FRANĒAIS HIV AND NUTRITION PREVIOUS PAGE NEXT PAGE SUBSCRIBE Chester Myers' Nutrition Series Information relating to HIV & Nutrition: HIV & Zinc and Copper revisited
Poor wound healing, anorexia, abnormal taste and smell, diarrhea, skin inflammation, skin stretch marks, nail abnormalities such as white spots or brittleness, anemia, impaired glucose tolerance, central nervous system malfunction, muscle deterioration, increased oxidative damage of cell membranes, decreased thymic hormone activity, increased apoptosis/cell death, T-helper cell dysfunction, low CD4+ cells, increased CD8+ cells, and reduced natural killer cell activity are some possible results of zinc deficiency. (Badgley, 1986; Chandra, 1984; Cunningham-Rundles et al, 1981; Forbes, 1984; Hoffer and Walker, 1978; Hunt and Groff, 1990; Odeh, 1992; Prasad, 1984; Stites and Terr, 1991).
In HIV disease, the most poignant observation may be that zinc supplementation has been observed to improve "accretion of lean tissue rather than fat after dietary zinc supplementation in children recovering from malnutrition" (Cavan et al, 1993). Interestingly, this study also wisely included supplementation with other micronutrients. All too often micronutrient supplementation studies have examined only one micronutrient without providing a broader baseline supplementation. In such studies, consequent imbalances are all too easily interpreted as being signs of toxic overdose of the one nutrient taken as the supplement, rather than the perhaps more likely effects of nutrient imbalance that may result from failure to simultaneously boost the baseline of other interrelated nutrients.
Copper deficiencies can cause reduced monocyte function, neutropenia, leukopenia, microcytosis, failure of erythropoiesis (formation and development of erythrocytes, i.e.,red blood cells), high oxidative damage to lipids, general oxidative damage, and, when caused by high zinc intake, high serum cholesterol (Hunt and Groff, 1990; Prasad et al, 1978; Turnlund, 1988).
Zinc and copper are two minerals that are essential for our health. Absorption of these into our bodies from food varies greatly; serum levels of both are regulated by a protein called metallothionein (Cousins, 1989), so that changing the level of one modifies the other in a see-saw fashion. From 14 to 41% of dietary zinc is absorbed in healthy people (Hunt and Groff, 1990; Sandstead, 1973); percentages of copper absorption are poorly known, but 25 to 60% has been suggested (Turnlund, 1988). The role of zinc in our bodies is linked with other materials, namely copper and sulfur-containing compounds called thiols (thiols include compounds such as N-acetyl cysteine, i.e., NAC). Zinc supplementation above normal dietary levels may be beneficial in HIV disease provided there is sufficient copper and cysteine (NAC) intake. Zinc supplementation without both copper and NAC, on the other hand, in my view is not to be recommended. I feel strongly that current information substantiates the several recommendations for daily zinc supplementation at levels of 50-100 mg, provided this is based on supplementation with a general multivitamin and multimineral (add up the zinc from the various sources to make sure 100 mg is not exceeded), 3-5 mg of copper (again, add up the amounts), and 1500-3000 mg of N-acetyl cysteine.
Background
Zinc
From 70 to over 100 enzymes in the human body are reported to require zinc; "zinc is a part of more enzyme systems than the rest of the trace elements combined". These enzymes/proteins include many from both the immune and digestive systems. Thus low levels of zinc interfere with digestion of our food, as well as our immune function. Immune dysfunction from zinc deficiency has been called "profound", and "severe deficiency is produced easily and rapidly" (Beisel, 1982).
Even for apparently healthy people, available data indicate that zinc deficiencies may not be uncommon in North America (Rivlin, 1990; Sandstead, 1973). A recent US study (Baum et al, 1994) noted that HIV- homosexual males may tend to be deficient in zinc in spite of intakes consistent with RDA recommendations. Earlier work from Europe indicated a similar trend on that side of the Atlantic (Bro et al, 1988). [COMMENT: low zinc levels in men can result from a high level of sexual activity since relatively high amounts of zinc are lost in seminal fluid (cum).]
