Zinc is one of the franchises of Björklund Pharma. The zinc franchise focuses on zinc deficiency, a globally widespread ailment. Worldwide is the overall frequency for zinc deficiency thought to be higher than 20% (Wuehler et al. 2005). Zinc deficiency may affect more than 2 billion people in the developing world (Wuehler et al. 2005). It has further been estimated that only 42.5% of U.S. elderly (≥71 years) have adequate zinc intake (Briefel et al. 2000). A few extra milligrams of zinc every day can make a huge difference. Zinc-containing supplements are a quick and easy, effective, and inexpensive remedy.
Zinc is an essential trace element, an important antioxidant (Russo and deVito 2011) in spite of not being a free radical scavenger, and a metalloenzyme required for the catalytic activity of at least 300 enzymes (Prasad 2012). It plays a role in immune system functioning (Prasad 1995), protein synthesis (Prasad 1995), wound healing (Heyneman 1996), DNA synthesis (IOM/FNB 2001), and cell division (Prasad 1995). Zinc is required for proper sense of taste and smell (Prasad et al. 1997). Zinc is part of a very large number of transcription factors, far more than the number of zinc-containing enzymes that are known (Oteiza and Mackenzie 2005, Prasad 2012).
Respiratory tract infections, including pneumonia, are the most common cause of death in children under the age of five (Srinivasan et al. 2012). In a study looking at children given standard antibiotic therapy, research published in BioMed Central’s open access journal BMC Medicine shows how zinc supplements drastically improved children’s chances of surviving the infection. The increase in survival due to zinc (on top of antibiotics) was even greater for HIV infected children (Srinivasan et al. 2012).
Zinc supports normal growth and development during pregnancy, childhood, and adolescence (Simmer and Thompson 1985, Fabris and Mocchegiani 1995). Prolonged zinc deficiency may therefore cause growth impairment (Sandstead et al. 1967, Prasad 2012). A child who is born with decreased zinc stores will remain at risk for zinc deficiency throughout childhood (Faber et al. 2009).
While many elderly have low intakes of zinc, it is also possible that the zinc requirement increases with age because of the age-related accumulation of mutations in mitochondrial DNA, leading to enhancement of mitochondrial production of reactive oxygen species (ROS), which in turn enhances the synthesis of zinc-binding apometallothionein in various cell types and organs (Bjørklund 2013).
Zinc is naturally present in some foods, is added to others, and is available as a dietary supplement (Lifschitz 2012). The recommended intake for zinc is 11 mg/day for men and 8 mg/day for women (Trumbo et al. 2001). Lower Zn intake is recommended for infants (2–3 mg/day) and children (5–9 mg/day) because of their lower average body weights (Trumbo et al. 2001).
Zinc deficiency occurs not only as a result of nutritional factors, but also in various disease states, including malabsorption syndromes, alcoholism and cirrhosis of the liver, acrodermatitis enteropathica, Crohn’s disease, and immune dysregulation (Prasad 1983, Faber et al. 2009, Russo and deVito 2011). An important clinical point to note is that, because zinc is primarily an intracellular nutrient, serum zinc levels can be normal in states of mild deficiency (Bales et al. 1994, Salgueiro et al. 2001).
The most common cause of zinc deficiency is dietary factors that reduce the availability of zinc, but inherited metabolic disturbances and intestinal diseases can also result in reduced zinc. Both these types of zinc deficiency can produce similar symptoms, such as dermatitis, diarrhea, alopecia, and loss of appetite (Hambidge et al. 1986, Russo and deVito 2011). These are symptoms of severe zinc deficiency. More moderate zinc deficiency, which leads to impaired immune function and increased mortality due to infections, as well as brain damage in the fetus when it affects pregnant women, are more common (Hambidge et al. 1986, Fischer Walker and Black 2004). Individuals with zinc deficiency often have suppressed immune function and frequent infections (Shankar and Prasad 1998, Lakshmi Priya and Geetha 2011) with the degree of immunosuppression depending on the severity of zinc deficiency.
Zinc supplements are commonly sold over the counter to treat several different brain disorders, including depression. It isn’t clear whether these supplements modify zinc content in the brain, or modify the efficiency of communication between these nerve cells (Pan et al. 2011). More than 50 years ago scientists discovered that high concentrations of zinc are contained in a specialized compartment of nerve cells, called vesicles, that package the transmitters which enable nerve cells to communicate. The highest concentrations of brain zinc were found among the neurons of the hippocampus, the center of learning and memory (Pan et al. 2011). Zinc’s presence in these vesicles suggested that zinc played some role in communication between nerve cells. The nerve cells in which the high concentrations of zinc reside are critical for a particular type of memory formation. Excessive enhancement of communication by the zinc-containing nerve cells occurs in epileptic animals and may worsen the severity of the epilepsy (Pan et al. 2011).
Geir Bjørklund and collaborators have studied the role of zinc and copper in autism spectrum disorders. The evidence from their research suggest that providing zinc to autistic children may be an important component of a treatment protocol, especially in children with zinc deficiency (Bjørklund 2013, Li et al. 2014, Macedoni-Lukšič et al. in press). Changes in the intestinal flora and function are common in autistic patients (de Theije et al. 2011, Finegold et al. 2012, MacFabe 2012, Midtvedt 2012); it is therefore conceivable that malabsorption due to pathological changes in the intestinal mucosa may play an important role as one of the causes of zinc deficiency in autism. Low intracellular zinc has been associated with DNA damage, which might be due to a combination of oxidative stress, impairment of antioxidant defences, and impairment of DNA repair (Russo and deVito 2011).
Since only exposure to high doses of zinc has toxic effects, acute zinc intoxication is rare (Plum et al. 2010). Copper and zinc are metabolic antagonists (Underwood 1977). Copper absorption is depressed when zinc is given in high excess of copper, or when zinc therapy is given for a long time without copper supplementation. Many of the toxic effects of zinc are in fact due to copper deficiency (Plum et al. 2010). On the other hand, a low level of zinc exacerbates copper toxicity (Bjørklund 2013).
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