Contact Me
Menu

Rethinking Copper Toxicity: A Critical Analysis of History, Research Methods, and the Iron Connection

Scroll to top
Scroll to top

As a practitioner and investigator of mineral metabolism, I’ve found myself increasingly questioning our fundamental assumptions about copper toxicity. The journey into this investigation has led me down fascinating paths through medical history, biochemistry, and methodological analysis. What I’ve discovered suggests we may need to radically rethink our understanding of copper’s role in human health and disease – not as a potential toxin to be feared, but as an essential conductor in the complex symphony of human metabolism.

The Evolution of a Medical Paradigm

The concept of copper toxicity has an interesting historical trajectory. Early researchers discussing “unbound copper” were working with limited analytical tools and an incomplete understanding of mineral metabolism. Over decades, this concept morphed and expanded, eventually becoming accepted wisdom in both conventional and alternative medicine. Yet when we trace this evolution carefully, we find surprisingly little evidence for copper existing in a truly “unbound” state in living systems.

In the early days of trace mineral research, scientists worked with crude tools by today’s standards. They could measure total copper content in tissues but couldn’t determine its biological state or function. This limitation proved crucial – it led to assumptions about copper’s behavior that persist today, despite our more sophisticated understanding of biochemistry.

The Biochemistry We Often Overlook

The story of copper in human biology begins with a striking comparison. Our bodies contain approximately 70-100 mg of copper, a remarkably small amount compared to our iron content of 4,000-5,000 mg. This copper exists in highly specific forms, always bound to proteins – whether as part of enzymes, bound to ceruloplasmin, or attached to other transport proteins like albumin. Despite decades of research, no one has demonstrated the existence of a “labile copper pool” similar to the well-documented labile iron pool.

This distinction becomes crucial when we consider how these metals behave in our bodies. Iron readily participates in the Fenton reaction, generating harmful free radicals that can damage tissues. It maintains a constant presence in what we call the labile iron pool – essentially reactive iron capable of driving oxidative damage. Copper, by contrast, remains under tight protein-bound control, suggesting our bodies evolved specific mechanisms to prevent it from participating in harmful reactions.

The Limits of Our Understanding

When scientists examine tissue for copper content, whether through biopsy or hair tissue mineral analysis, they encounter a fundamental limitation in their methodology. These tests reveal total copper content but tell us nothing about its biological state. A high copper reading might indicate properly functioning enzymes, copper bound to transport proteins, or copper that has separated from its usual protein partners. This limitation has led to potentially misleading interpretations, where elevated copper levels are assumed to indicate toxicity rather than disrupted copper metabolism or enzyme dysfunction.

Wilson’s Disease: A Story of Misunderstood Mechanisms

The story of Wilson’s disease provides a fascinating window into how our understanding of copper in human health evolved. When Samuel Alexander Kinnier Wilson first described the condition in 1912, he documented a complex neurological disorder with liver involvement. The copper connection remained undiscovered until 1948, when John Cumings found elevated copper content in brain and liver tissue.

Yet the early researchers overlooked something crucial – the role of iron metabolism. Recent research has revealed that Wilson’s disease is now recognized as a cause of hemochromatosis (aka iron overload) by some physicians, even in patients without genetic HFE markers. This finding forces us to question our basic assumptions about the condition.

The biochemistry tells an intriguing story. Wilson’s disease involves the ATP7B gene, affecting copper transport. But perhaps we’ve misunderstood the primary issue. Rather than copper accumulation itself being the problem, what if we’re seeing the effects of lost copper-dependent enzyme function? When these enzymes don’t work properly, iron regulation collapses. The symptoms we’ve long attributed to copper toxicity might actually result from iron dysregulation.

The Legacy of Iron Fortification

The story of our current mineral imbalances begins in 1939, when widespread iron fortification programs dramatically altered our exposure to this powerful metal. By 1969, fortification levels had increased by 50% in many countries, creating an unprecedented situation in human history. Combined with decreased dietary copper and other nutritional changes, this created what researchers would later describe as a perfect storm for mineral dysregulation.

