My experience with Zinc

When my son was diagnosed with an immune deficiency (CVID), the peadiatrician explained to me the importance of zinc to the immune system. Once he was finished with his immune treatments the peadiatrican made me vow to keep him on Zinc supplements for the rest of his childhood. 

He is still on Zinc supplements and I can’t help but believe that it has played a great role in his immunity over the last few years. I was surprised to find out that not everyone is aware of the important role Zinc has on our bodies until recently. For me it’s always been just accepted. 

A good friend of mine (an author I might add), did some extensive research on this subject to educate her family about Zinc, especially during these trying times. So if you have symptoms you can’t seem to find a cause for, read the piece below and perhaps Zinc is the thing that has been missing in your life.

P.S. All references are quoted at the bottom of her research. If you want to support her writing you’re welcome to visit her Amazon Profile here. 

Note:

Zinc must be taken with food to prevent gastric disturbance. All of the studies quoted below suggest taking at least 50mg of zinc per day to see the results of using zinc.

None of these dosages caused a deficiency in copper (zinc supplementation has been said to cause a copper deficiency and each study made point to say it did not do this in the study)

The best option is a) zinc lozenges and b) zinc gluconate (water soluble)

Zinc is best absorbed when taken with amino acids.

Why we need zinc

Zinc is an essential nutrient and a critical element in the structure and function of many protein complexes. It is the second most abundant transition metal, after iron, in the human organism. The human body comprises about 2 g of this element, with more than 99% located within the cells. Zinc deficiency is an emerging global problem, as nearly 2 billion people are at risk of such syndromes. (4)

Conditioned deficiency of zinc has been observed in patients with malabsorption syndrome, liver disease, chronic renal disease, sickle cell disease, and other chronic illnesses. Major clinical problems resulting from zinc deficiency in humans include growth retardation; cell-mediated immune dysfunction, and cognitive impairment. Zinc has been very successfully used as a therapeutic modality for the management of acute diarrhoea in children, Wilson’s disease, the common cold and for the prevention of blindness in patients with age-related dry type of macular degeneration and is very effective in decreasing the incidence of infection in the elderly. Zinc not only modulates cell-mediated immunity but is also an antioxidant and anti-inflammatory agent. (6)

Zinc is linked to growth (and early onset of sexual function) and those who receive ample zinc grow tall, and those that do not often fall into the ‘malnourished’ and dwarf category (6). Zinc deficiency also causes: Wilson’s disease, diarrhoea, dermatologic, alopecia, neuropsychiatric, weight loss, intercurrent infections, Gastrointestinal disturbances are severe and include diarrhoea, malabsorption, steatorrhea, lactose intolerance, congenital malformation of foetuses and infants, bullous pustular dermatitis of the extremities and oral, anal, and genital areas around the orifices, paronychia, and alopecia. Ophthalmic signs include blepharitis, conjunctivitis, photophobia, and corneal opacities. Neuropsychiatric signs include irritability, emotional instability, tremors, and also occasional cerebellar ataxia, male hypogonadism, emotional disorders, neurosensory disorders, and problems with healing of ulcers, growth retardation, rough skin, poor appetite, mental lethargy, delayed wound healing. Severe deficiency of zinc, if untreated, may become fatal.

The role of zinc and what looks like eczema / dandruff

(reference 6)

Zinc is also linked to a skin condition that looks like eczema but is acrodermatitis enteropathica (dandruff, acne, nappy rash). This is linked to a severe deficiency in zinc and are reversed using zinc supplementation.

The treatment of acrodermatitis enteropathica with zinc is furthermore a great success in the prevention of blindness, as zinc is not dangerous to the retina and the optic nerve.(7)

This original observation was quickly confirmed in other patients with acrodermatitis enteropathica (AE) throughout the world. The underlying pathogenesis of the zinc deficiency in these patients is due to malabsorption of zinc caused by a mutation in ZIP4, an intestinal zinc transporter. AE is a lethal, autosomal, recessive trait that usually occurs in infants of Italian, Armenian, or Iranian lineage. The disease develops in the early months of life soon after weaning from breastfeeding. The dermatologic manifestations of severe zinc deficiency in patients with AE include bullous pustular dermatitis of the extremities and oral, anal, and genital areas around the orifices, paronychia, and alopecia. Ophthalmic signs include blepharitis, conjunctivitis, photophobia, and corneal opacities. Neuropsychiatric signs include irritability, emotional instability, tremors, and occasional cerebellar ataxia. Weight loss, growth retardation, and male hypogonadism are also prominent clinical features. Congenital malformation of fetuses and infants born of pregnant women with AE has been commonly observed.

