The immune system weakens as the body ages, making older adults more susceptible to infections. Low levels of zinc impair immunity, particularly in older adults. A research team set out to determine if it was feasible to increase serum zinc concentrations in older adults in nursing homes who were zinc-deficient. Their work appears in the American Journal of Clinical Nutrition.
"Our previous work showed that 30 percent of nursing home residents have low serum zinc levels and those with low serum zinc levels had a significantly higher incidence of pneumonia and morbidity from it. Our new finding that serum zinc levels can be improved in older adults with zinc supplementation and that this is associated with enhancement of T-cell numbers and function strongly suggests that ensuring adequate zinc consumption by older adults could have a significant impact on reducing the incidence of and morbidity from infection, which is a major public health problem in older adults," said the study's lead author, Simin Nikbin Meydani, D.V.M., Ph.D., the director of the Jean Mayer USDA Human Nutrition Research Center on Aging (HNRCA) at Tufts University in Boston, and senior scientist and director of its Nutritional Immunology Laboratory.
The small double-blind, placebo-controlled trial involved adults age 65 or older from three Boston-area nursing homes. The study participants had baseline serum levels of zinc that ranged from moderately to very zinc-deficient. Participants were given zinc supplements or a placebo for three months. A total of 25 people completed the study, with 13 receiving the placebo (a daily multi-vitamin with only 5 mg of zinc), and 12 receiving a daily multi-vitamin with 30 mg of zinc. A serum-level of 70 micrograms per deciliter was used as the cut-off standard for adequate serum zinc level and measuring improvement from supplementation. The function of the immune response was assessed by determining the immune cell profile and function.
In addition to serum zinc concentrations, the researchers found that zinc supplementation improved the function of T-cells as determined by their ability to proliferate in response to stimuli that mimicked infection. Furthermore, they saw a positive correlation between serum zinc levels and the number and function of T-cells. This effect of zinc was attributed to increasing the number of T-cells rather than enhancing the function of each T-cell. At the end of three months, researchers found that:Zinc supplementation increased serum zinc concentrations in nursing home residents with low zinc levels.
Zinc supplementation increased both the number and effectiveness of T-cells in the treatment group at a much higher rate than the control group
The increase of serum zinc rose higher in the treatment group, at a rate of 16 percent, compared to those in the control group, which rose at a rate of 0.7 percent.
For those in the treatment group who were moderately zinc-sufficient at baseline, their serum zinc levels exceeded the cut-off standard.
Participants in the treatment group whose serum levels were measured as substantially zinc-deficient at baseline did not experience an increase to normal levels during the trial.
"Having a positive response to zinc supplementation may take some time in people who have been highly zinc deficient. We need to better understand how much supplementation is needed for certain people, and for how long a period, so that more refined recommendations can be made," added first author Junaidah B. Barnett, M.C.H. (N), Ph.D., scientist in the Nutritional Immunology Laboratory at the HNRCA.
"It is worth noting that zinc deficiency is not just a problem in nursing home residents; it also exists in non-institutionalized older adults," Meydani continued. "On average, zinc supplementation measurably improved serum zinc levels in these older adults, with most participants achieving serum zinc levels considered to be adequate."
Zinc is found in a wide variety of foods, including oysters, pork, red meat, poultry, seafood, and fortified breakfast cereals. Zinc is also found in beans, nuts, whole grains, cucumber peel, and dairy products and is common in multi-vitamins. The Office of Dietary Supplements of the National Institutes of Health notes that zinc deficiency is rare in North America, but that some groups of people are more likely to have trouble getting enough zinc, including those with digestive disorders and vegetarians. Too much zinc (the upper limit for adults is 40 mg/day) can be harmful. Some researchers suspect, however, the older adults do not absorb or use zinc as efficiently as others. In addition, while serum zinc levels are a commonly used measure to evaluate zinc deficiency, they might not accurately reflect cellular zinc status. Some cells might exhibit low zinc levels, which impacts their function, even when serum zinc levels are normal
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Effect of zinc supplementation on serum zinc concentration and T cell proliferation in nursing home elderly: a randomized, double-blind, placebo-controlled trial. Junaidah B Barnett, Maria C Dao, Davidson H Hamer, Ruth Kandel, Gary Brandeis, Dayong Wu, Gerard E Dallal, Paul F Jacques, Robert Schreiber, Eunhee Kong, and Simin N Meydani. American Journal of Clinical Nutrition. DOI.10.3945/ajcn.115.115188 . Published online January 27, 2016.
Meydani is also a professor at the Friedman School of Nutrition Science and Policy at Tufts and a member of the immunology program faculty at the Sackler School of Graduate Biomedical Sciences at Tufts.
This study is based upon work supported by the U.S. Department of Agriculture, Agricultural Research Service.
