I am not interested in the bloody system! Why has he no food? Why is he starving to death?                                          - Bob Geldof in The Observer, 1985

Activation and sustenance of immune responses during infection requires increased energy consumption. Protein energy malnutrition (PEM) is a critical, yet underestimated factor in susceptibility to infection, including the “big three” infectious diseases: HIV/AIDS, tuberculosis, and malaria. In this article, we discuss current concepts and controversies surrounding the complex influences of malnutrition on infection and immunity, and point to practical consequences of countermeasures in acute malnutrition.

We call for new strategies to overcome worldwide morbidity and mortality caused by chronic malnutrition in impoverished countries and by the newly emerging public health threat of overnutrition in industrialized societies.

Background 

In response to infection, the immune system first executes innate and then subsequently acquired host defense functions of high diversity. Both processes involve activation and propagation of immune cells and synthesis of an array of molecules requiring DNA replication, RNA expression, and protein synthesis and secretion, and therefore consume additional anabolic energy. Mediators of inflammation further increase the catabolic response. Studies in a simple system, involving measurement of the survival of malnourished bumblebee workers, showed that the energy cost of immunity further impairs fitness [1].

Consequently, the nutritive status of the host critically determines the outcome of infection.

Apart from deficiencies in single nutrients, such as vitamins, fatty acids, amino acids, iron, and trace elements, undernourishment based on PEM greatly increases susceptibility to major human infectious diseases in low-income countries, particularly in children [2–4].

Malnutrition is responsible, directly or indirectly, for 54% of the 10.8 million deaths per year in children under five and contributes to every second death (53%) associated with infectious diseases among children under five years of age in developing countries [5]. Infection causes energy loss on the part of the individual, which reduces productivity on the community level and perpetuates the alarming spiral of malnutrition, infection, disease, and poverty (Figure 1).

Malnutrition and Infection

Malnutrition increases risk of infection PEM is a common cause of secondary immune deficiency and susceptibility to infection in humans (Table 1). This causal relationship is further supported by animal studies. Severe PEM in children is clinically defined as less than 70% weight-to-height and/or the appearance of pitting edema on both feet, described as either marasmus, a chronic wasting condition, or kwashiorkor, characterized by edema and anemia.

Children with kwashiorkor often suffer from marked skin infections. Severe malnutrition during childhood affects thymic development, which compromises immunity in children by a long-term reduction of peripheral lymphocyte counts [6].

This immunodeficiency represents a key factor in susceptibility to infections and has therefore been termed nutritionally acquired immunodeficiency syndrome [7].

In severely malnourished patients, both acquired immunity—i.e., lymphocyte functions—as well as innate host defense mechanisms—i.e., macrophages and granulocytes—are affected.

Diminished immune functions render undernourished patients more susceptible to infections, notably those by opportunistic pathogens commonly prevalent in patients with HIV/AIDS [2–4,8,9].

The opportunistic fungus Pneumocystis carinii, frequently diagnosed in patients with AIDS, was repeatedly identified in malnourished children after the Second World War [9].

Noma is an opportunistic infection in children between one and four years with PEM, which occurs worldwide, but is most common in sub-Saharan Africa. The infection evolves from gingival inflammation to orofacial gangrene and is commonly preceded by other infections such as measles, malaria, severe diarrhea, and necrotising ulcerative gingivitis.

Noma coincides with the period of linear growth retardation in malnourished children [10]. In addition to promoting acute and chronic infections, PEM impairs the linear growth of children, leading to a further reduction in food intake, nutrient absorption, direct or catabolic nutrient losses, and increased metabolic requirements. It has been suggested that acute phase response and proinflammatory cytokines directly affect the bone remodelling required for longitudinal growth [11].

Correlation of malnutrition and growth retardation allows assessment of the individual nutritional state, which is usually measured as mid-upper arm circumference or body mass index (BMI).

BMIs are given either as weight-for-height to indicate acute PEM (wasting), or as weight-for-age (underweight) or height-for-age (stunting), correlations for chronic PEM.

A study in Kenya found a significant association between HIV infection and lower mid-upper arm circumferences and serum albumin concentration, another measure of malnutrition, but found no such association with BMI [12]. Independent of HIV, socioeconomic factors and severity of tuberculosis are important correlates of acute PEM or wasting [12].

Infection itself contributes to malnutrition. The relationship of malnutrition on immune suppression and infection is complicated by the profound effects of a number of infections on nutrition itself.

Examples of how infections can contribute to malnutrition are: (1) gastrointestinal infection can lead to diarrhea; (2) HIV/AIDS, tuberculosis, and other chronic infections can cause cachexia and anemia; and (3) intestinal parasites can cause anemia and nutrient deprivation [13].

Stimulation of an immune response by infection increases the demand for metabolically derived anabolic energy and associated substrates, leading to a synergistic vicious cycle of adverse nutritional status and increased susceptibility to infection.

Under inflammatory conditions such as sepsis, mediators increase the catabolic disease state characterised by enhanced arginine use. Furthermore, arginase is induced during infection and uses up arginine as substrate. It has been suggested that depletion of this amino acid impairs T cell responses [14], and exceeding the body’s arginine production leads to a negative nitrogen balance [15].

A study in Nigeria found that the severe metabolic demands made during acute measles infection further deteriorated the condition of malnourished children, leading to further weight loss, wasting, and reduced serum levels of essential amino acids [16]. Increased energy consumption due to immune responses may also affect the efficacy of live attenuated vaccines in populations ridden with PEM.

Arginine treatment has been shown to improve nitrogen balance and lymphocyte function and stimulate arginine transport in the liver. These benefits have made arginine an essential constituent of immunonutritive formulas currently in use for critically ill patients. PEM is an important health determinant for critically ill patients and increases susceptibility to infections in malnourished elderly patients and patients with anorexia.

A large and strictly controlled inpatient study in France pinpoints malnutrition as an independent risk factor for nosocomial infections, which account for 6%–10% of all in-hospital deaths worldwide [17]. Accordingly, nutritive management has to become an elementary part of intensive health care. In summary, nutritional quality and composition are pivotal for anti-infectious immunity.

Malnutrition Affects Immunity

Severe protein malnutrition in newborns and small children causes atrophy of the thymus with reduced cell numbers and subsequently ill-developed peripheral lymphoid organs, i.e., lymph nodes and spleen [6].

This causal chain leads to long-lasting immune defects characterized by leucopenia, decreased CD4 to CD8 ratio and increased numbers of CD4/CD8 double-negative T cells, and, therefore, the appearance of immature T cells in the periphery.

Malnourished children suffer in greater proportion from respiratory infections, infectious diarrhea, measles, and malaria, characterized by a protracted course and exacerbated disease. These malnourished children present with diminished functional T cell counts, increased undifferentiated lymphocyte numbers, and depressed serum complement activity (Table 1).

Reduced antibody responses to polysaccharide antigens of encapsulated bacteria such as Streptococcus pneumoniae and Haemophilus influenzae exacerbate susceptibility to these pathogens [2,4,18]. Moreover, immune defense at the epithelial barrier of the undernourished host is compromised due to altered architecture of the gut mucosa, such as flattened hypotrophic microvilli, reduced lymphocyte counts in Peyer’s patches, and reduced immunoglobulin A (IgA) secretion [7].

Availability of complement components is restricted by malnutrition, thereby affecting the capacity of professional phagocytes to engulf and eliminate pathogens. In mice with experimental PEM, phagocytosis and production of reactive oxygen intermediates (ROIs) and reactive nitrogen intermediates (RNIs) by macrophages is diminished, as is antigen presentation to T cells by dendritic cells [19].

Temporary PEM in mice challenged by experimental peritonitis resulted in impaired immune cell migration and extravasation, as indicated by reduced numbers of CD11b/CD18-positive cells at the site of infection, probably involving lower concentrations of the chemokine MIP-2.

Peripheral T lymphocytes from infected children with PEM had lower expression of the activation marker CD69, and predominantly showed an intermediate (CD45RAlow/CD45ROlow) rather than a memory phenotype (CD45ROhigh) when compared to healthy donors [20,21].

These T cells were biased towards type 2 T helper cell (Th2) responses, represented by decreased IFN-?/IL-2 (type 1 T helper cell [Th1]) and increased IL-4/IL-10 (Th2) production [22].