AE patients have an increased susceptibility to infections. Thymic hypoplasia, absence of germinal centers in lymph nodes, and plasmacytosis in the spleen are seen consistently. All T cell–mediated functional abnormalities are completely corrected with zinc supplementation. Abnormal chemotoxis is also corrected with zinc therapy in AE patients. The clinical course is downhill with failure to thrive and complicated by intercurrent bacterial, fungal, viral, and other opportunistic infections. Gastrointestinal disturbances are severe and include diarrhea, malabsorption, steatorrhea, and lactose intolerance. The disease, if unrecognized and untreated, is fatal.

Zinc supplementation, however, results in complete recovery.

The manifestations of a moderate deficiency of zinc include growth retardation, male hypogonadism in adolescents, rough skin, poor appetite, mental lethargy, delayed wound healing, cell-mediated immune dysfunctions, and abnormal neurosensory changes. These manifestations have been reported in subjects with nutritional deficiency of zinc and many subjects with conditioned deficiency of zinc. It is now apparent that a nutritional deficiency of zinc in humans is fairly prevalent throughout the world, particularly in areas where cereal proteins are primary in local diets.

Zinc is a second messenger for immune cells, and its intracellular status is directly altered by an extracellular stimulus and then intracellular zinc participates in signaling events. Zinc is required for all immunity of the body, the skin, and the eyes. Lack of zinc causes dry eyes which can lead to Macular Degeneration and lack of vision acuity (also causing conjunctivitis). Where there is a zinc deficiency there is inflammation which can lead to many illnesses, pain discomfort, and health issues even causing cancer, liver disease, hepatic coma, sickle cell disease, acute diarrhea in children, and even night blindness, and may indeed be related to the secondary zinc-deficient state induced by hyperzincuria (hyperzincuria is insulin dependent diabetes). (6)

Zinc presents chemical compatibility with several ligands present in histidine, aspartate, glutamate, glutamate, and cysteine residues in many proteins. Unlike other transition metals, zinc lacks and cysteine residues in many proteins. Unlike other transition metals, zinc lacks biological redox biological redox activity and facilitates bound water deprotonation by lowering water pKa, which activity and facilitates bound water deprotonation by lowering water pKa, which makes it a good makes it a good enzymatic cofactor [30]. Therefore, the chemical properties of zinc may be important enzymatic cofactor. Therefore, the chemical properties of zinc may be important for its cellular for its cellular functions. Zinc has been identified as a cofactor of hundreds of enzymes belonging to functions. Zinc has been identified as a cofactor of hundreds of enzymes belonging to all enzymatic all enzymatic classes. Moreover, enzyme-bound zinc plays a catalytic role and is directly classes. Moreover, enzyme-bound zinc plays a catalytic role and is directly involved in catalysis involved in catalysis and is found as a structural component in thousands of human proteins, and is found as a structural component in thousands of human proteins, constituting about 10% of the constituting about 10% of the human proteome. (4)

Zinc is also reported important in the pathophysiology of several groups of diseases, including neurodegenerative diseases and cancer. The majority of zinc present in the human body is in skeletal muscle and bone mass—approximately 60% and 30%, respectively. The eye has a relatively high content of zinc among other organs and tissues with the peak concentration in the RPE about 300 μg/g dry tissue. In the retinal tissue, zinc is mainly stored in intracellular compartments in ganglion cells, the horizontal and amsacrine cells as well as retinal Müller cells [33]. In addition, zinc can be present in photoreceptor outer segments (POSs), that are degraded by RPE cells. As endogenous zinc is co-released with glutamate from synaptic terminals of photoreceptors, it can possibly protect the retina from glutamate toxicity. (4)