Our bodies never evolved robust mechanisms for eliminating excess iron. Unlike many other minerals, iron primarily leaves the body through bleeding, leaving us poorly equipped to handle the modern burden of fortification. Meanwhile, copper-dependent enzymes play crucial roles in managing iron metabolism. When these enzymes don’t function properly, iron can accumulate and drive oxidative damage through the Fenton reaction.

The Foundation of Experimental Evidence

The experimental foundation for copper toxicity comes largely from animal studies, particularly in sheep, which helped shape our understanding of copper’s effects on living systems. In regions like Western Australia, researchers observed sheep developing liver disease, which they attributed to copper toxicity. Yet the story proves far more complex when examined closely.

These sheep grazed on pastures where mineral content varied with soil composition, seasonal changes, and complex mineral interactions. While researchers found correlations between copper exposure and liver disease, they often missed crucial pieces of the puzzle. The presence of other minerals, particularly molybdenum, significantly influenced copper’s biological effects. More importantly, these studies rarely examined the activity of copper-dependent enzymes or iron metabolism, leaving us with an incomplete picture of what truly caused the observed problems.

Cell culture studies, another cornerstone of copper toxicity research, present even more problematic methodological issues. These experiments typically expose cells directly to copper ions – a situation that rarely, if ever, occurs in living organisms. In real biological systems, copper travels bound to proteins, protected from engaging in harmful reactions. Drawing conclusions about copper toxicity from these artificial conditions is like studying water’s effects on fish by removing them from it – the context fundamentally changes the outcome.

The Symphony of Enzyme Function

Understanding copper’s role in living systems requires us to appreciate the intricate symphony of enzyme function. Through ceruloplasmin, copper orchestrates iron oxidation states, while its presence in superoxide dismutase protects against oxidative stress. Copper supports energy production in cellular respiration and facilitates the formation of connective tissue. When these copper-dependent processes fail, the resulting cascade of effects can masquerade as copper toxicity.

Without proper ceruloplasmin activity, iron metabolism falters. Without adequate superoxide dismutase, oxidative stress increases. These downstream effects might appear to implicate copper as the problem, when in fact, we’re seeing the results of compromised copper-dependent enzyme function. It’s akin to blaming a conductor for an orchestra’s poor performance when the real issue lies in the musicians’ inability to play their instruments.

Institutional Influences on Scientific Understanding

The direction of copper toxicity research hasn’t developed in a vacuum. The medical establishment faces significant challenges in reconsidering established paradigms, particularly when they involve widespread public health measures like iron fortification. Research funding tends to favor studies that support current understanding rather than challenge it, creating a self-reinforcing cycle where initial assumptions about copper toxicity guide future research directions.

The complexity of mineral interactions defies the reductionist approach favored by modern research methods. Iron and copper metabolism intertwine in ways that make studying them in isolation problematic. Yet most research examines them separately, potentially missing crucial interactions that could explain observed phenomena.

Reframing Our Understanding

These insights compel us to develop a new framework for understanding copper in human health. Rather than viewing copper as potentially toxic, we might better understand it as an essential component of biological systems that protect against iron-driven oxidative damage. When copper-dependent systems fail, the resulting problems might appear as copper toxicity but actually represent copper dysfunction.

This perspective suggests that what we call copper toxicity might often be copper dysregulation. Symptoms attributed to copper excess could instead reflect copper-dependent enzyme dysfunction, with iron dysregulation serving as the primary driver of observed tissue damage. Such a fundamental shift in understanding would require us to reconsider our treatment approaches entirely.

A New Clinical Perspective

The implications of this revised understanding reach deep into clinical practice. When we receive hair tissue mineral analysis results or other testing data, we must view them through a new lens. A high copper reading tells only part of the story – like finding excess building materials at a construction site. The real question isn’t about quantity but about function: Are copper-dependent enzymes operating properly? Has iron regulation broken down? These questions demand a more sophisticated approach to assessment and treatment.

Consider how this shifts our clinical perspective. When we see symptoms traditionally attributed to copper toxicity, we might instead investigate iron dysregulation and enzyme dysfunction. The copper we find accumulated in tissues might not be the villain but rather a sign of broader metabolic disruption. It’s similar to finding a buildup of postal workers during a mail strike – their presence indicates system dysfunction rather than causing it.