Experimentally undernourished weanling mice had predominantly T cells of the naïve quiescent phenotype (CD45RA+/CD62L+) [23,24]. In these mice, IFN-?- responses were depressed and IL-10 and the Th2-associated antibody, IgE, were increased, while IL-4 production remained normal [25]. These findings, however, should not be taken to suggest that PEM generally biases towards Th2 responses. Rather, PEM appears to alter immune responses, thus hampering protective immunity of any type.

Protective T cell responses against helminth infections are predominantly of the Th2 type comprising IL-4 production, expansion of eosinophils, and IgE secretion.

However, malnourished children are deficient for protective IgE antibodies against Ascaris lumbricoides [26,27]. By suppressing such responses in mice, PEM increases susceptibility to infection with the intestinal parasite, Heligmosomoides polygyrus [28].

Malnourished children suffering from helminth infections have high concentrations of total IgE. Yet these antibodies are neither worm-specific nor protective, and their memory T cells do not recognize helminth antigens [27,28].

Malnutrition and Tuberculosis: Yesterday and Today

Malnutrition is generally appreciated as a major risk factor in the onset of active tuberculosis [9]. This notion is largely based on historical reports but also on more recent experimental animal studies. One of the major disease burdens globally, tuberculosis is a well-documented example of the way in which malnutrition leads to worse disease outcomes.

During the First World War, Denmark was affected by a tuberculosis epidemic similar to that prevailing in countries at war. The Danish tuberculosis epidemic could be explained by widespread malnourishment, since the export of meat, fish, poultry, and dairy products meant that food was scarce inside the country. This tuberculosis epidemic plummeted once the German blockade of Denmark was established and food became available to the Danish population again, but the epidemic continued in other countries [9].

A comparative radiographic survey of prisoners of war held in German camps during the Second World War under similar living conditions found a tuberculosis prevalence of 1.2% versus up to 19.0% among the British and Russians, respectively, with more severe outcomes in the latter.

This difference in prevalence and severity is probably a direct consequence of the fact that only the British prisoners received—in addition to the regular prison diet—a Red Cross supplement of 30 grams of protein and 1,000 kilocalories per day. This causal relationship is in line with the positive correlation of below average BMI with increased risk of pulmonary tuberculosis [9].

More contemporary reports provide further support that malnutrition has an impact on the clinical outcome of tuberculosis [29]. A statistically significant number of patients with tuberculosis were malnourished in a recent study in Sri Lanka and skin test reactions for tuberculosis were negatively affected by malnutrition [30,31].

Hence, in poor settings, nutritional measures should be considered as an adjunct to anti-tuberculosis drug treatment. Animal experiments, mainly in the guinea pig tuberculosis model, document detrimental consequences of chronic PEM on immunity to Mycobacterium tuberculosis. In these experiments, lymphocyte stimulation as well as secretion of the Th1 cytokines IL-2, IFN-?, and TNF-?, involved in control of M. tuberculosis, were significantly reduced in animals with PEM [9].

Moreover, macrophages from such animals produced more transforming growth factor ? (TGF?), which further suppresses T cells and inflammation [32,33].

A study in murine tuberculosis reached similar conclusions and additionally found that malnourished mice showed hampered production of RNIs, which act as critical effectors against tuberculosis in mice. Consequently, malnourished mice suffered from higher bacterial burdens and died earlier of infection [34].

Finally, efficacy of BCG vaccination against tuberculosis was profoundly reduced in malnourished guinea pigs as compared to normally fed animals, due to impaired T cell priming and function [9,35]. Malnutrition, Leptin, and Immunity Top Leptin is a central mediator connecting nutrition and immunity. Levels of the pleiotropic hormone leptin, which regulates satiety, are reduced in patients with PEM.

Leptin concentrations correlate with body fat mass and are quickly reduced by fasting [36]. Leptin is a 16 kDa ?-helix type protein similar to the cytokines IL-6 and IL-12, and is mainly secreted by adipose tissue.

At least six receptors representing different splice forms encoded by one gene are broadly distributed on different cell types. The isoform is not only full-length ObRb expressed in the hypothalamus, but is also prevalent on lymphocytes and macrophages [36,37].

Leptin binding activates immune cells via the to ObRb JAK-2/STAT-3 and the MAPK pathway and induces TNF-?, IL-6, and IL-12 secretion in macrophages.

Leptin stimulates naïve T cells (CD45RA+) but blocks proliferation of memory T cells (CD45RO+). Concomitantly, leptin promotes IFN-? secretion by memory T cells, inhibits Th2 responses [38,39], and induces activation markers (CD69, CD25, and CD71) [40]. Apart from inducing lymphopoiesis, leptin seems to deliver survival signals to T cells by upregulating anti-apoptotic proteins T-bet and Bcl-xL [36].

Active tuberculosis is associated with cachexia, weight loss, and low serum concentrations of leptin [41–44]. Moreover, leptin-deficient mice are more susceptible to M. tuberculosis than wild-type mice, and T cell numbers, including those producing IFN-?, are reduced in infected lungs, suggesting that leptin contributes to protection against tuberculosis [45].

However, a causative correlation between severity of tuberculosis and leptin is not fully established, and leptin concentrations do not predict wasting in human tuberculosis [44]. Malnutrition causes immunosuppression through a variety of mechanisms, including the involvement of leptin and the hypothalamic-pituitary-adrenal axis.

PEM reduces leptin concentrations and increases serum levels of stress hormones, i.e., glucocorticoids [2,4,46–48]. Thus, it is likely that the hypothalamic-pituitary-adrenal axis plays a critical role in malnutrition-associated immune deficiency. In well-nourished people, infection and inflammation increase leptin levels in an IL-1-dependent manner and increase glucocorticoid concentrations, which subsequently can control inflammation [40,49,50]. Under conditions of PEM and low leptin concentrations, glucocorticoids impair macrophage functions by decreasing NF-kB translocation into the nucleus [49]. Macrophages from mice with experimental PEM are less sensitive to activation with lipopolysaccharides, partly due to decreased NF-kB translocation. Their ability to engulf pathogens and to produce cytokines and ROIs is impaired [51–54]. However, the suggestion that malnutrition suppresses macrophage functions due to elevated glucocorticoid levels was not supported by a recent study [55]. Further experiments are required to identify the mechanisms connecting PEM and immunosuppression.

More contemporary reports provide further support that malnutrition has an impact on the clinical outcome of tuberculosis [29]. A statistically significant number of patients with tuberculosis were malnourished in a recent study in Sri Lanka and skin test reactions for tuberculosis were negatively affected by malnutrition [30,31]. Hence, in poor settings, nutritional measures should be considered as an adjunct to anti-tuberculosis drug treatment.

Animal experiments, mainly in the guinea pig tuberculosis model, document detrimental consequences of chronic PEM on immunity to Mycobacterium tuberculosis. In these experiments, lymphocyte stimulation as well as secretion of the Th1 cytokines IL-2, IFN-?, and TNF-?, involved in control of M. tuberculosis, were significantly reduced in animals with PEM [9]. Moreover, macrophages from such animals produced more transforming growth factor ? (TGF?), which further suppresses T cells and inflammation [32,33]. A study in murine tuberculosis reached similar conclusions and additionally found that malnourished mice showed hampered production of RNIs, which act as critical effectors against tuberculosis in mice. Consequently, malnourished mice suffered from higher bacterial burdens and died earlier of infection [34]. Finally, efficacy of BCG vaccination against tuberculosis was profoundly reduced in malnourished guinea pigs as compared to normally fed animals, due to impaired T cell priming and function [9,35].

Outlook Top

Extrapolating the studies discussed, malnutrition can be considered a major risk factor for morbidity and mortality worldwide due to infections with bacterial, viral, and protozoal agents [2,8,9]. This causal relationship was suggested in the US Surgeon General’s Report in 1988 [71]. With more than 842 million chronically malnourished people worldwide [72], we agree with the notion that “…malnutrition may account for a greater population-attributable risk of tuberculosis than HIV infection, and certainly a much more correctable one” [9].

