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Недостаточность питания и ВИЧ / СПИД.

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СОДЕРЖАНИЕ

1. Иммунология питания.

2. Недостаточность питания и ВИЧ / СПИД.

3. Недостаточность питания и прогрессирование ВИЧ-инфекции индивидуалы к СПИДу.

4. Недостаточность питания и” передача" ВИЧ-СПИД.

5. Окислительный стресс и ВИЧ / СПИД.

6. Недостаточность питания и антиоксидантов в патогенезе СПИДа.

7. Питательная и антиоксидантная терапия для профилактики и лечения СПИДа.

8. Выводы.

9. Ссылки на литературу.

ИММУНОЛОГИЯ ПИТАНИЯ.

Влияние недоедания на лимфоидные органы описан в середине 19-го century (1). Лимфоидные ткани особенно уязвимы к повреждающим воздействиям недоедания и лимфоидной атрофии 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 имеют поврежденную задержанную кожу гиперчувствительность, плохая реакция пролиферации лимфоцитов к митогенам, более низкий синтез ДНК лимфоцита, уменьшенные номера розеттинг Т лимфоциты, поврежденное созревание лимфоцитов увиденное через повышенная активность дезоксинуклеотидилтрансферазы, сниженная сыворотка тимический фактор, меньше CD4 + клеток, снижение соотношения CD4+ / CD8+, нарушение продукция интерферона гамма и интерлейкина 2, измененного комплемента деятельность (особенно уменьшение C3, C5, фактора B и итога гемолитическая деятельность), плохая вторичная реакция антитела к некоторому антигены, уменьшенное сродство антитела, поврежденный секреторный ответ иммуноглобулина А, уменьшенное сродство антитела, и фагоцит дисфункция (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).

Внутриматочный недоедание вызывает длительную, даже постоянную депрессию иммунитета в потомстве (13-14).

Значительный данные вовлекают избыточное потребление липидов в нарушение иммунитета ответы (15). Потенциал повреждения свободными радикалами зависит от большая часть на уровне потенциально окисляемых жирных кислот, главным образом полиненасыщенные жирные кислоты (ПНЖК) в рационе (15). Высокие уровни были показаны, что будут диетические PUFAs иммунодепрессивны. Диетический жир смогите пройти свободн-радикал-посредничанную оксидацию до заглатывания, как может произойти, когда пища жарится (15). Животные кормили окисленные липиды показать отмечена атрофия тимуса и дисфункция Т-лимфоцитов (15).

На молекулярный уровень, повреждение к иммунокомпетентным клеткам несколькими недостаточность питания (PCM, витамин А, Витамин С, Витамин Е, цинк, медь, дефицит зеления) вызвано повышением свободных радикалов через оксидативный стресс (8-11, 15, 16).

CONCLUSIONS

A) Nutritional and antioxidant deficiencies have been documented in all patients with AIDS.

B) Nutritional and antioxidant deficiencies are a requisite prior to reacting positively on “HIV tests.”

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

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

E) 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.

F) Some of the nutritional and antioxidant supplements that have been used in the treatment and prevention of AIDS are: 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.

G) To prevent and treat AIDS in Africa, an absolute requisite is the provision of 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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206. Giraldo RA, Ródenas P, Flores JJ, Embid A. Tratamiento y prevención del sida: guía de principios básicos para una alternativa no tóxica, efectiva y barata. November 2002 http://www.robertogiraldo.com/esp/articulos/Tratamiento_y_Prevencion_2002.html

_______________________

* * 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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СОДЕРЖАНИЕ

1. Иммунология питания.

2. Недостаточность питания и ВИЧ / СПИД.

3. Недостаточность питания и прогрессирование ВИЧ-инфекции индивидуалы к СПИДу.

4. Недостаточность питания и” передача" ВИЧ-СПИД.

5. Окислительный стресс и ВИЧ / СПИД.

6. Недостаточность питания и антиоксидантов в патогенезе СПИДа.

7. Питательная и антиоксидантная терапия для профилактики и лечения СПИДа.

8. Выводы.

9. Ссылки на литературу.

ИММУНОЛОГИЯ ПИТАНИЯ.

Влияние недоедания на лимфоидные органы описан в середине 19-го century (1). Лимфоидные ткани особенно уязвимы к повреждающим воздействиям недоедания и лимфоидной атрофии 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 имеют поврежденную задержанную кожу гиперчувствительность, плохая реакция пролиферации лимфоцитов к митогенам, более низкий синтез ДНК лимфоцита, уменьшенные номера розеттинг Т лимфоциты, поврежденное созревание лимфоцитов увиденное через повышенная активность дезоксинуклеотидилтрансферазы, сниженная сыворотка тимический фактор, меньше CD4 + клеток, снижение соотношения CD4+ / CD8+, нарушение продукция интерферона гамма и интерлейкина 2, измененного комплемента деятельность (особенно уменьшение C3, C5, фактора B и итога гемолитическая деятельность), плохая вторичная реакция антитела к некоторому антигены, уменьшенное сродство антитела, поврежденный секреторный ответ иммуноглобулина А, уменьшенное сродство антитела, и фагоцит дисфункция (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).