Zinc deficiency is often caused by malnutrition, especially in the elderly (reviewed in [36]). Therefore, a low zinc diet in the elderly might contribute to AMD pathogenesis. Some studies suggest that the content of zinc in human AMD RPE/choroid can be lowered by 24% [37,38]. Therefore, diet supplementation with zinc may be an efficient and inexpensive strategy for AMD prevention. In the first prospective, randomized, double-masked, placebo-controlled oral intervention study in 151 subjects with drusen or macular degeneration, Newsome et al. showed that the zinc-treated group had significantly less visual loss than the placebo group after a follow-up of 12 to 24 months. (4) the Rotterdam Eye Study and the Blue Mountain Eye study confirmed beneficial effects of higher intake of dietary zinc on incident AMD (age related macular degeneration). Two features of zinc functioning in the eye may be related to AMD pathogenesis. First, zinc is present in higher concentrations in sub-retinal epithelial deposits (drusen), an established early hallmark of AMD. Second, RPE cells in the macula may contain less zinc than their counterparts in the peripheral parts of the retina, and the level of zinc in the macula may be affected by aging. (4)

Zinc and Dementia and AD (Alzheimer’s Dementia)

Zinc is an essential trace element, whose importance to the function of the central nervous system (CNS) is increasingly being appreciated. Alterations in zinc dyshomeostasis has been suggested as a key factor in the development of several neuropsychiatric disorders. In the CNS, zinc occurs in two forms: the first being tightly bound to proteins and, secondly, the free, cytoplasmic, or extracellular form found in presynaptic vesicles. (1)

a growing body of evidence suggests that a deficiency, rather than an excess, of zinc leads to an increased risk for the development of neurological disorders. Indeed, zinc deficiency has been shown to affect neurogenesis and increase neuronal apoptosis, which can lead to learning and memory deficits. Altered zinc homeostasis is also suggested as a risk factor for depression, Alzheimer’s disease (AD), aging, and other neurodegenerative disorders. (1)

We are in the midst of an epidemic of Alzheimer’s disease (AD), particularly in developed countries. We have previously hypothesized that ingestion of inorganic copper from drinking water and supplement pills and a high fat diet are main causal factors in AD. These two factors interact synergistically because copper oxidizes fats to molecules that are toxic, particularly to neurons. The epidemic correlates temporally with the use of copper plumbing in developed countries, and there is a great amount of additional data that draws the net tighter around a causative role for inorganic copper. (5)

Inorganic copper must not be confused with organic copper, the copper in food that is safely bound to protein. Inorganic copper is a simple salt of copper, not bound to anything, and is in part handled differently by the intestinal absorption mechanism, such that some of it contributes immediately to the serum free copper pool. This pool has been shown to be expanded in AD to correlate negatively with cognition, and to predict deterioration in cognition. (5)

While we believe ingestion of inorganic copper and a high fat diet are major causal factors, there are a number of other known risk factors in AD. Iron and copper are toxic through the same mechanism, generation of oxidant damage. In addition, the group has shown that possession of certain variants of the ATP7B gene is a risk factor for AD. Since ATP7B gene products control copper levels in the body, this risk factor also fits with the copper hypothesis. A risk factor for AD that we have recently observed has largely been ignored by the scientific community concerned with AD. This is zinc deficiency in AD patients. We have found that AD patients are zinc deficient. Zinc has many protective roles in neurons, and zinc deficiency may play a causal role in AD. We have found and will report here that zinc therapy appears to prevent at least some cognition decline. Our findings on zinc therapy may also lend further support to the copper hypothesis, because we have found that zinc therapy, in addition to restoring normal zinc levels, reduces serum free copper levels in AD. (5)

Available data indicates that the hippocampus seems to be the most responsive both to the deficiency as well as an overdose of zinc. Because the hippocampus is the region of the brain which plays a critical role in memory, learning and neurogenesis, the impact of zinc deficiency or zinc supplementation on these processes will be critical. Indeed, it was found that a zinc deficient diet, decreases the number of progenitor cells and immature neurons in the dentate gyrus (DG) and that reversal to a normal diet containing zinc restored a number of these cells. (1)

Zinc also appears to have an effect of oxidative stress. It was found that both high and extremely low concentrations of zinc are associated with increased oxidative and nitrosative stress, however, intermediate concentrations were found to be neuroprotective. This demonstrates once again the importance of zinc homeostasis in normal brain function. (1)