In the context of what is known as the 10/90 gap (10% of global health research funding is being targeted to health problems that account for 90% of the global disease burden) [73,74], research on infection and malnutrition are highly warranted for scientific, economic, and ethical reasons [75].

To conquer malnutrition, cost-efficient and practical approaches need to be established. Measures to counteract acute malnutrition are now available and were successfully applied in 2005 when Niger was affected by a famine. The crisis did not come as a surprise to the consortium of stakeholders, i.e., the government of Niger, its international partners, and the Famine Early Warning Systems Network of the US Agency for International Development. To avoid disturbance of the market and long-term development goals, food was sold to starving people for too high a price instead of being freely distributed. The catastrophe became apparent as vast numbers of malnourished children were brought to medical stations. Ready-to-use therapeutic food was delivered by doctors from Médecins Sans Frontières as an outpatient measure (community therapeutic care) with enormous success [76].

Usually children are hospitalized under such circumstances and given milk products as therapeutic food. Outpatient treatment during emergencies, however, decreases (1) duration of maternal absence from the family, thereby limiting children’s risk of malnourishment, (2) time needed to establish treatment centers, and (3) risk of spreading nosocomial infections among hospitalized children in a limited number of overcrowded places. New therapeutic food formulations with balanced contents of macro- and micronutrients, which are ready to use and do not need a clean water supply for their preparation, are important prerequisites for such rapid aid measures. In the past, life-threatening respiratory infections, diarrhea, and malaria were frequent complications requiring short-term inpatient anti-infectious treatment. Under the emergency conditions of the Niger famine in 2005, the measures employed by Médecins Sans Frontières kept child mortality at the rate of non-famine periods. Thus, there is a precedent of effective interventions for acute malnutrition in an emergency to avoid subsequent infections.

This measure, however, is unlikely to minimize mortality and morbidity due to chronic malnutrition worldwide. Further research and development in diverse areas ranging from biomedicine to public health are required to stop the downward spiral of chronic malnutrition, infection, disease, and reduced economic productivity in impoverished societies with the consequences of migration and economical and political instability or war (Figure 1). Diseases resulting from overnutrition in industrial societies are of equal concern and similar conditions are already spreading to developing countries. Under- and overnutrition and diet-related chronic diseases represent a critical risk factor for more than half of the world’s diseases and incur hundreds of millions of dollars in public expenditure [5], requiring the immediate attention of biomedical science and public health agencies alike.

References Top

1. Moret Y, Schmid-Hempel P (2000) Survival for immunity: The price of immune system activation for bumblebee workers. Science 290: 1166–1168. Find this article online
   
2. Scrimshaw NS, SanGiovanni JP (1997) Synergism of nutrition, infection, and immunity: An overview. Am J Clin Nutr 66: 464S–477S. Find this article online
   
3. Ambrus JL Sr, Ambrus JL Jr (2004) Nutrition and infectious diseases in developing countries and problems of acquired immunodeficiency syndrome. Exp Biol Med (Maywood) 229: 464–472. Find this article online
   
4. Woodward B (1998) Protein, calories, and immune defenses. Nutr Rev 56: S84–S92. Find this article online
   
5. World Health Organization (2005) Nutrition: Challenges. Available: http://www.who.int/nutrition/challenges. Accessed 29 March 2007.
   
6. Savino W (2002) The thymus gland is a target in malnutrition. Eur J Clin Nutr 56(Suppl 3): S46–S49. Find this article online
   
7. Beisel WR (1996) Nutrition in pediatric HIV infection: Setting the research agenda. Nutrition and immune function: Overview. J Nutr 126: 2611S–2615S. Find this article online
   
8. Field CJ, Johnson IR, Schley PD (2002) Nutrients and their role in host resistance to infection. J Leukoc Biol 71: 16–32. Find this article online
   
9. Cegielski JP, McMurray DN (2004) The relationship between malnutrition and tuberculosis: Evidence from studies in humans and experimental animals. Int J Tuberc Lung Dis 8: 286–298. Find this article online
   
10. Enwonwu CO, Falkler WA Jr, Phillips RS (2006) Noma (cancrum oris). Lancet 368: 147–156. Find this article online
    
11. Stephensen CB (1999) Burden of infection on growth failure. J Nutr 129: 534S–538S. Find this article online
    
12. Villamor E, Saathoff E, Mugusi F, Bosch RJ, Urassa W, et al. (2006) Wasting and body composition of adults with pulmonary tuberculosis in relation to HIV-1 coinfection, socioeconomic status, and severity of tuberculosis. Eur J Clin Nutr 60: 163–171. Find this article online
    
13. Scrimshaw NS, Taylor CE, Gordon JE (1968) Interactions of nutrition and infection. Monogr Ser World Health Organ 57: 3–329. Find this article online
    
14. Bronte V, Zanovello P (2005) Regulation of immune responses by L-arginine metabolism. Nat Rev Immunol 5: 641–654. Find this article online
    
15. Kurpad AV (2006) The requirements of protein & amino acid during acute & chronic infections. Indian J Med Res 124: 129–148. Find this article online
    
16. Phillips RS, Enwonwu CO, Okolo S, Hassan A (2004) Metabolic effects of acute measles in chronically malnourished Nigerian children. J Nutr Biochem 15: 281–288. Find this article online
    
17. Schneider SM, Veyres P, Pivot X, Soummer AM, Jambou P, et al. (2004) Malnutrition is an independent factor associated with nosocomial infections. Br J Nutr 92: 105–111. Find this article online
    
18. Caulfield LE, de Onis M, Blossner M, Black RE (2004) Undernutrition as an underlying cause of child deaths associated with diarrhea, pneumonia, malaria, and measles. Am J Clin Nutr 80: 193–198. Find this article online
    
19. Abe M, Akbar F, Matsuura B, Horiike N, Onji M (2003) Defective antigen-presenting capacity of murine dendritic cells during starvation. Nutrition 19: 265–269. Find this article online
    
20. Najera O, Gonzalez C, Toledo G, Lopez L, Cortes E, et al. (2001) CD45RA and CD45RO isoforms in infected malnourished and infected well-nourished children. Clin Exp Immunol 126: 461–465. Find this article online
    
21. Najera O, Gonzalez C, Toledo G, Lopez L, Ortiz R (2004) Flow cytometry study of lymphocyte subsets in malnourished and well-nourished children with bacterial infections. Clin Diagn Lab Immunol 11: 577–580. Find this article online
    
22. Rodriguez L, Gonzalez C, Flores L, Jimenez-Zamudio L, Graniel J, et al. (2005) Assessment by flow cytometry of cytokine production in malnourished children. Clin Diagn Lab Immunol 12: 502–507. Find this article online
    
23. Woodward B, Hillyer L, Hunt K (1999) T cells with a quiescent phenotype (CD45RA+) are overabundant in the blood and involuted lymphoid tissues in wasting protein and energy deficiencies. Immunology 96: 246–253. Find this article online
    
24. ten Bruggencate SJ, Hillyer LM, Woodward BD (2001) The proportion of CD45RA(+)CD62L(+) (quiescent-phenotype) T cells within the CD8(+) subset increases in advanced weight loss in the protein- or energy-deficient weanling mouse. J Nutr 131: 3266–3269. Find this article online
    
25. Neyestani TR, Woodward B (2005) Blood concentrations of Th2-type immunoglobulins are selectively increased in weanling mice subjected to acute malnutrition. Exp Biol Med (Maywood) 230: 128–134. Find this article online
    
26. Hagel I, Lynch NR, Di Prisco MC, Sanchez J, Perez M (1995) Nutritional status and the IgE response against Ascaris lumbricoides in children from a tropical slum. Trans R Soc Trop Med Hyg 89: 562–565. Find this article online
    
27. Hagel I, Lynch NR, Puccio F, Rodriguez O, Luzondo R, et al. (2003) Defective regulation of the protective IgE response against intestinal helminth Ascaris lumbricoides in malnourished children. J Trop Pediatr 49: 136–142. Find this article online
    
28. Ing R, Su Z, Scott ME, Koski KG (2000) Suppressed T helper 2 immunity and prolonged survival of a nematode parasite in protein-malnourished mice. Proc Natl Acad Sci U S A 97: 7078–7083. Find this article online
    