Source: Tufts University, Health Sciences Campus
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Disbalance of zinc (Zn2+) and copper (Cu2+) ions in the central nervous system is involved in the pathogenesis of numerous neurodegenerative disorders such as multisystem atrophy, amyotrophic lateral sclerosis, Creutzfeldt-Jakob disease, Wilson-Konovalov disease, Alzheimer's disease, and Parkinson's disease. Among these, Alzheimer's disease (AD) and Parkinson's disease (PD) are the most frequent age-related neurodegenerative pathologies with disorders in Zn2+ and Cu2+ homeostasis playing a pivotal role in the mechanisms of pathogenesis. In this review we generalized and systematized current literature data concerning this problem. The interactions of Zn2+ and Cu2+ with amyloid precursor protein (APP), β-amyloid (Abeta), tau-protein, metallothioneins, and GSK3β are considered, as well as the role of these interactions in the generation of free radicals in AD and PD. Analysis of the literature suggests that the main factors of AD and PD pathogenesis (oxidative stress, structural disorders and aggregation of proteins, mitochondrial dysfunction, energy deficiency) that initiate a cascade of events resulting finally in the dysfunction of neuronal networks are mediated by the disbalance of Zn2+ and Cu2+.
Ann Pharmacother. 2014 Nov;48(11):1515-20. doi: 10.1177/1060028014545356. Epub 2014 Jul 28.
Ascorbate- and zinc-responsive parkinsonism.
Quiroga MJ1, Carroll DW2, Brown TM3.
Author information
Abstract
OBJECTIVE:
To report a case of Parkinsonism rapidly responsive to intravenous replacement of vitamin C and zinc.
CASE SUMMARY:
A 66-year-old man with Parkinsonism, pleural effusion, and bipolar disorder was found to have low serum vitamin C and zinc levels. Intravenous replacement of these micronutrients led to resolution of the movement disorder in less than 24 hours.
DISCUSSION:
Parkinsonism has been associated with vitamin C deficiency, and recent cases of scurvy complicated by Parkinsonism have responded well to intravenous replacement of vitamin C. In this case, deficiency of zinc may have contributed to the development of a movement disorder. The likely pathophysiology of, and treatment recommendations for, Parkinsonism linked to deficiencies of vitamin C and zinc are reviewed.
CONCLUSIONS:
Whereas vitamin C has a strong link with Parkinsonism, the potential role of zinc has only been suspected. This case report highlights some of the potential links between zinc deficiency and Parkinsonism.
The green spots above are clumps of protein inside yeast cells that are deficient in both zinc and a protein that prevents clumping. Research by Colin MacDiarmid and David Eide is exploring how a shortage of zinc can contribute to diseases.
Photo: Colin MacDiarmid and David Eide/Journal of Biological Chemistry
Scientists at UW–Madison have made a discovery that, if replicated in humans, suggests a shortage of zinc may contribute to diseases like Alzheimer’s and Parkinson’s, which have been linked to defective proteins clumping together in the brain.
With proteins, shape is everything. The correct shape allows some proteins to ferry atoms or molecules about a cell, others to provide essential cellular scaffolding or identify invading bacteria for attack. When proteins lose their shape due to high temperature or chemical damage, they stop working and can clump together — a hallmark of Parkinson’s and Alzheimer’s.
The UW researchers have discovered another stress that decreases protein stability and causes clumping: a shortage of zinc, an essential metal nutrient.
Zinc ions play a key role in creating and holding proteins in the correct shape. In a study just published in the online Journal of Biological Chemistry, Colin MacDiarmid and David Eide show that the gene Tsa1 creates “protein chaperones” that prevent clumping of proteins in cells with a zinc shortage. By holding proteins in solution, Tsa1 prevents damage that can otherwise lead to cell death.
“Zinc is needed by all cells, all organisms, it’s not just for steel roofs, nails and trashcans.”
David Eide
For simplicity, the researchers studied the system in yeast —
For simplicity, the researchers studied the system in yeast — a single-celled fungus. Yeast can adapt to both shortages and excesses of zinc, says MacDiarmid, an associate scientist. “Zinc is an essential nutrient but if there’s too much, it’s toxic. The issue for the cell is to find enough zinc to grow and support all its functions, while at the same time not accumulating so much that it kills the cell.”
Cells that are low in zinc also produce proteins that counter the resulting stress, including one called Tsa1.
The researchers already knew that Tsa1 could reduce the level of harmful oxidants in cells that are short of zinc. Tsa1, MacDiarmid says, “is really a two-part protein. It can get rid of dangerous reactive oxygen species that damage proteins, but it also has this totally distinct chaperone function that protects proteins from aggregating. We found that the chaperone function was the more important of the two.”
“In yeast, if a cell is deficient in zinc, the proteins can mis-fold, and Tsa1 is needed to keep the proteins intact so they can function,” says Eide, a professor of nutritional science. “If you don’t have zinc, and you don’t have Tsa1, the proteins will glom together into big aggregations that are either toxic by themselves, or toxic because the proteins are not doing what they are supposed to do. Either way, you end up killing the cell.”
While the medical implications remain to be explored, there are clear similarities between yeast and human cells. “Zinc is needed by all cells, all organisms, it’s not just for steel roofs, nails and trashcans,” Eide says. “The global extent of zinc deficiency is debated, but diets that are high in whole
While the medical implications remain to be explored, there are clear similarities between yeast and human cells. “Zinc is needed by all cells, all organisms, it’s not just for steel roofs, nails and trashcans,” Eide says. “The global extent of zinc deficiency is debated, but diets that are high in whole grains and low in meat could lead to deficiency.”
If low zinc supply has the same effect on human cells as on yeast, zinc deficiency might contribute to human diseases that are associated with a build-up of “junked” proteins, such as Parkinson’s and Alzheimer’s. Eide says a similar protective system to Tsa1 also exists in animals, and the research group plans to move ahead by studying that system in human cell culture.
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