AD is a chronic neurodegenerative disorder and the most common cause of dementia. It is estimated that AD represents 60–80% of all dementia cases (Daviglus et al., 2010). The clinical features of AD vary from stable performance and cognitive health with only a gradual decline in the short-term memory to a serious state of cognitive impairment and into different forms of dementia (deterioration of memory, learning, orientation). (1)

Serum, cerebrospinal fluid (CSF) and brain zinc levels have been investigated in patients diagnosed with AD. Studies investigating zinc content in brain tissue suggests that an alteration in the zinc level seems to be fraction/region specific. Some alterations in the brain zinc levels were found when different brain regions were analyzed separately. Indeed, decreased zinc levels have been found in the neocortex, medial temporal gyrus, thalamus, and hippocampus, whilst increased levels were found in the amygdala, hippocampus, cerebellum, olfactory areas and superior temporal gyrus. The above-mentioned data strongly support the hypothesis that a deregulated zinc homeostasis is involved in the pathophysiology of AD. (1)

Post-mortem studies using different imaging techniques for zinc analysis have demonstrated significant increases in zinc levels in neuropil and plaques present in the brain of AD patients when compared to normal age-matched controls. On the other hand, lack of synaptic zinc prevents Aβ (APP cleaving enzyme) deposition. It was found that APP synthesis is regulated by zinc-containing transcription factors. Furthermore, the paper of Donnelly et al. demonstrated the beneficial effect of the selective intracellular delivery of zinc using bis complexes in the reduction of the extracellular levels of Aβ and suggested the role of these metal-loaded compounds as potential therapeutic agents for AD. In turn Greenough et al. reported that presenilin, which mediates the proteolytic cleavage of the β-amyloid precursor protein to release β-amyloid, is important for cellular cooper/zinc turnover and has the potential to indirectly impact on amyloid aggregation through zinc ion clearance. All of these data further emphasize the integral role of zinc in the mechanism of AD and support the hypothesis that restoring zinc homeostasis might be beneficial in the treatment of AD, although it also indicated the complex interactions between AD and zinc. (1)

There are several proteins/pathways that interact with zinc and that are also relevant to AD. One of these is MT. As noted earlier, MTs are zinc- binding proteins involved in the regulation of the transport, storage and transfer of zinc to various enzymes and transcription factors. Another important group of proteins involved in the homeostasis of zinc and the pathogenesis of AD are zinc transporter (ZnTs) proteins. Zhang showed that six ZnTs are extensively present in the Aβ, being therefore positive plaques in the cortex of human AD brains. Recent studies showed alterations in levels of ZnTs proteins in the brain of subjects diagnosed with the preclinical stage of AD (PCAD), mild cognitive impairment (MCI), early (EAD), and the late (LAD) stage of AD when compared to the control subjects. (1)

Recent progress in studies involving age related processes provide evidence that changes occurring in the brain during aging are related to zinc homeostasis and that zinc deficiency is a common cause of morbidity among the elderly. In aging, zinc deficiency is usually the result of an inadequate zinc dietary intake. It has been reported that only 40% of elderly people have a sufficient intake of zinc. Studies comparing low dietary zinc indicated that zinc is an important nutritional factor for a proper inflammatory/immune response. Accordingly, zinc has anti-inflammatory properties and a low zinc status is associated with increased susceptibility to infection plus intracellular zinc has been found to play a key role in signalling in immune cells. Interestingly, dietary supplementation reduced aged-associated inflammation. The other mechanism linking age, zinc and inflammation is associated with MTs. It was found that ageing is associated with a higher MT expression and consequently, low availability of intracellular zinc for normal immune responses. On the other hand, the supplementation of zinc in aging improves immune function and leads to decreased mortality from infections. (1)

First, since zinc deficiency is prevalent in patients with psychiatric and neurodegenerative disorders, the appropriate preventive measures should be considered especially in the elderly. Conversely, even if the beneficial effects of zinc supplementation were reported either in treatment or in the prevention of depressive or aging symptoms, zinc supplement users should be overly cautious and avoid overdosing. (do not exceed 100mg per kilogram of body weight). Recently, the zinc-homeostasis regulating proteins such as transporters and MTs have been gaining more prominence in related literature indicating they may be very important players in the pathophysiology of neurodegenerative disorders. (1)

