Nutritional deficiencies and hiv/aids.

ИММУНОЛОГИЯ ПИТАНИЯ.

Этот впервые описано влияние недостаточности питания на лимфоидные органы в середине 19^-го century (1). Лимфоидный ткани особенно уязвимы к повреждающим воздействиям недоедание, и лимфоидная атрофия видная особенность внутри лишение питания (2-5). Деление клеток является очень сингулярным характеристика функционирования иммунокомпетентных клеток. Все виды иммунных клеток и их продуктов, таких как интерлейкины, известно, что интерфероны и комплемент зависят от метаболизма пути которые используют различные питательные вещества как критические со-факторы для их действия и действия (5,6). Большая часть обороны хозяев механизмы изменяются при белковой калорийной недостаточности (ПКМ), а также как и при дефиците микроэлементов и витаминов (2,4,7,8).

Пациенты с ПКМ повреждали задержанную кожную гиперчувствительность, плохую реакция пролиферации лимфоцитов к митогенам, более низкому синтезу ДНК лимфоцитов, сниженное количество розеточных Т-лимфоцитов, нарушение созревание лимфоцитов, наблюдаемое через повышенный дезоксинуклеотидил активность трансферазы, снижение сывороточного тимического фактора, снижение CD4+ клетки, снижение соотношения CD4+ / CD8+, нарушение продукции интерферона гамма и интерлейкин 2, измененная активность комплемента (особенно снижение С3, С5, фактора В и общей гемолитической активности), плохой вторичная реакция антитела к некоторым антигенам, уменьшенное антитело аффинити, поврежденный секреторный ответ иммуноглобулина А, уменьшенный сродство антитела, и дисфункция фагоцита (2-7).

Человеческий недоедание обычно составной синдром множественного питательного вещества недоработки. Однако, изолированные дефициты микронутриентов случаются. Дефицит витамина А приводит к в уменьшении в весе тимус, уменьшенная пролиферация лимфоцита, поврежденный естественный убийца деятельность при клетки и макрофага, и увеличенное бактериальное придерживание к эпителиальные клетки (8-11). Дефицит витамина B6 производит отказ несколько компонентов как клетк-посредничанных, так и гуморальных иммунных реакций (2,4,7). Дефицит витамина С ухудшает фагоцитоз и опосредованный клетками иммунные реакции (12). Дефицит витамина Е также изменяет иммунитет отзывчивость (2,4,7). Дефицит цинка порождает лимфоидную атрофию, уменьшает реакции лимфоцитов и гиперчувствительность кожи задержанную (2,4,7). Дефицит меди и Селена ухудшает т-и В-лимфоциты функции (2,4,7). Диетические дефициты выбранных аминокислот такие по мере того как глутамин и аргинин также изменяют невосприимчивость (2,4,7).

Бета-каротин провитамин каротиноид который может увеличить Т-клетку и в-клетку иммунная функция, по возможности через преобразование к витамину A или мимо действует как антиоксидант (13,14). Ежедневное добавление бета-каротин среди пожилых добровольцев привел к увеличению Т-лимфоциты и клетки с рецепторами интерлейкина-2 (13). Furthermore, supplementation с бета-каротином или витамином A связанный с увеличенным клетчатым иммунитетом как в людях, так и в животных (13,15-17). Кроме того, витамин А повышает гуморальный иммунитет, продемонстрированный ответом антитела к столбняку (18) и Кори (19) антигены.

Supplementation with vitamin E in healthy elderly people significantly improved lymphocyte proliferation, IL-2 production, DTH, and response to T-cell-dependent vaccines, and reduced the incidence of infections (20,21).

Vitamin C is an antioxidant that plays a role in immune responses and the formation of connective tissues. Proliferation of T and B lymphocytes increased following supplementation with vitamin C (22), and increased levels of vitamin C have been associated with lower rate of infections (23).

Several B-complex vitamins have roles in immune functions. Vitamin B6 deficiency in healthy elderly individuals significantly reduced the total number of lymphocytes, lymphocyte proliferation, and IL-2 production in response to mitogens; these defects were corrected following B6 repletion (24). Riboflavin deficiency has been shown to impair the ability to generate antibodies (25). Clinical studies show that individuals with low serum vitamin B12 had impaired neutrophil function, while animal studies indicate that vitamin B12 supplements are associated with enhanced humoral and cellular immune responses (25).

Selenium is necessary for the proper functioning of the enzyme glutathione peroxidase, which acts as an antioxidant (26). Selenium deficiency is associated with impaired phagocytosis, decresed CD4 T-lymphocytes, and the occurrence of opportunistic infections (26). Selenium supplementation as parenteral nutrition improved immune response in patients with chronic gut failure (27).