Внутриматочный недоедание вызывает длительную, даже постоянную депрессию иммунитета в потомстве (13-14).

Значительный данные вовлекают избыточное потребление липидов в нарушение иммунитета ответы (15). Потенциал повреждения свободными радикалами зависит от большая часть на уровне потенциально окисляемых жирных кислот, главным образом полиненасыщенные жирные кислоты (ПНЖК) в рационе (15). Высокие уровни были показаны, что будут диетические PUFAs иммунодепрессивны. Диетический жир смогите пройти свободн-радикал-посредничанную оксидацию до заглатывания, как может произойти, когда пища жарится (15). Животные кормили окисленные липиды показать отмечена атрофия тимуса и дисфункция Т-лимфоцитов (15).

На молекулярный уровень, повреждение к иммунокомпетентным клеткам несколькими недостаточность питания (PCM, витамин А, Витамин С, Витамин Е, цинк, медь, дефицит зеления) вызвано повышением свободных радикалов через оксидативный стресс (8-11, 15, 16).

НЕДОСТАТОЧНОСТЬ ПИТАНИЯ И ВИЧ / СПИД.

Since the beginning of the AIDS epidemic, researchers have provided scientific evidence that supports the possibility that AIDS can be effectively prevented, treated, and overcome by guaranteeing an optimal nutritional status to the individual or the patient (17,18). However, it seems that propaganda spread by pharmaceutical companies to commercialize antiretroviral medications has prevented these ideas from being widely accepted, despite the toxicity of these medications.

Early in the AIDS era, well recognized researchers in the field of nutrition and immunology, such as Dr. Ranjit Kumar Chandra, noticed that: “There is an uncanny similarity between the immunological findings in nutritional deficiencies and those seen in acquired immunodeficiency syndrome, AIDS” (17).

“There is a similarity between the immune deficiency, multiple infections, and severe weigh loss seen in AIDS patients, and the association of protein caloric malnutrition (PCM) with reduced resistance to infection observed in malnourished children, particularly in the Third World.” “It is also possible that nutritional deficiency may play a significant role in the clinical course of the immunodeficient state.” “These similarities between AIDS and PCM suggest that nutrition may contribute to the immunodeficient state. The immunodeficiency in children with PCM can be reversed by nutritional rehabilitation, which suggests that restoration of nutritional state may be a useful adjunct to therapy for AIDS patients” (19).

As described above, the immunological alterations found in PCM are practically identical to those of AIDS: impaired delayed cutaneous hypersensitivity, lymphocyte proliferation response to mitogens, complement activity and secondary response to antigens. There is also a reduced number of rosetting T lymphocytes, increased deoxynucleotidyl transferase activity, decreased serum thymic factor, fewer helper T cells, impaired production of interferon gamma and interleukins 1 and 2, reduced antibody affinity, impaired secretory immunoglobulin A (IgA) antibody response and phagocyte dysfunction. The proportion of helper/inducer T lymphocytes recognized by the presence of CD4 positive antigen on the cell surface is markedly decreased. The ratio CD4/CD8 is significantly decreased. Lymphoid atrophy is a prominent feature of nutritional deprivation. Serum antibody responses are generally intact in PCM. Most complement components are decreased, especially C3, C5, factor B and total hemolytic activity (20-26).

“Nutritional problems have been a part of the clinical aspects of AIDS from its earliest recognition as a new disease” (20,24). “In fact, in many AIDS patients, death seams to be determined more by the individual's nutritional status than by any particular opportunistic infection. This is, when wasting of lean body mass approaches 55% of normal for age, sex, and height, death is imminent regardless of the forces resulting is such profound malnutrition” (20-24). Moreover, the severity of the clinical manifestations of AIDS is proportional to the degree of the nutritional deficiencies (27-30).

In addition to supporting optimal function of the immune system, nutrition is especially critical in children, as it provides the best opportunity for normal growth and development (31,32).

“All persons with HIV infection should be screened for nutritional problems and concerns at the time of their first contact with a health care professional, and routine monitoring should be performed on an ongoing basis” (31).

Scientific evidence strongly suggests that nutritional and antioxidant deficiencies are a prior requisite to both reacting positively on the tests for HIV (ELISA, Western blot, Viral Load) (33-36) and progressing to AIDS (37,38).


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