The neurons of many parts of the brain have high zinc levels, and it is clear that zinc plays many critical roles in neurons. In some neurons, high concentrations of zinc are secreted along with glutamate into the synapse. Glutamate initiates ring, and zinc quenches, or shuts down, the ring. With inadequate zinc, glutamate-induced ring persists and can damage the neuron. Excess glutamatergic excitotoxicity is believed to be a common occurrence in many neurodegenerative disorders, including AD. (5)

Another possible mechanism by which low availability of zinc in the brain can have harmful effects is through failure of adequate inhibition of calcineurin. Calcineurin activity is known to be high in AD brain, and this can have many negative downstream effects. Calcineurin is normally inhibited by zinc but is stimulated by beta amyloid. To add to the problem created by systemic zinc deficiency, there is another mechanism in the AD brain that depletes neurons of much-needed zinc. The beta amyloid plaques, that build up in the AD brain, are avid binders of zinc. Thus, it seems very likely that the neurons of the AD brain are seriously lacking in available zinc and probably many are injured and die as a result. (5)

At Adeona Pharmaceuticals, we developed a new zinc formulation with a zinc-binding agent that allowed the slow release of zinc. e kinetics of this formulation are such that in dissolution studies, peak zinc release is at 6–8 hours, and it is still releasing zinc at 24 hours. us, this pill caused no gastric intolerance, and because of the slow release, could be given one time/day, with around-the-clock elevation of serum zinc. We used this new zinc formulation in the controlled AD trial reported here. (5)

Zinc and Depression

Clinical studies demonstrate significantly lower serum zinc levels in patients suffering from major depression or unipolar depression than that in non-depressed patients. In some patients, a negative correlation between the serum zinc level and severity of depression was found. A lower serum zinc level was also found to accompany antepartum and postpartum depression. In this study the level of zinc was also negatively correlated with the severity of depressive symptoms. Low serum zinc levels have also been noted in depressed patients with end-stage renal disease undergoing haemodialysis. Moreover, treatment-resistant depressed patients have been shown to exhibit much lower serum zinc concentrations than their non-treatment resistant depressed counterparts.

Presented above data strongly indicated the importance of zinc deficiency in human depression and indicated the benefit of zinc supplementation in both the efficacy and the speed of the therapeutic response to antidepressants treatment. Thus, the understanding of the mechanisms involved in the antidepressant activity of zinc might contribute to the development of a new therapeutic strategy for the treatment of depression or depression-related diseases.  (1)

Zinc and Macular Degeneration

Age-related macular degeneration (AMD) is the leading cause of blindness in the Western world. AMD is a multifactorial disorder but complement-mediated inflammation at the level of the retina plays a pivotal role. Oral zinc supplementation can reduce the progression of AMD. To evaluate the effect of receiving zinc supplements on systemic complement catabolism, AMD patients received oral zinc sulphate.  Serum zinc concentration increased significantly during the supplementation period and returned to baseline levels two months after the zinc supplements were discontinued. (2)

Retina is exposed to high levels of oxidative stress from light exposure and metabolic processes. We tested in vitro whether zinc could also protect the RPE from an oxidative stress related damage from the complement system. The test results show that the amount of MAC deposited on RPE cells exposed to oxidative stress can be reduced in a dose dependent manner by zinc sulphate. Our findings suggest that increased complement catabolism in AMD patients can be reduced by the daily oral administration of 50 mg zinc sulphate. Continuous zinc supplementation may therefore be necessary to inhibit complement activity over longer periods of time. (2)

We then linked the degree of serum complement activation to the clinical stages of AMD and found that the level of serum complement activation is correlated with patients having large drusen and/or drusenoid RPE detachment. It has been demonstrated that 42% of patients with drusenoid RPE detachment progress to end-stage AMD and develop profound and irreversible visual loss within five years. The AREDS1 study showed that this group in particular benefits from zinc plus antioxidant supplementation. Our results suggest that this may be related to increased activation of the alternative complement pathway in this group, which would support the notion that patients with large drusen and/or drusenoid RPE detachment should receive supplements.  C5a returned to its baseline value within 2 months after the supplementation period also suggesting a reversible effect of zinc on C5a. (2)