The Research Horizon

Moving forward requires us to ask different questions. Instead of focusing solely on copper levels, we need to understand how copper-dependent enzymes influence iron metabolism in various conditions. The role of iron dysregulation in conditions currently attributed to copper toxicity demands closer examination. We need new ways to assess copper’s biological state and function, moving beyond simple measurements of quantity to understand quality of function.

The long-term effects of iron fortification on copper-dependent processes present another crucial area for investigation. We’ve conducted a massive nutritional experiment on populations worldwide through iron fortification, yet we’ve barely begun to understand its implications for copper metabolism and enzyme function.

The Story of Unintended Consequences

The history of copper toxicity reveals how easily we can misinterpret complex biological phenomena. When Samuel Wilson first described his eponymous disease, he couldn’t have known how copper and iron would come to intertwine in our understanding of the condition. The discovery of copper accumulation in tissues led to decades of focus on copper toxicity, potentially obscuring the more fundamental issue of iron dysregulation.

This story parallels other instances in medical history where initial observations led to incomplete conclusions. Like the early days of pellagra, when researchers focused on a seemingly toxic response to corn rather than the underlying niacin deficiency, we may have mistaken a downstream effect for a root cause.

Practical Applications and Future Directions

This evolved understanding suggests new approaches to both research and treatment. We need to develop methods for assessing enzyme function rather than merely measuring mineral levels. The interaction between copper-dependent processes and iron metabolism demands closer attention in both research and clinical settings.

The implications extend beyond individual treatment to public health policy. The wisdom of continued iron fortification requires reevaluation in light of its potential effects on copper-dependent processes. We might need to consider more nuanced approaches to mineral supplementation that account for these complex interactions.

Conclusions: A Call for Paradigm Shift

The evidence compels us to reconsider our understanding of copper toxicity fundamentally. What we observe in many cases might better be understood as a disruption of copper-dependent processes, leading to iron dysregulation and subsequent oxidative damage. This perspective doesn’t diminish the importance of proper copper metabolism but rather places it in a more nuanced context of mineral interactions and enzyme function.

The story of copper in human health continues to unfold. Like many scientific paradigm shifts, this new understanding doesn’t invalidate all previous observations but rather reframes them in a broader context. It suggests that the path forward lies not in fear of copper toxicity but in understanding and supporting copper’s essential roles in human health.

As practitioners and researchers, we must remain open to questioning established paradigms when evidence suggests alternative explanations. The story of copper toxicity reminds us that in biological systems, apparent simplicity often masks underlying complexity. Our understanding continues to evolve, and with it, our approach to health and disease must also evolve.

References

Bull, P. C., Thomas, G. R., Rommens, J. M., Forbes, J. R., & Cox, D. W. (1993). The Wilson disease gene is a putative copper transporting P-type ATPase similar to the Menkes gene. Nature Genetics, 5(4), 327-337.

Collins, J. F., Prohaska, J. R., & Knutson, M. D. (2010). Metabolic crossroads of iron and copper. Nutrition Reviews, 68(3), 133-147.

Cumings, J. N. (1948). The copper and iron content of brain and liver in the normal and in hepato-lenticular degeneration. Brain, 71(4), 410-415.

Gulec, S., & Collins, J. F. (2014). Molecular mediators governing iron-copper interactions. Annual Review of Nutrition, 34, 95-116.

Holmberg, C. G., & Laurell, C. B. (1948). Investigations in serum copper: II. Isolation of the copper containing protein, and a description of some of its properties. Acta Chemica Scandinavica, 2, 550-556.

Kell, D. B. (2009). Iron behaving badly: inappropriate iron chelation as a major contributor to the aetiology of vascular and other progressive inflammatory and degenerative diseases. BMC Medical Genomics, 2(1), 2.

Laurell, C. B. (1947). Studies on the transportation and metabolism of iron in the body. Acta Physiologica Scandinavica, 14(Suppl 46), 1-129.

Moon, J., Prasad, R., & Mercer, J. F. B. (2008). Molecular genetics of iron metabolism in mammals: Implications for disease. Annual Review of Genomics and Human Genetics, 9, 455-486.

Scheinberg, I. H., & Gitlin, D. (1952). Deficiency of ceruloplasmin in patients with hepatolenticular degeneration (Wilson’s disease). Science, 116(3018), 484-485.