29. Singal A, Pandhi D, Agrawal SK (2005) Multifocal scrofuloderma with disseminated tuberculosis in a severely malnourished child. Pediatr Dermatol 22: 440–443. Find this article online
    
30. Liebeschuetz S, Bamber S, Ewer K, Deeks J, Pathan AA, et al. (2004) Diagnosis of tuberculosis in South African children with a T-cell-based assay: a prospective cohort study. Lancet 364: 2196–2203. Find this article online
    
31. Metcalfe N (2005) A study of tuberculosis, malnutrition and gender in Sri Lanka. Trans R Soc Trop Med Hyg 99: 115–119. Find this article online
    
32. Dai G, McMurray DN (1999) Effects of modulating TGF-beta 1 on immune responses to mycobacterial infection in guinea pigs. Tuber Lung Dis 79: 207–214. Find this article online
    
33. Dai G, McMurray DN (1998) Altered cytokine production and impaired antimycobacterial immunity in protein-malnourished guinea pigs. Infect Immun 66: 3562–3568. Find this article online
    
34. Chan J, Tian Y, Tanaka KE, Tsang MS, Yu K, et al. (1996) Effects of protein calorie malnutrition on tuberculosis in mice. Proc Natl Acad Sci U S A 93: 14857–14861. Find this article online
    
35. McMurray DN, Dai G, Phalen S (1999) Mechanisms of vaccine-induced resistance in a guinea pig model of pulmonary tuberculosis. Tuber Lung Dis 79: 261–266. Find this article online
    
36. Matarese G, Moschos S, Mantzoros CS (2005) Leptin in immunology. J Immunol 174: 3137–3142. Find this article online
    
37. Matarese G, La Cava A, Sanna V, Lord GM, Lechler RI, et al. (2002) Balancing susceptibility to infection and autoimmunity: A role for leptin? Trends Immunol 23: 182–187. Find this article online
    
38. Lord GM, Matarese G, Howard JK, Baker RJ, Bloom SR, et al. (1998) Leptin modulates the T-cell immune response and reverses starvation-induced immunosuppression. Nature 394: 897–901. Find this article online
    
39. Lord GM, Matarese G, Howard JK, Bloom SR, Lechler RI (2002) Leptin inhibits the anti-CD3-driven proliferation of peripheral blood T cells but enhances the production of proinflammatory cytokines. J Leukoc Biol 72: 330–338. Find this article online
    
40. Faggioni R, Feingold KR, Grunfeld C (2001) Leptin regulation of the immune response and the immunodeficiency of malnutrition. Faseb J 15: 2565–2571. Find this article online
    
41. Cakir B, Yonem A, Guler S, Odabasi E, Demirbas B, et al. (1999) Relation of leptin and tumor necrosis factor alpha to body weight changes in patients with pulmonary tuberculosis. Horm Res 52: 279–283. Find this article online
    
42. Schwenk A, Hodgson L, Rayner CF, Griffin GE, Macallan DC (2003) Leptin and energy metabolism in pulmonary tuberculosis. Am J Clin Nutr 77: 392–398. Find this article online
    
43. van Crevel R, Karyadi E, Netea MG, Verhoef H, Nelwan RH, et al. (2002) Decreased plasma leptin concentrations in tuberculosis patients are associated with wasting and inflammation. J Clin Endocrinol Metab 87: 758–763. Find this article online
    
44. van Lettow M, van der Meer JW, West CE, van Crevel R, Semba RD (2005) Interleukin-6 and human immunodeficiency virus load, but not plasma leptin concentration, predict anorexia and wasting in adults with pulmonary tuberculosis in Malawi. J Clin Endocrinol Metab 90: 4771–4776. Find this article online
    
45. Wieland CW, Florquin S, Chan ED, Leemans JC, Weijer S, et al. (2005) Pulmonary Mycobacterium tuberculosis infection in leptin-deficient ob/ob mice. Int Immunol 17: 1399–1408. Find this article online
    
46. Monk JM, Makinen K, Shrum B, Woodward B (2006) Blood corticosterone concentration reaches critical illness levels early during acute malnutrition in the weanling mouse. Exp Biol Med (Maywood) 231: 264–268. Find this article online
    
47. Jacobson L (2005) Hypothalamic-pituitary-adrenocortical axis regulation. Endocrinol Metab Clin North Am 34: 271–292. Find this article online
    
48. Alleyne GA, Young VH (1967) Adrenocortical function in children with severe protein-calorie malnutrition. Clin Sci 33: 189–200. Find this article online
    
49. Auphan N, Didonato JA, Helmberg A, Rosette C, Karin M (1997) Immunoregulatory genes and immunosuppression by glucocorticoids. Arch Toxicol Suppl 19: 87–95. Find this article online
    
50. Van Molle W, Libert C (2005) How glucocorticoids control their own strength and the balance between pro- and anti-inflammatory mediators. Eur J Immunol 35: 3396–3399. Find this article online
    
51. McCarter MD, Naama HA, Shou J, Kwi LX, Evoy DA, et al. (1998) Altered macrophage intracellular signaling induced by protein-calorie malnutrition. Cell Immunol 183: 131–136. Find this article online
    
52. Redmond HP, Gallagher HJ, Shou J, Daly JM (1995) Antigen presentation in protein-energy malnutrition. Cell Immunol 163: 80–87. Find this article online
    
53. Redmond HP, Leon P, Lieberman MD, Hofmann K, Shou J, et al. (1991) Impaired macrophage function in severe protein-energy malnutrition. Arch Surg 126: 192–196. Find this article online
    
54. Redmond HP, Shou J, Kelly CJ, Leon P, Daly JM (1991) Protein-calorie malnutrition impairs host defense against Candida albicans. J Surg Res 50: 552–559. Find this article online
    
55. Stapleton PP, Barden CB, McCarter MD, Mackrell PJ, Freeman TA, et al. (2003) Serum leptin levels in acute protein deprivation. JPEN J Parenter Enteral Nutr 27: 132–136. Find this article online
    
56. Tanaka S, Isoda F, Ishihara Y, Kimura M, Yamakawa T (2001) T lymphopaenia in relation to body mass index and TNF-alpha in human obesity: Adequate weight reduction can be corrective. Clin Endocrinol (Oxf) 54: 347–354. Find this article online
    
57. Tanaka S, Isoda F, Kiuchi Y, Ikeda H, Mobbs CV, et al. (2000) T lymphopenia in genetically obese-diabetic Wistar fatty rats: Effects of body weight reduction on T cells. Metabolism 49: 1261–1266. Find this article online
    
58. Nieman DC, Henson DA, Nehlsen-Cannarella SL, Ekkens M, Utter AC, et al. (1999) Influence of obesity on immune function. J Am Diet Assoc 99: 294–299. Find this article online
    
59. Yamakawa T, Tanaka S, Yamakawa Y, Kiuchi Y, Isoda F, et al. (1995) Augmented production of tumor necrosis factor-alpha in obese mice. Clin Immunol Immunopathol 75: 51–56. Find this article online
    
60. Zarkesh-Esfahani H, Pockley AG, Wu Z, Hellewell PG, Weetman AP, et al. (2004) Leptin indirectly activates human neutrophils via induction of TNF-alpha. J Immunol 172: 1809–1814. Find this article online
    
61. Zarkesh-Esfahani H, Pockley G, Metcalfe RA, Bidlingmaier M, Wu Z, et al. (2001) High-dose leptin activates human leukocytes via receptor expression on monocytes. J Immunol 167: 4593–4599. Find this article online
    
62. Sanchez-Margalet V, Martin-Romero C, Santos-Alvarez J, Goberna R, Najib S, et al. (2003) Role of leptin as an immunomodulator of blood mononuclear cells: Mechanisms of action. Clin Exp Immunol 133: 11–19. Find this article online
    
63. Dixit VD, Schaffer EM, Pyle RS, Collins GD, Sakthivel SK, et al. (2004) Ghrelin inhibits leptin- and activation-induced proinflammatory cytokine expression by human monocytes and T cells. J Clin Invest 114: 57–66. Find this article online
    
64. Xia Q, Pang W, Pan H, Zheng Y, Kang JS, et al. (2004) Effects of ghrelin on the proliferation and secretion of splenic T lymphocytes in mice. Regul Pept 122: 173–178. Find this article online
    
