Re: Nutrition, Immunity and Infection

Excellent article, Rabbitears, thanks.

Re:
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I think this is a very interesting commentary. In my opinion, this supports the fact that people shouldn't try to "starve out the parasites" when there is an infection going on inside the body. Nutritional support is essential for the immune system.
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It seems like supporting work, doesn't it.







Re:
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http://www.pnas.org/cgi/content/full/93/25/14304

Proc. Natl. Acad. Sci. USA
Vol. 93, pp. 14304-14307, December 1996
Commentary
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Great commentary, in my opinion.
Some notes, if I may:









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Nutrition, immunity and infection: From basic knowledge of dietary manipulation of immune responses to practical application of ameliorating suffering and improving survival
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This could well mean "A 'new'/obvious/convenient look at some VERY OLD Knowledge".








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Thy food is such As has been belch'd on by infected lungs. William Shakespeare, Pericles, IV, vi, 178.
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Interesting note.







Some "translations" and comments:

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The causal relationship between the conjugal pair of famine and pestilence has been known for millennia. It is recognized that malnutrition and infection are the two major obstacles for health, development, and survival worldwide, and poverty and ignorance are the most significant contributing factors (1, 2). Epidemiological observations have confirmed that infection and malnutrition aggravate each other.
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'Starvation and Disease seem closely related'.









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However, nutrition does not influence all infections equally (3, 4). For some infections (e.g., pneumonia, bacterial and viral diarrhea, measles, tuberculosis), there is overwhelming evidence that the clinical course and final outcome are affected adversely by nutritional deficiency. For others (e.g., viral encephalitis, tetanus), the effect of nutritional status is minimal. For still others (e.g., influenza virus, human immunodeficiency virus), nutrition exerts a moderate influence.
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'The role of Nutrition in ALL Infections is not yet well understood by us'.








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...My interest in nutrition-immunity interactions was kindled by two cases: first, the story with an unhappy ending, of a child; second, the bleak scenario of the Third World. Eighteen-month-old Kamala was thin, her skin pale as wax, and her lungs screaming for air. She wore a spectral white death-mask in a frame of black hair....
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There was an OBVIOUS Process of Death occurring within the patient at that particular time according to those words above, my note.






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Her shrivelled body and swollen legs were typical of marasmic kwashiorkor, and she had an obvious fulminant infection. Lung aspirate revealed the opportunistic organism Pneumocystis carinii. Despite our best efforts, we lost the child. I speculated that malnutrition had robbed Kamala of her defenses against infection and led to premature demise.
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He may have been right at that precise moment even.
I wonder which steps were taken then.








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...Tuberculosis is a major cause of death in underprivileged populations. It has been estimated that 3 million to 4 million individuals die of the disease every year. In addition to environmental factors such as overcrowding, host immunity plays a crucial role in determining the final outcome. The delicate balance between the host's ability to kill Mycobacterium tuberculosis and the microorganism's efforts to evade the microbicidal armamentarium of the host makes fascinating study...
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Balance.







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A number of innate and adaptive mechanisms are responsible for killing Mycobacteria (8, 9). The major role played by macrophages has been reviewed extensively (10). Infection occurs commonly through the respiratory tract. Bacteria that survive mucociliary escalator of the upper respiratory tract are ingested by alveolar macrophages that contain numerous acidic phagocytic vacuoles and hydrolytic enzymes. Macrophage activation results in a drastic reduction in the number of viable bacteria that may be completely eradicated. However, some mycobacteria may survive the powerful microbicidal onslaught and escape into the cytoplasm where they multiply unhindered, leading ultimately to cell death, and release into the tissues where they enter other cells including macrophages.
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Very interesting Mechanism.







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Persistent organisms provide the antigenic stimulation and cell-mediated hypersensitivity reaction that leads to local accumulation of inflammatory cells and formation of granulomas. This process limits the spread of mycobacteria but is associated with tissue necrosis, fibrosis, and functional impairment. This stereotypic hide-and-seek game of evasion, activation, attack, and death is played out in response to many intracellular pathogens, e.g., Listeria monocytogenes (11).
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There you go.