Sternlieb, I., & Scheinberg, I. H. (1963). The role of radiocopper in the diagnosis of Wilson’s disease. Gastroenterology, 44, 550-553.

Wilson, S. A. K. (1912). Progressive lenticular degeneration: a familial nervous disease associated with cirrhosis of the liver. Brain, 34(4), 295-507.

Wilson, D. C., & Matthews, D. M. (1966). Metabolic inter-relationships between copper, zinc, and iron. Proceedings of the Nutrition Society, 25(1), 62-66.

Share This Post

More To Explore

Rethinking Copper Toxicity: A Critical Analysis of History, Research Methods, and the Iron Connection

As a practitioner and investigator of mineral metabolism, I’ve found myself increasingly questioning our fundamental assumptions about copper toxicity. The journey into this investigation has led me down fascinating paths through medical history, biochemistry, and methodological analysis. What I’ve discovered suggests we may need to radically rethink our understanding of copper’s role in human health and disease – not as a potential toxin to be feared, but as an essential conductor in the complex symphony of human metabolism.

The Evolution of a Medical Paradigm

The concept of copper toxicity has an interesting historical trajectory. Early researchers discussing “unbound copper” were working with limited analytical tools and an incomplete understanding of mineral metabolism. Over decades, this concept morphed and expanded, eventually becoming accepted wisdom in both conventional and alternative medicine. Yet when we trace this evolution carefully, we find surprisingly little evidence for copper existing in a truly “unbound” state in living systems.

In the early days of trace mineral research, scientists worked with crude tools by today’s standards. They could measure total copper content in tissues but couldn’t determine its biological state or function. This limitation proved crucial – it led to assumptions about copper’s behavior that persist today, despite our more sophisticated understanding of biochemistry.

The Biochemistry We Often Overlook

The story of copper in human biology begins with a striking comparison. Our bodies contain approximately 70-100 mg of copper, a remarkably small amount compared to our iron content of 4,000-5,000 mg. This copper exists in highly specific forms, always bound to proteins – whether as part of enzymes, bound to ceruloplasmin, or attached to other transport proteins like albumin. Despite decades of research, no one has demonstrated the existence of a “labile copper pool” similar to the well-documented labile iron pool.

This distinction becomes crucial when we consider how these metals behave in our bodies. Iron readily participates in the Fenton reaction, generating harmful free radicals that can damage tissues. It maintains a constant presence in what we call the labile iron pool – essentially reactive iron capable of driving oxidative damage. Copper, by contrast, remains under tight protein-bound control, suggesting our bodies evolved specific mechanisms to prevent it from participating in harmful reactions.

The Limits of Our Understanding

When scientists examine tissue for copper content, whether through biopsy or hair tissue mineral analysis, they encounter a fundamental limitation in their methodology. These tests reveal total copper content but tell us nothing about its biological state. A high copper reading might indicate properly functioning enzymes, copper bound to transport proteins, or copper that has separated from its usual protein partners. This limitation has led to potentially misleading interpretations, where elevated copper levels are assumed to indicate toxicity rather than disrupted copper metabolism or enzyme dysfunction.

Wilson’s Disease: A Story of Misunderstood Mechanisms

The story of Wilson’s disease provides a fascinating window into how our understanding of copper in human health evolved. When Samuel Alexander Kinnier Wilson first described the condition in 1912, he documented a complex neurological disorder with liver involvement. The copper connection remained undiscovered until 1948, when John Cumings found elevated copper content in brain and liver tissue.

Yet the early researchers overlooked something crucial – the role of iron metabolism. Recent research has revealed that Wilson’s disease is now recognized as a cause of hemochromatosis (aka iron overload) by some physicians, even in patients without genetic HFE markers. This finding forces us to question our basic assumptions about the condition.

The biochemistry tells an intriguing story. Wilson’s disease involves the ATP7B gene, affecting copper transport. But perhaps we’ve misunderstood the primary issue. Rather than copper accumulation itself being the problem, what if we’re seeing the effects of lost copper-dependent enzyme function? When these enzymes don’t work properly, iron regulation collapses. The symptoms we’ve long attributed to copper toxicity might actually result from iron dysregulation.