65. Netea MG, Joosten LA, Lewis E, Jensen DR, Voshol PJ, et al. (2006) Deficiency of interleukin-18 in mice leads to hyperphagia, obesity and insulin resistance. Nat Med 12: 650–656. Find this article online
    
66. Turnbaugh PJ, Ley RE, Mahowald MA, Magrini V, Mardis ER, et al. (2006) An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 444: 1027–1131. Find this article online
    
67. Perez-Guzman C, Vargas MH (2006) Hypocholesterolemia: A major risk factor for developing pulmonary tuberculosis? Med Hypotheses 66: 1227–1230. Find this article online
    
68. Perez-Guzman C, Vargas MH, Quinonez F, Bazavilvazo N, Aguilar A (2005) A cholesterol-rich diet accelerates bacteriologic sterilization in pulmonary tuberculosis. Chest 127: 643–651. Find this article online
    
69. Joshi N, Caputo GM, Weitekamp MR, Karchmer AW (1999) Infections in patients with diabetes mellitus. N Engl J Med 341: 1906–1912. Find this article online
    
70. Guptan A, Shah A (2000) Tuberculosis and diabetes: An appraisal. Ind J Tub 47: 2–8. Find this article online
    
71. United States Department of Health and Human Services (1988) The Surgeon General’s report on nutrition and health. Washington (D. C.): DHHS Publishing. pp. 427–463.
    
72. World Food Programme (2004) Hunger facts. Available: http://www.wfp.org/aboutwfp/facts/hunger?_facts.asp . Accessed 29 March 2007.
    
73. Blackburn GL (2001) Pasteur’s Quadrant and malnutrition. Nature 409: 397–401. Find this article online
    
74. World Health Organization (2003) Investing in health: A summary of the findings of the Commission on Macroeconomics and Health. Available: 29 March 2007.
    
75. The World Bank (2006) Repositioning nutrition as central to development: A strategy for large-scale action. Available: http://siteresources.worldbank.org/NUTRI?TION/Resources/281846-1131636806329/Nutr?itionStrategy.pdf . Accessed 29 March 2007.
    
76. Tectonidis M (2006) Crisis in Niger—Outpatient care for severe acute malnutrition. N Engl J Med 354: 224–227. Find this article online

It was 1981 when Dr. Michael Gottlieb reported five patients to the Centers for Disease Control (CDC) because each had an uncommonly intensive infection.

The men had Pneumocystis Carini pneumonia (incorrectly identified as PCP, now known to be Pneumocystis Jiroveci); they also suffered from cytomegalovirus (CMV) infections, and intestinal and/or oral Candida Albicans overgrowth. Kaposi's Sarcoma lesions were reported at other clinics, in New York and San Francisco, and noted on the page following Dr. Gottlieb's report.

Dr. Gottlieb's Los Angeles report, and the KS "outbreak" in NYC and San Francisco, spurred a race among epidemiologists at the CDC and NIH - and simultaneiously at the Pasteur Institute - to find a cause celebre, a 'bug' that was making gay folk sick, even though the reasons for these illnesses caused by the mens' immunocompromised state was plainly attributable to behavioral causes.

The late seventies were characterized by a mentality of free-flowing sex, love, drugs, and rock and roll, and sex. In the late seventies and early eighties, there were thousands of other gay men who were dealing with irritable bowel syndrome (IBS) - caused by parasites and candida overgrowth, sometimes severe or entrenched enough to cause wasting and other so-called "rare" illneses.

Dr. Michael Gottlieb described these infections in his 1981 report to the CDC on five patients of his Los Angeles office. What is not in the report is the setting of this medical drama about to unfold on center stage for the next 30 years.

Intravenous drug use, exotic pills, 8 or 12 hour sex parties, and the many sacrificed meals and lost nights of sleep set up an environment favorable to mycobacteria (CMV), fungal organisms (Candida, PCP), and viral antigens like Kaposi's sarcoma, a human herpes virus. All of these organisms are present in a majority of humans but don't typically manifest in illness, under the immune system's capable control.

Some of the sexual activites gay men enjoy, like rimming, are unfortunately high-risk for parasites, which commonly travel the fecal-oral route. In Africa, due to the lack of water filtration systems, this route is quite common. Less than half of the sub-Saharan population has access to clean drinking water.

Research has repeatedly shown that parasitic infections over time damages the immune system, restricts absorption of nutrients from food, and settle in organs beyond the digestive tract, in the lungs for example. It is notable that pneumocystis pneumonia is a fungal parasite.

Candida overgrowth, another fungal infection, occurs routinely in the intestines post-antibiotics. It is no surprise, then, that IBS was common. In the gilded age of gay liberation, sex was carefree; it was as easy to find antibiotic pills as it was to get laid, if you caught something from your midnight snack.

Despite the wild sex parties of the time, these "CDC five" who are the subject of Dr. Gottlieb's infamous report, hadn't had direct sexual contact with each other - an interesting sidebar despite the "sex kills" mentality coming out of the AIDS madness.

One wonders if there were 5 straight people, not having had direct sexual contact with each other, presenting with pneumonia, CMV and IBS candida overgrowth, would they have not been reported to the CDC, and might we never have had AIDS?

The fact is that the only "unusual" thing about these men is that they preferred sex with men - note the wording in the CDC report: "all active homosexuals." (When the CDC refers to heterosexuals, are they qualified by their "active" sex life?)

Statistics indicate that around 60% of the general population would test positive for the CMV bacteria. As stated, all of the other offending organisms also are common but not commonly fatal. Therefore, a diagnosis of immunodeficiency is a no-brainer, but a prognosis of "eat well" and "get some rest" was apparently not exciting enough for the public health establishment, and certainly too boring for the career epidemioligist.

As anyone knows, when the body gets run down, illness is likely to follow. It is a known fact that protracted parasitic infections cause AIDS symptoms. So there is in fact nothing unusual at all about these five men getting sick given each of their behaviors leading to their illness.

Kaposi's sarcoma (KS) that afflicted other cohorts of men from New York and San Francisco was also blamed on the imaginary "AIDS virus," but a 1990 study concluded that KS had nothing to do with HIV.

"Differences in clinical findings, CD4+ and CD8+ cell counts, and P24 antibody and antigen levels indicate that the occurrence of KS may be independent of HIV induced severe immunodeficiency."²

Research shows that KS was and is directly attributable to the the hepatitis B vaccine. An experimental formulation of the hepatitis B vaccine was administered to thousands of gay men in New York, San Francisco, between 1979 and 1981 - the year a "gay related immune deficiency" syndrome called GRID was described in the media, later to become known as AIDS.

When all the facts are considered, the response of the CDC was fatefully overwrought in 1981. The sexual proclivities of gay men became a hot topic and maybe was titillating to certain repressed NIH / CDC epedemiologists. But beyond some gay men's choice of recreational activity, and the reaction of overzealous government employees and entrepreneurial medical workers like Robert Gallo who saw dollar signs in other people's suffering, not much else was unusual about some guys getting sick from partying and playing too much.

Nope, there was nothing unusual at all about what was to become AIDS, and what would curse generations of gay men, and consign them and later, sub Saharan Africa to the longest running pharmaceutical and human surveillance experiment in history.

The dose of trimethoprim sulfa is too high. It was the dose that we were taught to give, but we recognized fairly early, probably by '83 at least, that this was too high a dose...because it was toxic, yes. People got too sick on this high dose.

Early in the epidemic, people with KS had a better prognosis than later, after the first couple, three years of the epidemic. This was because the oncologists were just blasting the KS patients with chemotherapy and further depressing their immune system, and so their life expectancy went down.

So there was this dip in the life expectancy of KS patients. In fact, the early response, despite what the dermatologists and oncologists may say, was to overtreat these patients with chemotherapy. This hurt patients in terms of their life expectancy, because they were treated aggressively for their visible KS lesions.¹

- Dr. Stephen Follansbee

See page 2 of the MMWR report on the New York and San Francisco KS outbreak.Essay by Kirk Cordell, ©2006.

