There is no evidence that lipid supplementation is of benefit 56 , Nutrition and HIV are strongly related and complement each other. Boletín de la Asociación Médica de Puerto Rico. For example, HIV replication was enhanced in monocytes cultured with retinoid [ 59 ]. When children do not receive a sufficient amount of nutrients while they are growing, they may suffer from growth retardation. Though HIV-specific humoral immune responses can be detected during primary infection, they mostly comprise low-avidity env specific IgG antibodies with little or no neutralising activity [ 12 ]. HIV or human immunodeficiency virus infection has assumed worldwide proportions and importance in just a span of 25 years.
This leads to a longer recovery time and susceptibility to infection. Over nutrition negatively affects wound healing because it impedes white blood cells, oxygen and nutrients' abilities to get where needed. Severe weight loss is also known as cachexia. Your muscles will shrink and your bones will protrude.
You will have an increased chance of a hip fracture or pressure ulcers. Your hair will fall out and your skin will be rough and dry. If you suffer from malnutrition, you have an increased risk of organ failure. You will be more susceptible to jaundice, edema, liver failure, anemia, pneumonia, heart failure, gastroenteritis, kidney failure, sepsis and urinary tract infections. If you suffer from obesity, also known as over nutrition, you have a greater chance of suffering from a stroke, heart disease, high blood pressure, certain cancers and diabetes.
Malnutrition can lead to loss of concentration, memory and focus, which can result in increased stress. Certain diagnostic tests should be avoided, such as ADHD, until a person's nutritional health can be evaluated.
Some of the effects of malnutrition are behavioral. When your body's organs are affected, it disturbs your mental balance. You can experience several emotional irregularities including depression, irritability, rigidity, overwhelming sadness and anxiety.
If you suffer from an obsessive-compulsive disorder, your symptoms may become worse. Children suffering malnutrition can develop ailments, disorders and diseases that may affect them for the rest of their lives. If caught early enough, several of the effects of malnutrition can be reversed. This is especially so if the situation was only short term. A child suspected of being malnourished should be evaluated by a doctor. The doctor will be able to conduct a physical exam and check for underlying conditions that lead to malnutrition.
He will ask questions about the child's diet and eating habits. In addition, the doctor may also order blood tests, measure the child's body mass index, check height and weight and order other tests as deemed necessary. If an underlying condition is causing the child's condition, the doctor will recommend ways to help combat the malnutrition, which may include a referral to a specialist. If the problem lies with the amount and type of food the child eats, a dietitian will come up with a food plan and may recommend vitamin and mineral supplements.
The best way to treat malnutrition is to prevent it from occurring in the first place. A balanced diet is needed to maintain good health. Consumption of a variety of foods will help you accomplish this goal. The food groups in a healthy diet include proteins, fats, carbohydrates, dairy, fruit and vegetables. Last Updated 16 September, Overall Effects of Malnutrition 1. Body Mass Changes Lean body mass is naturally lost as you age but it can also be lost when you are malnourished.
Even in households with HIV-infected members, nutritional impacts can be seen if the infected adult becomes too sick to work and provide food for themselves and their families [ 5 , 6 ]. Dietary intake also varies inversely with level of virus, suggesting that viral replication directly or indirectly suppresses appetite [ 7 ].
Malnutrition is frequent and is considered a marker for poor prognosis among HIV-infected subjects [ 8 ]. Also, in acute viral infections such responses could be seen but they were generally not present in patients with chronic progressive infections. Antiviral immunity involves both the arms of the immune system. The protective component of cell-mediated immunity involves the cytotoxic CD8 T-lymphocytes. Schmitz and colleagues had demonstrated the effects of CD8 T lymphocytes in monkeys experimentally infected with simian immunodeficiency virus SIV.
Humoral immunity to HIV is expressed by neutralising antibodies. Anti-HIV antibodies are able to bind cell-free virus and potentially prevent established infection in the challenged host. Neutralising antibodies attaching to CD4 binding site of HIV have been identified which appear to prevent the virus from attaching to and infecting T cells. Though HIV-specific humoral immune responses can be detected during primary infection, they mostly comprise low-avidity env specific IgG antibodies with little or no neutralising activity [ 12 ].