Absorption of zinc from the digestive tract occurs in sections of the small intestine known to be often deteriorated in those living with HIV. While common measurements of zinc levels in the blood serum don't necessarily make it possible to predict low body levels from low serum levels (Bogden et al, 1990), the known digestive difficulties and increased metabolism, common with HIV, make it very likely that zinc levels deteriorate early in the disease (at least in the absence of supplementation). Furthermore, serum zinc levels are lower than the levels that provide maximum function of certain cells such as the peripheral blood mononuclear cells (Harrer et al, 1992). Thus, an apparently adequate serum level may not necessarily rule out functional deficiencies, and immune dysfunction has been singled out as a functional deficiency that may be likely when serum zinc levels are still normal (Rivlin, 1990). [One reviewer has suggested that measurement of both serum zinc levels and alkaline phosphatase is currently an appropriate assessment of zinc status (Arnaud et al, 1993). More specifically, "quantitative measurement of alkaline phosphatase activity in neutrophils before and after zinc supplementation" may be beneficial (Hunt and Groff, 1990).] Thymic hormone failure, common in HIV disease, has been attributed to zinc deficiency. While total thymulin levels remain normal, the active form is low because of low zinc levels (Arnaud et al, 1993; Bro et al, 1988; Cunningham-Rundles et al, 1981; Fabris et al, 1988; Mocchegiani et al, 1992; Ott et al, 1993).
Zinc occurs in a variety of foods. Good sources are most meats and poultry, eggs, shrimp and crabmeat. Oysters are remarkable in having very high levels. [For other reasons, oysters should not be eaten raw by those living with HIV. High levels of cooked oysters may also be inadvisable since they may also contain high levels of certain toxic heavy metals.]
Absorption of zinc into the body decreases when foods are cooked, especially when browning occurs. Many vegetables (legumes) and cereals are high in phytic acid which binds to zinc when calcium is present, and this makes the zinc poorly available to the body. If high levels of calcium are not present, phytic acid binding of zinc is not significant (Forbes, 1984; Hunt and Groff, 1990). It may therefore be wise to minimize dairy products and calcium supplements when eating meals high in vegetable/cereal content. NOTE: the evidence indicates calcium interferes with zinc absorption only when phytic acid is present. In addition, the body doesn't store zinc. The only 'store' is made up of those many proteins /enzymes that contain zinc; when dietary zinc intake is not enough, these proteins/enzymes (including muscle proteins) are cannibalized in a sequential fashion, those holding their zinc least tightly losing their zinc the fastest. An enzyme called carbonic anhydrase which is important for respiration is given high priority, and apparently maintains its zinc content when other body stores become depleted (Beisel, 1976; Hunt and Groff, 1990). Conversely, alkaline phosphatase becomes deprived of its zinc quite readily, thus making activity of this enzyme a good monitor for body zinc status (as already noted).
Low zinc levels may be complicated by low metallothionein, the protein that regulates zinc and copper levels in the serum, liver etc. This protein is made of about 30% of the amino acid cysteine. This amino acid becomes deficient early in the course of HIV infection, so that, uncorrected, not only is zinc likely to be deficient, but its regulation within the body is also likely compromised (see HIV & Cysteine, revisited, in this series, and listed at the end of this monograph). Futhermore, absorption of zinc from the gut into the body may also rely on compounds derived from cysteine (O'Dell, 1990; Pattison and Cousins, 1986; Reeves et al, 1993).
Studies have shown that zinc deficiency or its effects can be reversed by supplementation (Beisel, 1982; Black et al, 1988; Cavan et al, 1993; Cunningham-Rundles et al, 1981; Libanore et al, 1987). These studies include reversal of immune depression, such as diminished proliferative response by lymphocytes and neutrophil dysfunction when caused by zinc deficiency. In states of malabsorption such as occurs with Crohn's disease, supplementation at levels as high as 300 mg per day has been suggested to be necessary (Chandra, 1984). In HIV disease, Shambaugh (1989) suggested levels of 150 mg per day for up to 6 months may be necessary to correct even marginal zinc deficiencies.
A well-publicized study (Chandra, 1984) of high levels of zinc supplementation (300 mg per day) in healthy males observed effects that could be interpreted as being from copper deficiency, but otherwise "none of the subjects showed evidence of any untoward side effects". This study noted that 2000 mg of zinc can cause vomiting, abdominal cramps, and diarrhea. This study also noted the importance of supplementation at levels as high as 300 mg per day for those with zinc malabsorption such as with Crohn's disease. Curiously, this study has been cited in support of an unfocussed opinion that above either 15 mg or 300 mg per day of zinc may be toxic (Galvin, 1992). Other individuals have gone one step further by indicating 25 mg per day is a toxic level (Holley et al, 1992).