When the rabid AIDS promoters hit the media channels and the Internet gloating over the death of leading HIV "rethinker" Christine Maggiore, it will be in the sadistic manner of which only AIDS-lovers are capable, and they will twist the truth into a scary fable meant to coax you into taking your meds.

Yet, it would be prudent to resist any temptation to believe their false assumption that Christine Maggiore succumbed to an "AIDS-related" illness, specifically, HIV-related pneumonia. If she tested negative, after testing positive, and her son tests negative, how is that HIV-related? Even if she was HIV positive, on what basis is her death attributed to HIV?

In an international study of bacterial pneumonia outcomes, conducted in part by the University of Alberta, researchers concluded that pneumonia doesn't appear to harm HIV-positive patients any more than those who are HIV-negative.

There was also negligible difference in the mortality rate; total deaths among the HIV patients was 3.5 per cent (two of 58 patients), and 4.8 per cent (seven of 174) among the HIV-negative patients.

Mourners and revelers alike, consider the following, as noted on Medicine.net.

Currently, over 3 million people develop pneumonia each year in the United States. Over a half a million of these people are admitted to a hospital for treatment. Although most of these people recover, approximately 5% will die from pneumonia. Pneumonia is the sixth leading cause of death in the United States.

The latest numbers from the CDC put pneumonia as the 8th leading cause of death in the United States as of the last officially available government numbers from 2005.

It is disrespect of the lowest form; not giving time to honor a departed soul. Christine Maggiore was a tireless fighter, for what she believed in wholeheartedly. To hear the evil cackling on some blogs, such as Aetiology, is to hear the desperate rantings of those trying to convince themselves of their stories in the midst of so many questions of their position.

One blogger mocked Maggiore's death from pneumonia as an event extraordinarily rare and remotest of possibility, that a person unaffected by AIDS, HIV positive or not would endure.

It's not very difficult to consult the CDC website to find the top 15 causes of death in the USA, and to find pneumonia at numbers 6 and 8 for the two most recent national population studies.

Their wild, baseless accusations of how many deaths AIDS-dissenters directly cause, based upon UN numbers that are faulty to begin with, bear no relation to reality, as if Duesberg, or any dissenter is running public health policy on a continent thousands of miles away.

Defending against this libelous accusation gives these bloggers unwarranted credit. Remember these are the same people who vilify those who advocate good nutrition, food and sanitation technology transfer, and parasite remediation, as "quacks".

One week they condemned the then South African public health minister and demanded her exit because she advised people to eat garlic and some local pomme de terre. The next week there was a prominent feature in an academic health journal discussing a study's newest findings about the far-reaching circulatory and immune function health benefits of garlic.

To say that the bloggers to whom I refer have a credibility problem is an understatement. To respect their arguments and character is impossible, although this writer would never consider saying they should be silenced, through any means.

Using a tragic and untimely death to advance the causes of unsubstantiated pseudo-science through fascist style censorship, and to achieve the unstated goal of market penetration and profits is abominable, and creates a karma problem.

One nimrod even suggested putting Duesberg in prison for espousing his scientific opinion. Ah, Duesberg. I disagree with some of Duesberg's theories, to which he clings maddeningly and stubbornly. But Duesberg is an important scientific explorer and much of the field of biological science owes him a great debt, and a measure of respect. I'm quite certain, the sad excuse for a citizen who suggested that he be decommissioned is anything but a scientific explorer.

Of all the disciplines, the science people have and should continue to encourage dissent in the journey to uncover knowledge.

Voltaire, the French philosopher said in a letter to a contemporary, "I detest what you write, but I would give my life to make it possible for you to continue to write."¹ Those at Etiology should study this quote and put it to memory.

Is it clear that what was referred to as PCP - an acronym for pneumocystis carinii pneumonia even related to AIDS? Kaposi's sarcoma, another early AIDS-defining illness, is now known to be entirely unrelated to HIV.

PCS, a fungal infection of the lungs, started as a small cluster of contagious infections under the tutelage of Los Angeles-based Dr. Gottlieb, who was in close touch with the Feds at CDC.

It eventually morphed first into GRID (gay-related immune deficiency) and then into "AIDS" in this concerted effort to see it not as any other cluster but as a homosexual cluster of immune dysfunction, as if therein lived the aetiology of the great and powerful mystery of gay men who fell ill.

No matter that almost every parasite harmful to humans causes immune dysfunction, and they are usually contagious.

As titillating as gay sex may have been at the time, and feasible may it be that PCP was a proximity-related fraternally infectious bubble, it still has never been proven that PCP, or KS, for another matter, was related to someone's testing positive for HIV.

The tests of course came later, after the initial PCP/ KS clusters had run their course when Gallo monetized the whole mess with the erstwhile "HIV test" marketed for gay men. Erstwhile, because if you've read the labels of any such test, they don't actually test for HIV.

History speaks volumes and it is instructional in this quote from interviews conducted in 1993 and 1994 by Sally Smith Hughes, Ph.D with Dr. John Ziegler from The AIDS Epidemic in San Francisco: The Medical Response, 1981-1984, Volume IV, an oral history conducted in 1993 and 1994," at the Regional Oral History Office, The Bancroft Library, University of California, Berkeley, 1997.

Hughes
In the early days, when it was pretty much you alone seeing AIDS patients at the VA, how did you deal with opportunistic infections? You presumably are not an expert on infectious disease. How did you handle patients with problems that really weren't in your territory?

Ziegler
Well, they were partly in my territory, insofar as a chemotherapist renders people immunodepressed with cytotoxins. So as a profession, we have to deal with opportunistic infections. In fact, a lot of the early cases of Pneumocystis pneumonia were seen in leukemia patients who were treated with prednisone. So I was pretty familiar with the opportunistic infections, and we just treated them as part of our daily oncologic experience.

I read of an NCI [National Cancer Institute] program called SEER [Surveillance, Epidemiology and End Results] which found that the incidence of KS prior to 1980 in various participating cities, San Francisco being one of them, was several times higher than in cities such as Atlanta and Denver where AIDS is relatively rare.46 What does that mean?

Ziegler
There's a long story around KS and its epidemiology. But the short version is that most people think that KS is caused by an infectious agent, not HIV, but an agent that is passed along with it, and that these were really two independent epidemics, both following pretty much the pattern of advanced promiscuity in the homosexual community in the seventies. And in point of fact, the dermatologists, when they looked back and began to see that there were a fair number of patients in their gay practices who had Kaposi's sarcoma but who ended up not having HIV.

Q. Who is The Editor? A. Kirk Cordell

November 30, 2008

"Coming of age"

by The Editor

This year's aptly themed World AIDS Day, for those in the AIDS industry, a high holiday, certainly has different meanings among different people.

A headline grabbed me this week and it is telling of the ludicrous corner these people have backed themselves into. 

With the red ribbons of World AIDS Day observance everywhere, the newsflash reminded me that my entire adult life has been in the shadow of AIDS and promised death, and 3 decades of AIDS research have come full circle. 

It is obvious they don't know what they're doing.

The headline stated backwards that viral load has no statistically significant impact on CD4 counts, according to the research.

The backdoor actual headline described the researchers' inabilty to detect a link between what they term "virolgic failure" and CD4 T-cell counts.

Over 1600 antiretroviral newbies were monitored over intervals across a six month span.  What they found is obvious to those with real life experience outside the lab.

Suppression of what is improperly dubbed "viral load" - a misappropriated lab DNA count exxaggerated by laboratory magnification - is pointless.

Success of suppression means no DNA count. But this count does not measure virus particles, only DNA litter, remnants from unknown acttivty that has never been proven to be HIV activity.

The PCR DNA test as it is usually called, is not even authorizd by the US Food and Drug Adminsitration to diagnose HIV, so to base life-eroding and life-taking medication decisions on a rationale so tenuous is and was always wrong.

Now that it has been proven in the field, more than once, at more than one lab, how can the world bodies and national governments endorse, even force medicines on people if they can't even tell you the benefits of such treatment.

"The proportion with no increase in CD4 count from baseline did not differ between those with suppressed or unsuppressed VLs at 6, 18, and 24 months after ART (antiretroviral therapy) initiation."1

These are the exact words Moore et. al. published in their paper, CD4+ T-Cell Count Monitoring Does Not Accurately Identify HIV-Infected Adults With Virologic Failure Receiving Antiretroviral Therapy.