Significant neutralising titers are believed to take place after chronicity has set in. HIV evolves various strategies to establish chronicity in human body. Initial CTL responses cause downregulation of viremia and prevent disease progression, but later it induces the selection of virus mutants capable of escaping the immune response [ 14 ].
Immune activation in HIV is supported by an experiment by Pandrea et al. High T-cell turnover in chronic HIV infection is attributed to overlapping and nonsynchronized bursts of proliferation, differentiation, and death in response to T-cell receptor- TCR- mediated stimulation and inflammation [ 16 , 17 ]. Antiretroviral therapy ART results in a marked reduction of T-cell activation and apoptosis and helps to decrease naive T-cell consumption and restore their numbers [ 18 ].
Chronic HIV infection also causes immunological or direct virotoxic effects on gastrointestinal tract which shows blunted villi, crypt hyperplasia, and damaged epithelial barrier with increased permeability and malabsorption of bile acid and vitamin B12, microbial translocation, and enterocyte apoptosis.
There is a decrease of luminal defensins and massive CD4 T-cell depletion but high concentration of infected CD4 T cells [ 19 ]. Malnutrition is considered to be the most common cause of immunodeficiency worldwide [ 20 ]. Malnutrition, immune system, and infectious diseases are interlocked in a complex negative cascade [ 1 ]. Malnutrition elicits dysfunctions in the immune system and promotes increased vulnerability of the host to infections [ 21 ].
Every type of immunological deficiency induced by malnutrition can be included under the NAIDS umbrella. Protein-energy malnutrition PEM , now known as protein-energy undernutrition, is an energy deficit due to chronic deficiency of all macronutrients [ 22 ]. In children, PEM causes widespread atrophy of lymphoid tissues, particularly T-lymphocyte areas.
The thymus involutes causing a reduction in the thymus-derived lymphocyte growth and maturation factors, arrest of lymphocyte development, reduced numbers of circulating mature CD4 helper cells, and impairment of antibody production to T-dependent antigens.
Imbalance in Th1-Th2 activation occurs depending on nature of stimuli and altered regulatory pathways, including responses mediated by the nuclear factor-kB NF-kB [ 23 ], a major transcription factor involved in the development of innate and adaptive immunity.
However, CD8 suppressor cells are relatively preserved. The lymphocytes not only get reduced in blood, but also impaired show T-lymphocyte mitogenesis and diminished activity in response to mitogens [ 24 ]. According to Chandra [ 25 ], in children with PEM, there is a decrease or reversal of the T-helper-suppressor cell ratio and total numbers of T-lymphocytes decrease due to reduced numbers of these T-cell subpopulations. In malnourished children, changes such as dermal anergy, loss of delayed dermal hypersensitivity DDH reactions, and loss of the ability of killer lymphocytes to recognize and destroy foreign tissues were noted [ 20 ].
Necropsy studies on malnourished patients have also shown profound depletion of the thymolymphatic system and severe depression of cell-mediated immunity. Chronic thymic atrophy with peripheral lymphoid tissue wasting along with depletion of paracortical cells and loss of germinal centres was noted. This was suggested to have led to various types of infections from which these patients actually died [ 26 ].
B-lymphocyte numbers and functions generally appear to be maintained though immunoglobulin concentrations get reduced including secretory IgA sIgA , which is responsible for mucosal immunity. This may be due to increased bacterial adherence to nasopharyngeal and buccal epithelial cells or altered expression of membrane glycoprotein receptors [ 27 ]. It has been speculated that the existing antibody production is conserved or even increased during generalized malnutrition but new primary antibody responses to T-cell-dependent antigens and antibody affinity are impaired [ 20 ].
The failure of antibody formation is reversed within a few days of protein therapy as amino acids become available for the synthesis of immune proteins [ 28 ]. It also reduces complement formation, and interferon and lower interleukin 2 receptors [ 26 ]. In patients with severe generalized malnutrition, functional status of the immune system should be assessed by simply looking at the tonsils in young children.
In adequately nourished children they are usually huge but are virtually undetectable in children with severe PEM. Deficiencies of other nutrients also adversely affect the immune mechanisms. Deficiencies of essential amino acids can depress the synthesis of proteins responsible for production of cytokines released by lymphocytes, macrophages, and other body cells, complement proteins, kinins, clotting factors, and tissue enzymes activated during acute phase responses [ 24 ].