Copper
Copper is also a mineral essential in small amounts for proper health. As with zinc, copper is also part of different proteins/enzymes, mostly three proteins in blood plasma. A significant feature of copper deficiency is that it is a possible source of anemia due to a resulting defective iron metabolism secondary to a defective protein, called ceruloplasmin, which mediates use of iron by the body (Hunt and Groff, 1990).
Supplementation with zinc, especially at levels of 150 mg per day or higher, without a simultaneous increase in copper intake results in copper deficiencies. These are reversed by appropriate copper supplementation (Black, et al, 1988; Prasad et al, 1978; Turnlund, 1988).
Those foods that are good sources of zinc also contain good levels of copper. Beef/lamb liver, prunes, raisins and nuts contain very high levels of copper.
Copper absorption not only occurs in the small intestine, but also in the stomach. Because of this, in the absence of supplementation, serum zinc deficiencies could be accompanied initially by a simultaneous elevation of serum copper. It is also possible that low absorption of zinc across the small intestine mucosal membrane could permit increased absorption of copper in the stomach. Subsequent supplementation with zinc without copper would be expected to rapidly reverse this, and result in copper defiency - this could be just as bad for immunity as the initial zinc deficiency and may take longer to correct.
The story for copper levels in HIV disease has not been crystal-clear. However, a study presented at the San Francisco AIDS Conference (abstract THC677) noting an increase in copper level to accompany zinc decrease is probably the most consistent, although a report the following year (Florence Conference abstract WB2098) reported the opposite, i.e., copper deficiency. Bogden et al (1990) suggested that their observation of increasing copper levels in progressing from asymptomatic to ARC to AIDS may have been the result of weight loss. Since copper absorption is less likely to be compromised (it is absorbed in both the stomach and small intestine), and since zinc requirements are more likely to be elevated to a greater extent, it is logical that in the absence of zinc supplementation copper levels will initially become elevated, especially in early HIV disease. On initiation of zinc supplementation, it is important to remember the importance of also maintaining a balance of copper intake. While from 5X RDA levels (i.e., 75 mg per day for males, or 60 mg per day for females) to 100 mg per day of zinc intake have been recommended for those living with HIV, a level of 3 to 5 mg of copper supplementation is likely to be sufficient to balance the increased zinc inctake.
HIV and Zinc and Copper
As early as 1984 it was apparent that serum zinc levels were likely to be severely stressed with HIV disease (Cunningham-Rundles, 1984); other research noted that decreases in both T4 cells and the T4/T8 ratio correlated with zinc deficiency (Beach et al, 1982; abstr. ThC677, San Francisco AIDS Conf. 1990). It was several years before there was general medical documentation that serum zinc levels may be low in those with HIV disease (abstr. ThC677, ThBu206, San Francisco AIDS Conf. 1990; abstr. MC3128, MB3128, WB90, WB2098, WB2166, Florence AIDS Conf. 1991; abstr. PoB3675, PoB3707, PuB7502, Amsterdam AIDS Conf. 1992; Bogden et al, 1990; Libanore et al, 1987; Beach et al, 1992; Falutz, 1990; Falutz et al, 1988; Harrer et al, 1992; Shambaugh, 1989). Furthermore, use of AZT has been associated with still greater decreases in zinc levels (abstr. WB2098, Florence AIDS Conf. 1991).
In some cases, as already noted, low serum zinc may be common among gays irrespective of HIV status. Not all studies, however, have noted zinc reductions in those with HIV. One study noted low levels in HIV+ people with Group IV HIV disease, but not in those with swollen lymph glands (generalized lymphadenopathy) (Falutz et al, 1988). Another study failed to find any lowering of zinc status in either people with ARC or AIDS (Walter et al, 1990). This latter study recorded lower zinc levels for control subjects; thirty-five percent of these were female and it is not stated whether the males were gay.
In a study of the relative decrease in antioxidant status during the course of HIV infection, Sappey et al (1992) compared 16 control HIV- people with 25 HIV+ people of CDC stage II status, and 18 HIV+ people of CDC stage IV status. The following serum levels of zinc were recorded:
Controls 12.3±2.5 µL
Stage II 10.5±2.7 µL
Stage IV 7.9±1.4 µL.
The authors noted the "decrease is progressive with the severity of the disease".