Important to note is that zinc concentrations were in physiological levels and therefore have biomedical significance. We can conclude that zinc inhibits systemic complement activation and local MAC deposition preventing RPE cell damage. However, a steep increase in serum zinc following the initiation of treatment indicated that supplementation had been successful. Because of the slow natural progression of AMD, this study was never designed to measure a direct protective effect of zinc on visual acuity. In summary, in our study increased levels of serum complement catabolism correlates with the stage of AMD. Our study demonstrate that increased levels of complement catabolism can be normalized by the daily oral administration of 50 mg zinc sulphate. Findings from the present study might explain how zinc slows AMD progression in subgroups of patients with AMD. (2)

Age-related macular degeneration (AMD) is the leading cause of visual impairment and blindness in the United States and elsewhere among people 65 years or older. Oxidative damage to the retina may be involved in the pathogenesis of AMD. This randomized clinical trial was designed to evaluate the effect of high doses of zinc and selected antioxidant vitamins on the development of advanced AMD in a cohort of older persons. The treatment benefit of antioxidants plus zinc and zinc alone was present for each of the events predefined in the study protocol to be signs of advanced AMD. A small randomized trial suggested a benefit of large doses of zinc on visual acuity in persons with AMD. (3)

Observational and experimental data suggest that antioxidant and/or zinc supplements may delay progression of age-related macular degeneration (AMD) and vision loss. (3)

Recently it was showed that AMD was linked with several adverse effects in the retina, including delayed retrograde melanosome transport, increased deposition of pigment granules, and impaired autophagy in zebrafish. As shown by Julien et al., the metal ion concentration of RPE melanosomes is regulated by zinc, and reduced metal-binding activity of melanosomes is associated with degenerative processes in the retina. Therefore, melanosomes and their properties, especially their zinc-binding activity, may be a key element in the triad zinc–autophagy–AMD. (4)

Zinc for the treatment of the common cold.

The common cold is one of the most frequently occurring diseases in the world (59,60). More than 20 viruses cause the common cold, and these include rhinovirus, coronavirus, adenovirus, respiratory syncytial virus, and parainfluenza virus. Annu- ally adults in the United States may develop a common cold 2–4 times in a year, and children may develop colds 6–8 times in a year. The morbidity and subsequent financial loss resulting from absenteeism from work are substantial. Previously prescribed treatments have not provided a consistent relief of symptoms. (6)

We conclude that zinc acetate lozenges given within 24 h of the onset of common cold in proper doses are very effective in decreasing the duration and severity of the common cold. We propose that the beneficial effects seen in the zinc group were due to the antioxidant and anti-inflammatory effects of zinc. We also suggest that a decrease in plasma ICAM-1 levels due to zinc therapy may have decreased the docking of the cold viruses on the surface of somatic cells. (6)

Studies reporting the duration and severity of cold symptoms suggest that zinc significantly reduced the overall duration and severity of common cold symptoms if the therapy was started within 24 h of the onset of the cold. Zinc supplementation for prevention of the common cold showed that the incidence of the common cold, school absenteeism, and use of antibiotics were decrease. (6)

Physicians and health practitioners must realize that one cannot treat common cold symptoms by swallowing zinc tablets, zinc syrup, or zinc lozenges. Zinc lozenges must be used orally and allowed to dissolve slowly in the mouth, which will then allow ionic zinc to be released, absorbed, and transported to the virally infected nose. (6)

Atherosclerosis and zinc

Atherosclerosis is a slowly progressive chronic inflammatory disease characterized by focal arterial lesions that ultimately block the blood vessels, which leads to angina, myocardial infarction, cerebrovascular ischemia and stroke, and even death. Inflammation, oxidative stress, and/or endothelial dysfunction caused by known risk factors such as age, sex, smoking, hypertension, diabetes, and obesity are involved in the development and progression of atherosclerosis. Our previous studies showed that zinc deficiency increases the generation of inflammatory cytokines, increases oxidative stress, and induces endothelial cell dysfunction. (6)

Our study showed that zinc supplementation (45 mg el-emental zinc as gluconate) daily was effective in lowering plasma CRP concentration. This is the first documentation to show that zinc is effective in downregulating the plasma CRP level in the elderly. (6)

Zinc deficiency increased oxidative stress and zinc supple- mentation decreased oxidative stress in cell culture models and humans. We confirmed in this study that zinc supplementation decreased oxidative stress in elderly subjects and human vascular endothelial and monocytic cells. Thus, de- creased oxidative stress by zinc may decrease the LDL oxidation and exhibit an atheroprotective effect. (6)