"The CD4 cell count monitoring does not accurately identify individuals with virologic failure among patients taking ART.

NotAIDS! has been saying for some time that many of the same immunosuppresive symptoms attributed to HIV can be a misdiagnosis of intestinal or other parasite infections.

Research has been published here that shows identical proteins and surface proteins are expressed by various parasites as by HIV, such as p24, gp160.

Not long ago, there was a splashy announcement in the mainstream press that "HIV lives in the gut" and hides out in the lymphatic tissue.  Interesting, since intestinal parasites hang out in the same neighborhood.

How coincidental that Irritable Bowel Syndrome affected a great many gay men in the 1970s, but this "syndrome" - a eupheism for intestinal parasites - disappeared suddenly around 1981, and was replaced with something called GRID - Gay Related Immune Deficiency -, ultimately becoming known as AIDS.

To fit the HIV/AIDS model, any disease occuring in the presence of a silly little antibody to an even sillier little retrovirus named unimaginitively,  Human Immunodeficiency Virus, is "coinfection." 

Keeping this in mind, divert for a moment and ask yourself, when you have the flu, or  a cold, is it said that you are "coinfected" with mononucleosis or meningitis - which you had when you were in college and for which you still have antibodies?

As far as the HIV/AIDS model is concerned, it is reported that "coinfection" with HIV and the  parasite, cryptospordium, is a leading cause of mortality from AIDS. 

What a surprise.   

Now read the following Author's Summary of just-completed research into the connection between intestinal parasites and, not just the progression to AIDS, but to the prevalence of AIDS in regions where parasitic infections are endemic due to an shameful lack of water purification and sanitation systems.

 Please note that the AIDS industry is busy sending millions of dollars to these regions for pharmaceutical products, rather than building much more cost-efficient solutions, like sewage systems and drinking water filtration facilities. 

The other question you need to ask, is whether there is even a remote possibility that without HIV, a long-term parasite infection will cause AIDS - meaning a syndrome of immune deficiency as indicated by a plethora of infections which normally the body would defeat.

If there is this possibility, then AIDS researchers all over the world may want to think about switching tracks, from the glamorous celebrity that is an insignficant retrovirus, to a field definitely with more ick-factor, and less star-appeal

- The Editor

Interestingly, symptoms once attributed to AIDS, like "wasting" or KS lesions (human herpes virus-8) or PCP [known as Pneumocystis (carinii) jiroveci Pneumonia] rarely occur or if they do rarely are fatal. Pneumonia is more often than not misdiagnosed as its symptoms are generalized and subacute, whether or not the person is HIV+.

Furthermore, "PCP has been documented recently in persons who are mildly immunocompromised, including those with chronic lung disease" (Contini C, Villa MP, Romani R, Merolla R, Delia S, Ronchetti R. Detection of Pneumocystis carinii among children with chronic respiratory disorders in the absence of HIV infection and immunodeficiency. J Med Microbiol 1998;47:329–33.} ]]> http://notaids.com/en/commonsense 2008-03-22T15:41:12-05:00 2008-03-24T12:53:58-05:00 The Editor

Poor sanitation threatens public health

6 in 10 Africans remain without access to proper toilet

20 MARCH 2008 | GENEVA --

Sixty-two per cent of Africans do not have access to an improved sanitation facility -- a proper toilet -- which separates human waste from human contact, according to the WHO/UNICEF Joint Monitoring Programme for Water Supply and Sanitation.

A global report will be published later this year, however, preliminary data on the situation in Africa was released today as part of World Water Day 2008.

The Day, built around the theme that “Sanitation matters," seeks to draw attention to the plight of some 2.6 billion people around the world who live without access to a toilet at home and thus are vulnerable to a range of health risks.

"Sanitation is a cornerstone of public health," said WHO Director-General Dr Margaret Chan. "Improved sanitation contributes enormously to human health and well-being, especially for girls and women. We know that simple, achievable interventions can reduce the risk of contracting diarrhoeal disease by a third."

Although WHO and UNICEF estimate that 1.2 billion people worldwide gained access to improved sanitation between 1990 and 2004, an estimated 2.6 billion people - including 980 million children – had no toilets at home.

If current trends continue, there will still be 2.4 billion people without basic sanitation in 2015, and the children among them will continue to pay the price in lost lives, missed schooling, in disease, malnutrition and poverty.

“Nearly 40% of the world’s population lacks access to toilets, and the dignity and safety that they provide," said Ann M. Veneman, UNICEF Executive Director. “The absence of adequate sanitation has a serious impact on health and social development, especially for children. Investments in improving sanitation will accelerate progress towards the Millennium Development Goals and save lives.”

Using proper toilets and hand washing - preferably with soap - prevents the transfer of bacteria, viruses and parasites found in human excreta which otherwise contaminate water resources, soil and food.

This contamination is a major cause of diarrhoea, the second biggest killer of children in developing countries, and leads to other major diseases such as cholera, schistosomiasis, and trachoma.

Improving access to sanitation is a critical step towards reducing the impact of these diseases. It also helps create physical environments that enhance safety, dignity and self-esteem.

Safety issues are particularly important for women and children, who otherwise risk sexual harassment and assault when defecating at night and in secluded areas.

Also, improving sanitation facilities and promoting hygiene in schools benefits both learning and the health of children.

Child-friendly schools that offer private and separate toilets for boys and girls, as well as facilities for hand washing with soap, are better equipped to attract and retain students, especially girls. Where such facilities are not available, girls are often withdrawn from school when they reach puberty.

In health-care facilities, safe disposal of human waste of patients, staff and visitors is an essential environmental health measure.

This intervention can contribute to the reduction of the transmission of health-care associated infections which affect 5% to 30% of patients.

“The focus on sanitation is fundamental to human beings,” says Pasquale Steduto, UN-Water chairman. “The MDG target on sanitation is seriously lagging behind schedule. The entire UN System has a shared responsibility in mobilizing concrete actions towards its achievement; investments must increase immediately.”

UN-Water is the coordinating mechanism of the UN agencies, programmes and funds that play a significant role in tackling global water and sanitation concerns.

World Water Day provides an opportunity to draw attention to the International Year of Sanitation 2008, a year in which the UN General Assembly in December 2006 has called for a focus on addressing sanitation and hygiene problems.

The International Year of Sanitation 2008 aims to raise the profile of sanitation issues on the international agenda and to accelerate progress towards meeting the Millennium Development Goal target of reducing by half the proportion of people living without access to improved sanitation by 2015.

Within the UN system, the focal point for the International Year of Sanitation is the United Nations Department of Economic and Social Affairs, in collaboration with the UN-Water Task Force on Sanitation.

Sanitation is not a dirty word. Sanitation matters.

For further information contact:

WHO:
Ms Fadela Chaib
WHO Communications Officer/spokesperson
Tel.: +41 22 791 3228
Mobile: +41 79475 5556
Email: ChaibF@who.int

Ms Sari Setiogi
Media Relations Office
Health Security and Environment
Tel.: +41 22 791 3576
Email: SetiogiS@who.int

Ms Nada Osseiran
Advocacy & Communications Officer
Public Health and Environment
Tel.: +41 22 791 4475
Email: OsseiranN@who.int

UNICEF:
Veronique Taveau
UNICEF Geneva Regional Office
Tel.: +41 22 909 5716
Mobile: +41 79 216 9401
Fax: +41 22 909 5907
Email: vtaveau@unicef.org

Veronique Cordier
UNICEF Media – International Year of Sanitation
Tel.: +1 212 326 7516
Email: vcordier@unicef.org

Women in New Jersey have suffered a civil rights defeat in the State of New Jersey when the legislature recently passed a bill that forces each pregnant woman and her newborn to be tested for HIV.

Despite the fact that only two infants tested positive in 2006 in New Jersey, and none in 2007, the State opted to blast personal liberty and violate civil rights with a law that is both unncessary and cruel.

Women who are pregnant have a high "false positive" rate, and when specificity and accuracy are evaluated in the general population, all HIV tests are of questionable value.