Beach et al (1992) observed marginally lower serum zinc in HIV+ subjects compared with HIV- gay controls. The difference was not statistically significant. Interestingly, serum copper was higher in the HIV+ subjects than in the controls. Although not considered by the authors, it would seem logical that this elevation in copper may have resulted from a real zinc decline. While it seems that zinc deficiencies may become profound in advanced HIV disease (Sappey et al, 1992), so-called early disease states have been generally documented with serum zinc levels that are low, but not lower than in HIV- gays. The data from Sappey and co-workers would make it seem likely that increased zinc deficiency may start early in HIV infection, but that the currently used assays don't detect deficiency until it is more severe; functional deficiency may precede deficiencies detected by common assay. Comments by Harrer and co-workers (1992) also would argue for this conclusion. Another factor is that serum zinc levels decrease as part of the body's normal reaction to infection (Cousins, 1988; Koj, 1989); this results when the liver takes up higher than normal levels, apparently in order to meet increased needs of zinc-requiring enzymes to fight the infection (Beisel, 1976). Thus infection is initially accompanied by the acute phase response (APR) whereby humoral immunity is activated along with fever promotion, suppression of serum zinc and iron levels, changes in glucose metabolism, changes in energy utilization, and very large changes in blood proteins (Beisel, 1976; Dezube et al, 1992; Yamada et al, 1990). While some reports of low serum zinc levels may reflect only the acute phase response in early stages of HIV disease, it is still apparent that real decline of zinc does occur (Sappey et al, 1992), and probably should be expected if HIV disease progresses without a compensating adjustment of dietary intake.
In her monograph HIV Treatment Strategy, Part II: Therapeutic Basics for People Living with HIV, Dr. Lark Lands includes a quote from Dr. Richard Beach, at the 1992 Amsterdam International Conference on AIDS: "patients who were put on AZT who had low plasma levels did not do nearly as well on the drug as those who had normal levels of zinc."
There are reports noting benefits from zinc supplementation for those living with HIV. An early such report (Libanore et al, 1978) noted increases in T4 and T8 cell counts, and the T4/T8 ratio, after 10 mg zinc sulphate supplementation for 21 days in people with ARC, but increases of T4 cells and decline of T8 cells for those with LAS (lymphadenopathy syndrome). Gordon (1992) reported marked improvements with aggressive zinc therapy that included intravenous zinc therapy. Improved cell-mediated immune response, increased life expectancy, lower incidence of Kaposi's sarcoma, and fewer opportunistic infections were reported, although unmasking of herpes infection necessitated acyclovir treatment. For the study where cell-mediated immunity was assessed, an oral dose of 220 mg of zinc sulphate (i.e., about 75 mg of zinc) was administered orally.
Some studies have examined dietary zinc intake and disease progression (Abrams et al, 1993; Graham et al, 1991; Tang et al, 1993).
Graham and co-workers noted "neither dietary copper and zinc nor their levels in toenails were associated with HIV-1 seropositivity or progression to AIDS", but that "serum copper levels were higher... and .. serum zinc levels were lower in the seropositive progressors than the seropositive nonprogressors and the seronegatives". This study continued to note that "in a logistic regression, higher serum copper and lower serum zinc predicted progression to AIDS independently of baseline CD4+ lymphocyte level, age, and calorie-adjusted dietary intakes of both nutrients". They concluded, however, that these markers resulted from disease activity/progression, and that a lack of correlation with dietary intake did not argue for supplementation. They did, however, state that their "findings do not completely exclude [that zinc supplementation might be useful]".
Three authors of the former study are also authors with Tang and other co-workers in a 1993 report of data from 281 HIV-1 seropositive homosexual/bisexual men. In this study it is noted that "increased intake of zinc was monotonically and significantly associated with an increased risk of progression to AIDS", while disease progression was not observed to relate to copper intake (the report implies that copper levels were elevated). While the higher level of supplemental zinc intake was 155 mg per day, in fact, few in the study had intakes this high (see below). Certainly, at 155 mg per day there may have been problems from copper balance.