Role of zinc in diabetes

Diabetes mellitus is one of the most common chronic dis- eases, and according to WHO, estimate nearly 300 million individuals are affected by this disorder. Diabetes is one of the major causes of blindness, increased risk of cardiovascular disorder, end-stage renal disease, and nontraumatic limb amputation. Insulin, produced by the b cells of the pancreas, is essential for glucose clearance from the blood to muscle, fat, and liver cells. The hallmark of diabetes is a loss of control of glycemia due to lack of insulin, which may be relative or absolute depending on the type of diabetes. (6)

Type 1 diabetes mellitus alone accounts for 5%–10% of all cases of diabetes. It is caused by autoimmune destruction of pancreatic b cells, resulting in virtually no production of insulin. Without insulin, carbohydrate cannot be used for energy; therefore, fats become the main intracellular source of energy. This results in generation of ketone bodies leading to ketoacidosis. Exogenous insulin administration is the main treatment for this situation. (6)

Type 2 diabetes mellitus accounts for >90% of the cases of diabetes and is due to insulin resistance; there is no problem in insulin production initially by the b cells. Eventually, however, islet b cell function also declines, leading to overt diabetes. These patients ultimately also require exogenous insulin for treatment. (6)

Zinc is crucial for the pancreas and the regulation of blood glucose. Insulin is stored in a crystalline form as a zinc insulin complex. Hence, the zinc concentration of the pancreatic b cells is among the highest in the body. Addition of zinc to insulin in vitro extended the duration of insulin action. In the 1930s, zinc ions were added in vitro to produce protamine zinc insulin to control the blood sugar in diabetic patients. (6)

In the presence of zinc ions, both insulin and proinsulin dimers aggregate into hexamers containing bound zinc. ZnT8 mRNA and protein has been shown to be almost exclusively confined to pancreatic islets and to participate in the regulation of insulin secretion. ZnT8 is believed to be crucial for both zinc transport in the insulin granules and insulin crystallization, which could not occur unless zinc is present. Zinc is a potent physiological regulator of insulin signal transduction. An adequate supply of zinc is crucial for insulin biosynthesis and storage, especially when there is hyperglycaemia. (6)

Recent studies by Jansen et al. showed that zinc supplementation may be a potential treatment adjunct in type 2 diabetes because zinc also promotes insulin signalling. (6)

The decrease in total body zinc in diabetic patients may be due to either hyperzincuria or decreased intestinal zinc absorption. Decreased zinc in plasma, lymphocytes, granulocytes, platelets, and hyperzincuria has been observed in diabetic patients. Zinc deficiency contributes to diabetic complications such as increased susceptibility to infections due to immune dysfunction, increased generation of inflammatory cytokines, and increased oxidative stress.  (6)

Scientific References:

1. Zinc homeostasis and neurodegenerative disorders Front Aging Neurosci. 2013 Jul 19; 5:33.  doi: 10.3389/fnagi.2013.00033. eCollection 2013. s

2. Zinc Supplementation Inhibits Complement Activation in Age-Related Macular Degeneration

3. Arch Ophthalmol. 2001 October ; 119(10): 1417–1436.  A Randomized, Placebo-Controlled, Clinical Trial of High-Dose Supplementation With Vitamins C and E, Beta Carotene, and Zinc for Age-Related Macular Degeneration and Vision Loss:

4. Zinc and Autophagy in Age-Related Macular Degeneration Received: 22 June 2020; Accepted: 13 July 2020; Published: 15 July 2020
5. Zinc Deficiency and Zinc Therapy Efficacy with Reduction of Serum Free Copper in Alzheimer’s Disease Received 2 July 2013; Accepted 4 September 2013
6. Discovery of Human Zinc Deficiency: Its Impact on Human Health and Disease Adv. Nutr. 4: 176–190, 2013.
7. Hautarzt. 1976 Mar;27(3):95-100. Acrodermatitis enteropathica–zinc as a life-saving drug

Harper Collins. Interviewed by journalist David Kentner, Poppet gained exposure across North America with the release of her debut novel Darkroom. Previously published by Night Publishing, Tirgearr Publishing, Endaxi Press, and Thorstruck Press, Poppet now has more than 50 titles to her credit.