The Legacy of Iron Fortification

The story of our current mineral imbalances begins in 1939, when widespread iron fortification programs dramatically altered our exposure to this powerful metal. By 1969, fortification levels had increased by 50% in many countries, creating an unprecedented situation in human history. Combined with decreased dietary copper and other nutritional changes, this created what researchers would later describe as a perfect storm for mineral dysregulation.

Our bodies never evolved robust mechanisms for eliminating excess iron. Unlike many other minerals, iron primarily leaves the body through bleeding, leaving us poorly equipped to handle the modern burden of fortification. Meanwhile, copper-dependent enzymes play crucial roles in managing iron metabolism. When these enzymes don’t function properly, iron can accumulate and drive oxidative damage through the Fenton reaction.

The Foundation of Experimental Evidence

The experimental foundation for copper toxicity comes largely from animal studies, particularly in sheep, which helped shape our understanding of copper’s effects on living systems. In regions like Western Australia, researchers observed sheep developing liver disease, which they attributed to copper toxicity. Yet the story proves far more complex when examined closely.

These sheep grazed on pastures where mineral content varied with soil composition, seasonal changes, and complex mineral interactions. While researchers found correlations between copper exposure and liver disease, they often missed crucial pieces of the puzzle. The presence of other minerals, particularly molybdenum, significantly influenced copper’s biological effects. More importantly, these studies rarely examined the activity of copper-dependent enzymes or iron metabolism, leaving us with an incomplete picture of what truly caused the observed problems.

Cell culture studies, another cornerstone of copper toxicity research, present even more problematic methodological issues. These experiments typically expose cells directly to copper ions – a situation that rarely, if ever, occurs in living organisms. In real biological systems, copper travels bound to proteins, protected from engaging in harmful reactions. Drawing conclusions about copper toxicity from these artificial conditions is like studying water’s effects on fish by removing them from it – the context fundamentally changes the outcome.

The Symphony of Enzyme Function

Understanding copper’s role in living systems requires us to appreciate the intricate symphony of enzyme function. Through ceruloplasmin, copper orchestrates iron oxidation states, while its presence in superoxide dismutase protects against oxidative stress. Copper supports energy production in cellular respiration and facilitates the formation of connective tissue. When these copper-dependent processes fail, the resulting cascade of effects can masquerade as copper toxicity.

Without proper ceruloplasmin activity, iron metabolism falters. Without adequate superoxide dismutase, oxidative stress increases. These downstream effects might appear to implicate copper as the problem, when in fact, we’re seeing the results of compromised copper-dependent enzyme function. It’s akin to blaming a conductor for an orchestra’s poor performance when the real issue lies in the musicians’ inability to play their instruments.

Institutional Influences on Scientific Understanding

The direction of copper toxicity research hasn’t developed in a vacuum. The medical establishment faces significant challenges in reconsidering established paradigms, particularly when they involve widespread public health measures like iron fortification. Research funding tends to favor studies that support current understanding rather than challenge it, creating a self-reinforcing cycle where initial assumptions about copper toxicity guide future research directions.

The complexity of mineral interactions defies the reductionist approach favored by modern research methods. Iron and copper metabolism intertwine in ways that make studying them in isolation problematic. Yet most research examines them separately, potentially missing crucial interactions that could explain observed phenomena.

Reframing Our Understanding

These insights compel us to develop a new framework for understanding copper in human health. Rather than viewing copper as potentially toxic, we might better understand it as an essential component of biological systems that protect against iron-driven oxidative damage. When copper-dependent systems fail, the resulting problems might appear as copper toxicity but actually represent copper dysfunction.

This perspective suggests that what we call copper toxicity might often be copper dysregulation. Symptoms attributed to copper excess could instead reflect copper-dependent enzyme dysfunction, with iron dysregulation serving as the primary driver of observed tissue damage. Such a fundamental shift in understanding would require us to reconsider our treatment approaches entirely.

A New Clinical Perspective

The implications of this revised understanding reach deep into clinical practice. When we receive hair tissue mineral analysis results or other testing data, we must view them through a new lens. A high copper reading tells only part of the story – like finding excess building materials at a construction site. The real question isn’t about quantity but about function: Are copper-dependent enzymes operating properly? Has iron regulation broken down? These questions demand a more sophisticated approach to assessment and treatment.