Abrams and co-workers presented different results from 269 HIV-1 seropositive men. The following compares the results:
Quartiles Hazard 95% confidence # with
of intake ratio level AIDS
Abrams et al 14.1 mg 1.0 0.5, 1.7 21
14.2-15.9 1.8 1.0, 3.1 25
15.9-18.1 1.2 0.7, 2.0 29
18.2 1.0 - 25
Tang et al 11.6 1.00 - 21
11.6-14.1 1.33 0.75-2.38 26
14.1-20.0 1.69 0.95-3.02 28
20.0 2.06 1.16-3.64 33
The time from dietary intake assessment to study completion was 6-7 years in both cases. Abrams et al did not consider their results regarding zinc intake as statistically significant due to a "lack of variation in zinc intake". They noted that their group had generally high intakes "especially as a result of supplementation", and that overall "a high nutrient intake was associated with a significant decrease in the risk of AIDS when the models were adjusted for health status at baseline". Considering that the hazard ratio appeared to decrease at the higher level of zinc intake for the Abrams et al group, and that the 95% confidence levels of the higher intake levels in the Tang et al study spans a wide range (wider than any of the other nutrients listed!) including down to a low value of 1.16, it seems likely that there may be (an)other influencing factor(s). Dr. Lands (personal communication) has pointed out that, in the Washington/Baltimore area where the Tang et al study was done, the food portion of zinc intake may have been accompanied by a corresponding high level of toxic heavy metals such as mercury and cadmium. Furthermore, an increase in negative effect was observed when supplemental levels (up to 155 mg/day) were added to food levels. Negative effects would be expected at this level if copper intake were not adjusted accordingly; furthermore, in HIV disease, it is important to ensure cysteine/thiol levels are adequate. Without corresponding data on copper levels and body cysteine status, it is difficult to attach much significance to what might be considered as an apparent negative influence from zinc supplementation in the Tang et al study. This is an area, however, that clearly needs controlled studies to examine all the interrelated parameters.
It would seem that the two groups of people in the latter two studies may be somewhat different, although, in general, both studies concluded that disease progression was slower among those with higher intakes of a number of micronutrients. The role of copper seems not to have been assessed, so that interpretation of the apparent trends with zinc intake are difficult to interpret.
Th1 vs Th2
Higher levels of CD8+ cells, and thus lower CD4+/CD8+ ratios , have been noted to be characteristic of many long-term survivors. Furthermore, disease progression correlates with loss of cell-mediated immunity (CMI), also called delayed-type hypersensitivity (DTH). Some people feel that events that support cell-mediated immunity (the Th1 response) encourage long-term survival for those living with HIV (Lanzavecchia, 1993; Pantaleo et al, 1993; Shearer and Clerici, 1992). The Th1 response tends to see-saw with humoral immunity, the Th2 response, so that what increases one may suppress the other. Humoral immunity involves antibodies, and is believed to be a more recent evolutionary development. In general, cell-mediated immunity is more sensitive to malnutrition, especially of the protein-calorie type, than is humoral immunity (Stites and Terr, 1991). Both humoral and cell-mediated immunity are suppressed by zinc deficiency (Beisel, 1982), but it appears that cell-mediated may be the more sensitive (Harrer et al, 1992). Zinc deficiency has been reported to increase CD8+ counts while suppressing CD4+ counts (Stites and Terr, 1991). Odeh (1992) noted that zinc deficiency causes a decrease in T-cell function while leaving B-cell function unaltered. In a study of zinc supplementation in HIV disease, however, both CD4+ and CD8+ counts have been observed to increase (Libanore et al, 1987). The CD4+/CD8+ ratio also increased, and currently the significance of this is difficult to interpret. Some might even say that this is perhaps therefore one argument for not supplementing with zinc in HIV disease (the study did not indicate copper status which confounds reasonable interpretation of the results). Since zinc deficiency seems to become progressively worse with disease progression, at least in the absence of supplementation, then it seems reasonable to try to ensure adequate zinc levels are maintained. Keep in mind the rather long list of possible effects of zinc deficiency - first page. Surely other ways must be sought for suppression of HIV.
There are various reports of test tube studies where zinc has been shown to either have negative or positive effects on parts of the virus. Interpretation of such studies needs to be done with discretion. Use of high levels of zinc to 'hurt' the virus is unlikely to be achieved at levels of intake that would not also be harmful to you, the host. Similarly, the body's need for zinc in so many of its components and functions would also make it unwise to consider zinc deprivation in an attempt to 'hurt' the virus. After all, the virus also needs amino acids for its growth, yet one would hardly stop eating protein to kill the virus thusly. Dr. Lands has noted that a comparable method of killing the virus would be simply to place a plastic bag over one's head - the virus will die simply because its host is killed. One might call this the "plastic bag approach". It is not to be recommended!