Because the protein markers used in these tests, like p24 or gp41 (p=protein gp=surface protein or glycoprotein, number X=molecular weight in kilodaltons), are not specific to the possibly benign retrovirus identified as HIV, there are some who argue that all positive HIV tests are false positives .

Biologically, pregnant women are much more likely to exhibit these or the other nonspecific protein markers that are used in diagnosing HIV.

Therefore, any policy, or worse, any law that forces expectant mothers to take what some consider to be a useless and irrelevant HIV test, risks causing catastrophic trauma to the pregnant woman, leading to depression, suicide, elective abortion, or the unnecessary administration of highly toxic substances like AZT or Nevirapine to the newborn and/or mother.

A bill signed into law Wednesday by the Senate president, Richard J. Codey, in his capacity as acting governor, requires two tests for pregnant women, at the beginning of the pregnancy and again in the third trimester, unless the mother objects. If the mother objects, the objection will be noted and the newborn will then be tested for HIV, with the only exception being on religious grounds. Newborns will also be tested if the woman tests positive.¹

Like the many national laws around the world, including the United States, denying entry of HIV positive individuals, official government policy and law are based on faulty HIV positive tests, and at the foundation, a faulty theory of HIV.

The reality is that studies have not in fact uncovered any process by which the elusive so-called "human immunodeficiency virus" kills CD4 immune t-cells, or any other actual cause-and-effect pathogenic process.

Riki E. Jacobs, who heads the Hyacinth AIDS Foundation, a New Jersey nonprofit AIDS service organization, is even opposed to the new law passed late 2007.

"I am adamantly opposed to this bill. New Jersey already reduced the perinatal rate of transmission with mandatory counseling of pregnant women. The issue is getting those women who are not in prenatal care in for services and testing. I definitely think it is an invasion of privacy."

Both the American Civil Liberties Union of New Jersey and the New Jersey National Organization for Women chapter have questioned the legality of the bill, signed into law by Richard J. Codey, NJ senate president, and acting governor.

What's even more confounding is that it appears infants can be born testing "HIV positive" even though the mother doesn't, which destroys the entire assumption about "mother to child transmission" or "MTCT" in AIDS industry careerists' lingo.

A Reuters news brief reported recently the results of a London study.

Infants can be born with HIV infection even if their mother tests negative for the virus in pregnancy, the results of a brief report show.

The study, which is published in the Archives of Disease in Childhood, involved a review of the prenatal test histories for 25 infants diagnosed with HIV infection at a referral hospital in London from 2001 to 2005. The study focused on 21 of the cases in which prenatal care had been provided in the UK.

Twelve of the mothers had not been tested for HIV infection during pregnancy, Dr. Hermione Lyall, from St. Mary's NHS Trust in London, and colleagues report. Of the remaining nine, four tested positive, but five did not.

Infants whose mothers were not diagnosed with HIV infection fared worse than other infants. Infected infants typically had severe infections, which proved fatal in six cases.

The important message is that a negative prenatal HIV test in the mother does not mean an infant is not infected with HIV and this possibility should be considered for any child with symptoms of immunodeficiency, the investigators emphasize.²

##

1. "N.J. Orders HIV Testing For Pregnant Women - Some Groups Call Law Unneeded and Intrusive" By Keith B. Richburg, Washington Post Staff Writer Friday, December 28, 2007; Page A03
2. Negative prenatal test doesn't assure infant free of HIV, Reuters, Thu, Jan 31, 2008 (Reuters Health)

Clean drinking water, a luxury most of us take for granted, is sadly unavailable for a billion or so of our brothers and sisters around the world.

NotAIDS! has published various charts and editorials about the shameful lack of attention to the world's most solvable health problems.

Having enough food to eat isn't a question for most people of the West, many of whom are overweight, and a frightening majority of whom are obese.

But in developing nations, and amongst the lower income in the cities and towns of the rich West, malnutrition is shockingly common.

In a surprising shift towards common sense, some important voices are joining the call to correct these gross imbalances.

The Associated Press recently published an article by Maria Cheng, "Experts Call for Rethinking AIDS Money." She quotes some of the statistics NotAIDS! has graphically represented over the past two years, data which has been available for some time, but for some reason until now hasn't been sexy enough for the likes of celebrity ambassadors such as the always-sunglassed Bono.

As the charts show, easily curable conditions cause the most premature deaths, like parasites in untreated drinking water, or malnutrition.

Dr. Richard Horton, editor of Lancet, a British medical journal, had this to say, "We have a system in public health where the loudest voice gets the most money. AIDS has grossly distorted our limited budget."

This evaluation of spending budgets is certain to be uncomfortable to AIDS researchers and the techno-medical-government complex who fatten themselves at the expense of HIV positive guinea pigs and unwitting taxpayers.

In her January 18, 2008 essay, Maria Cheng notes some important points the "Rethinkers" have been discussing for years.

The world invests about $8 billion to $10 billion in AIDS every year, more than 100 times what it spends on water projects in developing countries. Yet more than 2 billion people do not have access to adequate sanitation, and about 1 billion lack clean water.

In a recent series in the journal Lancet, experts wrote that more than one-third of child deaths and 11 percent of the total disease burden worldwide are due to mothers and children not getting enough to eat — or not getting enough nutritional food.

"If we look at the data objectively, we are spending too much on AIDS," wrote Dr. Malcolm Potts, an AIDS expert at the University of California, Berkeley.

Even the World Health Organization (WHO), sharply criticized on the pages of NotAIDS! for its propagation of misguided health policies, admits global health funding priorities are screwy.

Dr. Kevin De Cock, director of the AIDS department at WHO sheepishly remarks on his work in Kenya. "It did feel a bit peculiar to be investing so much money into anti-retrovirals while the people there were dealing with huge problems like water and sanitation."

As celebrity spokespeople with the best intentions glamorized AIDS funding, less sexy problems like clean water projects, sanitation systems, and food for the billions of our brothers and sisters around the world took backstage.

Ironically, the popularity of the AIDS cause was spurred on by the death of Hollywood actor Rock Hudson, who few know didn't even test HIV positive. Mr. Hudson died just months after quadruple bypass surgery, and whose copious consumption of liquor and 4-packs of cigarettes a day led to his dramatic decline and untimely demise.

Many researchers in the AIDS world like to use the term, "resource poor" when referring to the war-torn, poverty stricken nations ravaged by the imperial colonialism of the last two centuries.

The term couldn't be more inaccurate. The lands of Africa, for example, rich in natural resources and mineral deposits, are pillaged by the corporate interests of the West, whose policies and public discourse, and AIDS work fattens the wallets of pharmaceutical companies, and whose politicians hide the criminal ransacking that continues unabated.

The middle classes of the West are busy trying to maintain a moderate quality of life, taking for granted the faucet in the kitchen, the food in the refrigerator, the weekly trash collection, while the entrenched poverty of billions of our bretheren continues.

While billions go hungry, and billions suffer cholera and dysentery from parasite infested waters collected in street puddles, billions of dollars are poured into the black hole of AIDS research, ultimately landing in the bank accounts of pharmaceutical companies.

But "trying to redirect AIDS money will take a long time," complains Dr. Richard Wamai, a Kenyan doctor at Harvard's School of Public Health. "It's a bit like trying to stop an ocean liner."

"No one is beating the drum for basic health problems," said Daniel Halperin, an AIDS specialist also at Harvard University's School of Public Health.

It's time we listen more carefully.

##

Through these extreme rises and falls, Arenas is always writing, his typewriter his most faithful lover and weapon (by way of smuggled manuscripts) against the dark forces that surround him. As Time magazine's Richard Corliss wrote, Arenas is "a serious actor's dream role: to be a gay Jesus in a modern Passion Play," and Javier Bardem--the first Spanish actor to receive an Oscar nomination--inhabits the role with subtle ferocity, charting this emotional odyssey with outer reserve but blazing infernos of internal passion. And while Schnabel suffers from a hyperactive camera, there's poetry here--visual, dramatic, and literal--and vibrant humor to temper the deep tragedy of Arenas's life. Schnabel also uses his actor friends to good advantage: a nearly unrecognizable Sean Penn adds an ironic touch to his brief appearance as a peasant, and Johnny Depp is both funny and fearsome in dual roles as a drag queen and vicious army interrogator. --Jeff Shannon