Arginine deficiency diminishes the production of nitric oxide, and hence, the antioxidants, allowing damaging effects of free oxygen radicals [ 24 ]. Arginine has also been shown to enhance phagocytes of alveolar macrophages, depress T suppressor cells, and stimulate T helper cells [ 29 ]. Particularly the omega-3 fatty acids, serve as the key precursors for the production of eicosanoids like prostaglandins, prostacyclins, thromboxanes, and leukotrines that play a variety of host defensive roles.
Thus their deficiency in the diet can impair cytokine synthesis [ 30 ]. Vitamin A has an important role in nucleic acid synthesis, and its deficiency is also characterized by lymphoid tissue atrophy, depressed cellular immunity, impaired IgG responses to protein antigens, and pathologic alterations of mucosal surfaces.
Experimental animals with vitamin A deficiency have decreased thymus and spleen sizes, reduced natural killer cell, macrophage and lymphocyte activity, lower production of interferon, and weak response to stimulation by mitogens [ 31 ].
B-group vitamins like thiamin, riboflavin, pantothenic acid, biotin, folic acid, and cobalamin can influence humoral immunity by diminishing antibody production. Pyridoxine deficiency has also been associated with reduced cell-mediated immunity.
Folic acid and vitamin B are essential to cellular replication. Experimental deficiencies of these vitamins were shown to interfere with both replication of stimulated leukocytes and antibody formation. In anemia due to folic acid deficiency, cell-mediated immunity is depressed [ 32 ].
In vitamin C deficiency, phagocytic cells cannot produce tubulin, therefore, with impaired chemotaxis, microorganisms cannot be engulfed and destroyed [ 33 ].
Vitamin D acts as an immunoregulatory and a lymphocyte differentiation hormone [ 34 ]. In vitamin E deficiency, leukocyte especially lymphocyte killing power gets reduced. In animals it was shown to interfere with antibody formation, plaque-forming cells, and other aspects of cell-mediated immunity.
At higher than recommended levels, it has been shown to enhance immune response and resistance to disease [ 35 ]. Zinc is also the fundamental component of thymic hormones and shares a similar role as vitamin A in nucleic acid synthesis. Zinc deficiency influences both lymphocyte and phagocyte cell functions and affects more than metalloenzymes that are zinc dependent [ 36 ].
During infections, reticuloendothelial cells sequester iron from the blood and phagocytes release lactoferrin with a higher iron binding capacity than bacterial siderophores. The net effect is to deprive the infectious agent of iron for its replication and inhibit the spread of infection [ 34 ]. Iron deficiency results in impaired phagocytic killing, less response to lymphocyte stimulation, fewer natural killer cells, and reduced interferon production [ 37 ]. Selenium serves as an antioxidant and contributes to antibody responses and cytotoxicity of natural killer cells [ 38 ].
In children with HIV infection, selenium concentration in plasma appeared to correlate with their immune functions [ 39 ]. Similar changes were also seen in patients with copper deficiency [ 40 ]. Copper concentrations often increase during infection as a result of stimulation of the hepatic production of ceruloplasmin.
Conversely, plasma zinc concentration often declines due to internal redistribution to the liver. Antimicrobial systems in the neutrophils are affected by malnutrition. These include both oxygen-dependent systems responsible for the respiratory burst, and oxygen-independent systems, such as lactoferrin, lysozymes, hydrolase, and proteases [ 34 ].
Cytokines are substances that play an important role in coordinating inflammatory response of the body to various external and internal stimuli. They may be proinflammatory, which are essential to initiate defence against various pathogens, and anti-inflammatory, which downregulate the inflammatory process by suppressing production of the proinflammatory cytokines and balance the inflammatory response. Excess production of both are counterproductive.
Severe malnutrition alters the ability of T lymphocytes to respond appropriately to IL-1 rather than simply affecting synthesis of this monokine [ 42 ]. During catabolic states, interleukin 1 is released by leukocytes which causes endocrine changes that lead to amino-acid mobilization, primarily from skeletal muscle. These amino acids are used for gluconeogenesis in the liver, and the nitrogen released is excreted in urine [ 43 ].
Thus, a continual conversion of alanine carbon to glucose carbon occurs with acute infection.