[A way to encourage the Th1 (cell-mediated immunity) response might be to keep vegetable polyunsaturated fats, such as those from soy, corn, sunflower oils, to a minimum. In fact, deficient amounts (for other reasons, not recommended!) may promote Th1 immunity (Stites and Terr, 1991). It's been noted, however, that deficiency of essential fatty acids is highly unlikely. This issue was highlighted by dietitian Jennifer Jensen, in counselling to the California Pharmacists Association 1993 Education meeting in San Diego. It would seem wise to rely on regular food (e.g., legumes) for getting essential fatty acids, or on controlled supplementation with selected oils such as evening primrose oil. It would seem especially wise to avoid major amounts of oils such as corn, soy, sunflower, and safflower oils (except for those special varieties which contain increased levels of monounsaturated fats at the expense of the polyunsaturated fats). Look for canola or olive oil, and/or MCT as major constituents of the oil/fat of liquid food supplements, or use those with no fat.]
How much zinc and copper to take?
The normal concentration of plasma zinc is in the range of 85 to 120 µg/dL, i.e., 5.5-12 mg/100mL, or 13.0-18.3 µmol/L. The normal concentration for copper is in the range of 75 to 150 µg/dL (Hunt and Groff, 1990). To maintain these levels, for healthy people RDA recommended daily intakes are 12 or 15 mg for zinc (women and men, respectively) and 1.5 to 3 mg for copper. Some seem to consider this intake of zinc low even for healthy people and 15-50 mg per day has been suggested (Weiner, 1987).
A review of zinc issues (Odeh, 1992) suggested "treatment with zinc supplements as an adjuvent therapy" for HIV disease, and noted the role of the sulfur-containing compounds such as metallothionein in zinc regulation in the body. Odeh argues that zinc supplementation may ameliorate "the deleterious effects" of -tumour necrosis factor, a cytokine which tends to increase to excessively high levels in people living with HIV.
Shambaugh (1989) has noted that 150 mg per day of zinc supplementation may be necessary to correct even marginal zinc deficiency. Chandra notes that up to 300 mg per day may be necessary in cases of zinc malabsorption such as with Crohn's disease. There are, however, concerns at these levels of supplementation on a long-term basis. In general, it is wise to make sure that there is adequate copper intake at any level of supplemental zinc intake.
A 1990 consideration of zinc toxicity (Fosmire) gave three categories of zinc supplementation levels: (i) levels "commonly consumed in self-selected supplements" (15-100 mg per day); (ii) pharmacological dosages" (100-300 mg per day); and (iii) "amounts sufficient to induce acute toxicity" (higher amounts). Fosmire notes that reports of overt toxicity resulted from zinc intakes in the order of 12,000 mg of elemental zinc over a 2 day period, and that "all symptoms disappeared with chelation therapy". At levels of 100-300 mg per day, copper deficiency resulted. Fosmire also notes that copper deficiency from such zinc supplementation may take considerable time to reverse. At levels under 100 mg per day, "some adverse consequences" may result, but again, only copper deficiency is noted as a problem. Fosmire notes that most studies of apparent zinc toxicity failed to "evaluate copper status", but where studied the role of copper deficiency was readily evident. One study with women noted zinc might also compete with iron status. Fortunately, iron status is more readily monitored.
Keusch and Thea (1993) have suggested that some people may not report their intake of supplements, and that, as a result, this may cause apparently contradicting results from different studies. This may be a very real factor. A major influence may be a distrust of opinions from some sources, even sources that are nominally professional. For example, while there is little evidence of toxicity from high levels of vitamin/mineral supplementation, it is not uncommon for some individuals to merely recognize the greater likeliness of deficiency while emphasizing out of proportion the dangers of excess intake.
The area of HIV disease has certainly not been exempt from such distortion. One example (Galvin, 1992) reviews some of the many known deficiencies that occur with HIV, and then proceeds to emphasize the dangers of toxic overdose, even omitting major literature that claims the opposite of some of her opinions.
Many of those living with HIV have done a great deal to educate themselves and may readily sense misconstrued concern that possibly derives more from dogma than knowledge of established literature. There is a very real danger that others who are less well-informed, but who are aware that their informed friends who take a balanced supplementation do so because they feel their wellness benefits from it, may embark on a supplementation program that results in imbalance. This may be critical in certain areas such as with zinc-copper-thiols.
