be left without access to basic services, essential supplies, and social assistance," said Rotigliano. "But beyond the immediate response, it is crucial that we invest in long-term solutions by strengthening systems and building resilience within communities to handle recurring outbreaks and humanitarian emergencies better."

#####
Note to Editors: Malawi Appeal | Humanitarian Action for Children: https://www.unicef.org/appeals/malawi

In the first quarter of 2023, thanks to the support of donors and partners, UNICEF supported the Government of Malawi to achieve the following:

Reached over 1.2 million people with a sufficient quantity and quality of water for drinking and domestic needs, over 3 million with critical water, sanitation, and hygiene supplies, and over 200,000 with appropriate sanitation services.

Supported over 19,000 children and adults in accessing treatment at cholera treatment centres.

Trained more than 11,000 healthcare and community workers in infection prevention and control, as well as case management of cholera.

Provided cash transfers to 20,921 households in Blantyre and Zomba, two key affected districts.

Trained 243 teachers on cholera prevention and management in 92 schools, benefiting 167,379 young learners.

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Over half a million children at risk of malnutrition in Malawi

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Lilongwe, 19 May 2023 - At least 573,000 children under five are at risk of suffering from malnutrition in Malawi, UNICEF warns. Despite recent progress in reducing chronic malnutrition, acute food insecurity-compounded by recurrent climate shocks, preventable disease outbreaks, economic instability, and chronic underfunding in the social sectors - threatens to reverse past gains.