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Bloom and colleagues (12-16) have conducted a number of studies to elucidate the principal mechanisms by which murine mononuclear phagocytes kill M. tuberculosis. Now, Bloom and colleagues take us one major step forward by examining the effects of a low protein diet on anti-mycobacterial immunity (17). Young adult mice fed a diet containing 2% protein died rapidly following challenge with M. tuberculosis; their immune responses were compared with those of animals fed a diet containing 20% protein. Malnourished animals showed a reduced expression of interferon , tumor necrosis factor , and inducible nitric oxide synthase in the first 2 weeks after infectious challenge. Interestingly, these changes were observed in the lungs but not in the liver, and the effects wore off after 2 weeks after challenge. There was no significant effect on total nitric acid production in vivo. Granulomatous inflammation was studied at the light, immunohistochemical, and electron microscopic levels, and was impaired in the low-protein group, confirming and extending earlier observations (18). The immunologic changes and risk of death could be reversed by reverting to a normal high-protein diet.
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The proposition "Ensure a Hypernutritional Pathway" may seem to make [even more] sense now also according to this.









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The seminal work of Bloom and colleagues raises many new questions. Are the findings nutrient-specific? Did body weight and lymphoid organ weight differ in the two animal groups? It is possible that at least some of the observed effects may be the result of concomitant deficiencies of micronutrients such as zinc.
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Yeah, sure, ANYTHING is possible. This is where Science comes in, in my opinion, and where those 'whild-shot' approaches and measures taken by some doctors seem to fail, always in my humble opinion [for example: "..you've got a Zinc deficiency, take these Zinc capsules x times a day and that should do it for you.."].

The mechanism seems a bit more complex and more variables seem to be involved, as I've said before and based on observations, of course.










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It is recognized that inadequate diets result in poor appetite, malabsorption, and decreased growth. Thus, the consumption and absorption of nutrients that are critical for optimum immune responses (e.g., zinc, selenium, vitamin A, pyridoxine, vitamin E) are compromised. This confounding variable can be sorted out by including a pair-fed comparison group. Would the quality of dietary protein make a difference? In general, animal proteins are superior to vegetable proteins in sustaining growth and maintaining immunity;
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Some thoughts to consider, especially for those who discard Meat and/or animal products as part of their diets.








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there are subtle differences in immune responses of animals fed casein-based and whey-based diets.
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So begins what I call "the puzzle".









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What is the threshold of nutritional deficiency that results in a significant impairment of anti-mycobacterial defenses?
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I'll submit right here that [the effects of] this "threshold" may be [just] a function.












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The 2% protein diet is a very drastic nutritional insult and quite unlike what happens in the majority of deprived human populations. What is the explanation for the marked heterogeneity of survival time in genetically similar mice challenged with the same mycobacterial burden? What is the basis of tissue specificity of macrophage handling of the microorganisms? It has been shown that CD8 T cells specific for listeriolysin O mediate significant immunity in the liver but not in the spleen (19). Is one cell type essential for antibacterial defense at one site but not at another location, as has been shown for neutrophils and Listeria (20).
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I wonder if those are the significant questions to ask with regard to this issue.










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Would deficiencies of other nutrients result in impaired anti-mycobacterial immunity similar to that observed in mice on low-protein diet? For instance, deficiencies of vitamin A (1, 21, 22) and zinc (1, 23-25) alter a wide range of immune responses. Would the immunologic abnormalities be reversible in young animals whose mothers had been subjected to a chronic nutritional insult before and/or during gestation? Both in small-for-gestation low-birth-weight infants (26, 27) and in animal models of intrauterine undernutrition or zinc deficiency (28, 29), the immunologic impairment is profound and long lasting. What is the status of other immunologic mechanisms that play an important role in defense against intracellular pathogens, e.g., CD4+ and CD8+ T cells (19, 30, 31); and T cells (32, 33); interleukins 2, 4, 6, 8, and 12 (31, 33-38); natural killer cell activity (39); fibronectin (40); and heat-shock protein (41)? Neutralizing antibodies (42), gene knockout mice (43), and adoptive transfer assays (19) with bone marrow chimeric or transgenic rodent hosts can be deployed to study the specific role of individual immune processes. What is the impact of genetic host factors on antigen recognition and immunologic defense (44)?
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Many questions, possibly a loss of 'focus', I think.