There is a great need for informed nutritional counselling that reflects logic based on the extensive literature regarding HIV and nutrition, and immunity and nutrition in the broader sense.
For HIV+ people, educator Dr. Lark Lands gives an excellent review of nutrients for people living with HIV (HIV Treatment Strategy, Part II: Therapeutic Basics for People Living with HIV", 1994). Dr. Lands has one of the most extensive experiences in HIV disease, working closely with a number of HIV primary care physicians and patients. For zinc, the daily intake level suggested by Dr. Lands is 25-75 mg per day, in addition to what is contained in a multivitamin/mineral (which should be the basis for supplementation). Dr. Lands also emphasizes that more than 100 mg per day on a long-term basis may be toxic. This level is in line with the 75-100 mg per day suggested by registered dietitian Jennifer Jensen (on recommendation by Dr. Chandra to a meeting of the American Dietetic Association). Ms. Jensen has both extensive experience in HIV and nutrition, and advanced graduate level education in nutritional biochemistry. Both Dr. Lands and Jennifer Jensen are emphatic about the importance of an appropriate copper level of 2-4 mg per day accompanying this zinc supplementation.
The recommendations by both Dr. Lands and Ms. Jensen are in agreement with levels of zinc supplementation of 75 mg/day recommended at the 1992 Amsterdam International AIDS Conference by University of Miami researcher Dr. Baum and colleagues (abstract PoB 3675).
It is unfortunate that studies indicating zinc toxicity, or negative effects from zinc intake above that from normal food consumption, have not done detailed study of copper as a parameter. That is, for those studies where an apparent zinc toxicity was observed, the toxicity was likely due to a resulting copper deficiency rather than excessive zinc per se. In support of this, a modern textbook on human nutrition and metabolism lists only copper and thiol deficiencies as the major concerns re zinc supplementation above 40 mg per day, for apparently healthy individuals! The requirement of copper as a companion to zinc supplementation seems quite unequivoval (Prasad et al, 1978). For those living with HIV, it would seem equally important that zinc supplementation be accompanied by supplementation with N-acetyl cysteine (NAC). Since NAC supplementation seems an absolute recommendation for those living with HIV (the various presentations at the Conference on Oxidative Stress in HIV/AIDS, NIH, 1993), this caveat is probably a redundant reminder. It would seem reasonable to conclude that until there are well-controlled studies of zinc AND copper intake in the presence of adequate cysteine, reports of zinc toxicity should be viewed with extreme caution, particularly in a disease where it seems zinc deficiency is far more likely than EITHER zinc normalcy OR zinc excess.
Even though serum zinc levels are difficult to interpret, it would nonetheless seem wise that your doctor regularly monitor, e.g., every 3 months, your levels of both zinc and copper. Depending on diet, time of day, stress at the time etc. your individual readings may vary somewhat - if you are interested, you may average every last three readings to get an indication of trends which would suggest to you to either increase or decrease your level of supplementation.
Related monograph:
Zinc Supplementation in HIV/AIDS
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In this series:
HIV & Diet revisited
HIV & Dietary Supplements revisited
HIV & Nutrients revisited
HIV & Cysteine revisited
HIV & Copper and Zinc revisited
HIV & Vitamin B12
HIV & Carnitine
HIV & The Gut
HIV & Use of Tylenol - About Acetaminophen toxicity
HIV & Liquid Food Supplements
Author, Chester Myers, holds both honours B.Sc. and M.Sc. (1969) degrees in physical chemistry from Dalhousie University, and a Ph.D. (1975) from the University of Toronto (biophysical chemistry) where he investigated the mechanism of action of one of the digestive enzymes. In addition to publishing in the scientific literature and having authored several patents, he has written extensively on topics regarding health and HIV. The latter include articles in The Positive Side, Canadian AIDS News, and monographs available from the AIDS Committee of Toronto (ACT), the Community AIDS Treatment Information Exchange (CATIE), and various other organizations.
Disclaimer:
The material in this publication is for information purposes only. It does not endorse any particular treatment program nor strategy; neither is it intended as medical advice nor as a replacement for medical advice.
©This document is copyrighted by Chester Myers. All materials may be reprinted and/or distributed without prior permission. However, reprints may not be edited. |
