Effects of Copper Deficiency on the Immune System

Author(s):  
Joseph R. Prohaska ◽  
Omelan A. Lukasewycz
The Lancet ◽  
1978 ◽  
Vol 312 (8091) ◽  
pp. 686 ◽  
Author(s):  
J.L Sullivan ◽  
H.D Ochs

Author(s):  
Sir Peter Gluckman ◽  
Mark Hanson ◽  
Chong Yap Seng ◽  
Anne Bardsley

Copper is an essential trace mineral with a central role in oxidation#amp;#x2013;reduction reactions. It is involved in connective tissue formation and disulphide bonding of keratin. Clinical deficiency for copper is uncommon but has been increasing in prevalence, resulting from malnutrition or lack of trace metals in the food source, even in Western diets. Secondary copper deficiency can be induced by excess intake of zinc or iron and is sometimes seen in individuals taking supplements of these minerals. Copper requirements are increased in pregnancy, and suboptimal supply may have adverse effects on developing tissues and organ systems including the lung, skin, bones, and immune system. Despite the increased need, supplementation is generally not recommended in pregnancy. An increased intake of foods high in copper, such as nuts, and a proportionate lowering of low-copper foods (e.g. fats/oils) may be advisable in women with potentially marginal copper status.


Author(s):  
U. Bielenberg

Copper deficiency can cause cardiovascular lesions in experimental animals. Previous experiments have shown that the biochemical and itDrphologic lesions induced by deprivation of dietary copper can be suppressed by feeding diets containing starch or can be magnified by a high sucrose diet. In a recent study it was found that the more severe signs of copper deficiency in rats fed sucrose as compared to starch were due to the fructose moiety of sucrose. Although fructose as compared to starch markedly enhanced the symptoms of copper deficiency, the possibility that an effect of dietary carbohydrates due to the nature of the simple carbohydrate (fructose vs glucose) cannot be excluded. The present study was designed to determine if the severity of copper deficiency in rats fed sucrose as compared to starch is due to the glucose as well as the fructose moiety of sucrose. This portion of the study assessed the morphologic changes in aortas of seventy weanling male rats who were fed, for 9 weeks, copper deficient or copper supplemented diets containing either 62% starch, fructose or glucose. The starch-fed copper supplemented group served as the most normal controls. Rats were sacrificed after 9 weeks of dietary treatments. Copper deficiency was verified by reduced serum ceruloplasmin activity and serum and hepatic copper concentration.


2006 ◽  
Vol 12 ◽  
pp. 96-97
Author(s):  
Mihaela Cosma ◽  
Daniel L. Hurley

2014 ◽  
Vol 222 (3) ◽  
pp. 148-153 ◽  
Author(s):  
Sabine Vits ◽  
Manfred Schedlowski

Associative learning processes are one of the major neuropsychological mechanisms steering the placebo response in different physiological systems and end organ functions. Learned placebo effects on immune functions are based on the bidirectional communication between the central nervous system (CNS) and the peripheral immune system. Based on this “hardware,” experimental evidence in animals and humans showed that humoral and cellular immune functions can be affected by behavioral conditioning processes. We will first highlight and summarize data documenting the variety of experimental approaches conditioning protocols employed, affecting different immunological functions by associative learning. Taking a well-established paradigm employing a conditioned taste aversion model in rats with the immunosuppressive drug cyclosporine A (CsA) as an unconditioned stimulus (US) as an example, we will then summarize the efferent and afferent communication pathways as well as central processes activated during a learned immunosuppression. In addition, the potential clinical relevance of learned placebo effects on the outcome of immune-related diseases has been demonstrated in a number of different clinical conditions in rodents. More importantly, the learned immunosuppression is not restricted to experimental animals but can be also induced in humans. These data so far show that (i) behavioral conditioned immunosuppression is not limited to a single event but can be reproduced over time, (ii) immunosuppression cannot be induced by mere expectation, (iii) psychological and biological variables can be identified as predictors for this learned immunosuppression. Together with experimental approaches employing a placebo-controlled dose reduction these data provide a basis for new therapeutic approaches to the treatment of diseases where a suppression of immune functions is required via modulation of nervous system-immune system communication by learned placebo effects.


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