Zinc plays an important role in the growth, development, and function of natural killer cells, macrophages, neutrophils, and T and B lymphocytes (28). Zinc supplementation has resulted in significant reductions in the severity of diarrhea, malaria, and acute respiratory infections among children (29).

Intrauterine malnutrition causes prolonged, even permanent, depression of immunity in offspring (30,31).

Considerable data implicate excess lipid intake in the impairment of immune responses (32). The potential for free radical damage is dependent in large part on the level of potentially oxidizable fatty acids, mainly polyunsaturated fatty acids (PUFAs) in the diet (32). High levels of dietary PUFAs have been shown to be immunodepressive. Dietary fats may undergo free radical-mediated oxidation prior to ingestion, as can occur when foods are fried (32). Animals fed oxidized lipids show marked atrophy of the thymus and T lymphocyte dysfunctions (32).

At the molecular level, the damage to immunocompetent cells by several nutritional deficiencies (PCM, Vitamin A, Vitamin C, Vitamin E, zinc, copper, zelenium deficiencies) is caused by increased free radicals through oxidative stress (8-11,32,33).

CONCLUSIONS

A) Nutritional and antioxidant deficiencies have been documented in all patients with AIDS as well as in persons who react positively on “tests for HIV.”

B) Scientific data indicate that nutritional and antioxidant deficiencies are a requisite prior to reacting positively on “tests for HIV.”

C) Nutritional and antioxidant deficiencies are also a requisite of “HIV-positive” individuals prior to the development of the clinical manifestations of AIDS.

D) Reactivity on “tests for HIV” in sub-Saharan Africa cannot be explained by sexual or vertical transmission. It is very probable that reacting positively on the so-called tests for HIV in Africa is a result of chronic exposure to poverty and its consequences, such as malnutrition, infections, and parasites.

E) Nutritional and antioxidant deficiencies play a major role in the pathogenesis of AIDS.

F) Nutritional and Antioxidant supplements are being used successfully in preventing and treating AIDS. An optimal nutritional and antioxidant status can guarantee success in preventing and treating AIDS.

G) Some of the nutritional and antioxidant supplements that have been used in the treatment and prevention of AIDS are; combinations of amino acids, vitamin A and carotenoids, vitamin C, vitamin E, selenium, n-acetyl cisteine, l-gluthamin, zinc, cooper, manganese, alphalipoic acid, coenzyme Q10, B-complex vitamins, and flavonoids or vitamin P.

H) To prevent and treat AIDS in Africa, it is an absolute requisite to provide at least the minimum food needs to HIV-positive individuals, to AIDS patients, and to all African communities. Moreover, diets rich in fresh and organic fruits, vegetables, and cereals, as well as diets rich in bifidogenic foods (yogurt, kumis) are known to be immune stimulants.

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_____________________________________

1 Physician, specialist in internal medicine, infectious and tropical diseases. New York. E-mail: [email protected] Website: www.robertogiraldo.com

 

Roberto A. Giraldo
www.RobertoGiraldo.com

 

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ИММУНОЛОГИЯ ПИТАНИЯ.

Этот впервые описано влияние недостаточности питания на лимфоидные органы в середине 19^-го century (1). Лимфоидный ткани особенно уязвимы к повреждающим воздействиям недоедание, и лимфоидная атрофия видная особенность внутри лишение питания (2-5). Деление клеток является очень сингулярным характеристика функционирования иммунокомпетентных клеток. Все виды иммунных клеток и их продуктов, таких как интерлейкины, известно, что интерфероны и комплемент зависят от метаболизма пути которые используют различные питательные вещества как критические со-факторы для их действия и действия (5,6). Большая часть обороны хозяев механизмы изменяются при белковой калорийной недостаточности (ПКМ), а также как и при дефиците микроэлементов и витаминов (2,4,7,8).

Пациенты с ПКМ повреждали задержанную кожную гиперчувствительность, плохую реакция пролиферации лимфоцитов к митогенам, более низкому синтезу ДНК лимфоцитов, сниженное количество розеточных Т-лимфоцитов, нарушение созревание лимфоцитов, наблюдаемое через повышенный дезоксинуклеотидил активность трансферазы, снижение сывороточного тимического фактора, снижение CD4+ клетки, снижение соотношения CD4+ / CD8+, нарушение продукции интерферона гамма и интерлейкин 2, измененная активность комплемента (особенно снижение С3, С5, фактора В и общей гемолитической активности), плохой вторичная реакция антитела к некоторым антигенам, уменьшенное антитело аффинити, поврежденный секреторный ответ иммуноглобулина А, уменьшенный сродство антитела, и дисфункция фагоцита (2-7).

Человеческий недоедание обычно составной синдром множественного питательного вещества недоработки. Однако, изолированные дефициты микронутриентов случаются. Дефицит витамина А приводит к в уменьшении в