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Finally, it would be useful to confirm the interesting observations reported in the study by Chan et al. (17) on a larger number of animals that would permit an adequate statistical analysis and to extend these investigations to newly diagnosed as well as chronically infected patients with pulmonary tuberculosis.
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Which would be a (re)statement of the obvious, in my opinion. But of course something healthy to do all the time.







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There is exciting new information on another face of host-parasite interaction. Viruses can mutate and show altered virulence because of nutritional deficiencies in the hosts they infect. Beck and coworkers (45) showed that selenium deficiency enhanced the heart-damaging potential of coxsackievirus.
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Based on paragraphs like these many will "rush ahead" I'm sure, and will start to introduce "Selenium supplements" as an attempt to correct Balance. In my opinion and based on observations, there may be quite more at stake.








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...If confirmed, these exciting data will have far-reaching epidemiologic implications and may explain the emergence of novel infectious diseases in populations with endemic nutritional deficiencies...
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That's right, IF confirmed.







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Our knowledge in nutrition-immunity interactions has opened up exciting possibilities for nutritional intervention for both primary and secondary prevention of infection in high-risk groups.
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Often I've had to learn to translate the expression "opening up exciting possibilities" as another synonym for "creating a new market". Just a pertinent note here, of course not necessarily this case.









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Nutritional deficiencies are seen often in hospitalized patients.
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A VERY interesting observation, in my opinion. Patients and families, you've been warned.











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These individuals are susceptible to develop life-threatening opportunistic infections.
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Heh.








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Recent animal work (46) has highlighted the value of nutrient-enriched diets in improving immune responses and survival following challenge with organisms such as Listeria (Figs. 1 and 2), and limited clinical studies have confirmed these observations. Similarly, a large proportion of the elderly have reduced dietary intakes and low blood levels of various nutrients (47). They are also prone to respiratory infection. Several investigations have shown a correlation between nutritional status and incidence of infection in old age. The results of a few recent intervention trials indicate that modest supplements of micronutrients improve immune responses and more significantly, reduce the incidence of respiratory infection and antibiotic usage (48). In addition, post-vaccination immune responses are higher in subjects given nutritional supplements than in untreated controls. These observations have profound clinical and public health implications.
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Absolutely, I think as well. It means, or it should mean "Try to Nourish yourself [INTELLIGENTLY] to the Best of your ability SPECIALLY during Disease".

[also, it's good to note that "to nourish" doesn't mean "to eat a lot" at all - that's where 'Intelligence'/skill comes in, I think]







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The era of nutritional manipulation of the immune system has finally dawned
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Finally, huh?







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and it brings with it the promise of using diet and nutrition as innovative powerful tools to reduce illness and death caused by infection.
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Which is a (re)statement of the obvious. Something that Science doesn't need, in my opinion. What I DON'T like about this paragraph is that it calls "Diet and Nutrition" "Innovative Powerful Tools" as 'a [future] promise'. Powerful Tools? Well of course they are! They've always been, can't you see? Med school doesn't know this YET? Innovative they say? From whose perspective, I wonder, when it's been Medicine used since the ages [as far as I know]? So then what kind of medicine is being practiced today, I ask, that seems to ignore these apparently simple and obvious and powerful observations? It would seem certainly not the kind of Medicine practiced "in the past", now would it?

I wonder from which perspective the FDA's "brains" would look at these 'findings' today. [keeping in mind that this article seems to be from 1996] Ten years have passed already. What has been done with/about these 'findings'? Tweet