Consider how this shifts our clinical perspective. When we see symptoms traditionally attributed to copper toxicity, we might instead investigate iron dysregulation and enzyme dysfunction. The copper we find accumulated in tissues might not be the villain but rather a sign of broader metabolic disruption. It’s similar to finding a buildup of postal workers during a mail strike – their presence indicates system dysfunction rather than causing it.

The Research Horizon

Moving forward requires us to ask different questions. Instead of focusing solely on copper levels, we need to understand how copper-dependent enzymes influence iron metabolism in various conditions. The role of iron dysregulation in conditions currently attributed to copper toxicity demands closer examination. We need new ways to assess copper’s biological state and function, moving beyond simple measurements of quantity to understand quality of function.

The long-term effects of iron fortification on copper-dependent processes present another crucial area for investigation. We’ve conducted a massive nutritional experiment on populations worldwide through iron fortification, yet we’ve barely begun to understand its implications for copper metabolism and enzyme function.

The Story of Unintended Consequences

The history of copper toxicity reveals how easily we can misinterpret complex biological phenomena. When Samuel Wilson first described his eponymous disease, he couldn’t have known how copper and iron would come to intertwine in our understanding of the condition. The discovery of copper accumulation in tissues led to decades of focus on copper toxicity, potentially obscuring the more fundamental issue of iron dysregulation.

This story parallels other instances in medical history where initial observations led to incomplete conclusions. Like the early days of pellagra, when researchers focused on a seemingly toxic response to corn rather than the underlying niacin deficiency, we may have mistaken a downstream effect for a root cause.

Practical Applications and Future Directions

This evolved understanding suggests new approaches to both research and treatment. We need to develop methods for assessing enzyme function rather than merely measuring mineral levels. The interaction between copper-dependent processes and iron metabolism demands closer attention in both research and clinical settings.

The implications extend beyond individual treatment to public health policy. The wisdom of continued iron fortification requires reevaluation in light of its potential effects on copper-dependent processes. We might need to consider more nuanced approaches to mineral supplementation that account for these complex interactions.

Conclusions: A Call for Paradigm Shift

The evidence compels us to reconsider our understanding of copper toxicity fundamentally. What we observe in many cases might better be understood as a disruption of copper-dependent processes, leading to iron dysregulation and subsequent oxidative damage. This perspective doesn’t diminish the importance of proper copper metabolism but rather places it in a more nuanced context of mineral interactions and enzyme function.

The story of copper in human health continues to unfold. Like many scientific paradigm shifts, this new understanding doesn’t invalidate all previous observations but rather reframes them in a broader context. It suggests that the path forward lies not in fear of copper toxicity but in understanding and supporting copper’s essential roles in human health.

As practitioners and researchers, we must remain open to questioning established paradigms when evidence suggests alternative explanations. The story of copper toxicity reminds us that in biological systems, apparent simplicity often masks underlying complexity. Our understanding continues to evolve, and with it, our approach to health and disease must also evolve.

References

Bull, P. C., Thomas, G. R., Rommens, J. M., Forbes, J. R., & Cox, D. W. (1993). The Wilson disease gene is a putative copper transporting P-type ATPase similar to the Menkes gene. Nature Genetics, 5(4), 327-337.

Collins, J. F., Prohaska, J. R., & Knutson, M. D. (2010). Metabolic crossroads of iron and copper. Nutrition Reviews, 68(3), 133-147.

Cumings, J. N. (1948). The copper and iron content of brain and liver in the normal and in hepato-lenticular degeneration. Brain, 71(4), 410-415.

Gulec, S., & Collins, J. F. (2014). Molecular mediators governing iron-copper interactions. Annual Review of Nutrition, 34, 95-116.

Holmberg, C. G., & Laurell, C. B. (1948). Investigations in serum copper: II. Isolation of the copper containing protein, and a description of some of its properties. Acta Chemica Scandinavica, 2, 550-556.

Kell, D. B. (2009). Iron behaving badly: inappropriate iron chelation as a major contributor to the aetiology of vascular and other progressive inflammatory and degenerative diseases. BMC Medical Genomics, 2(1), 2.

Laurell, C. B. (1947). Studies on the transportation and metabolism of iron in the body. Acta Physiologica Scandinavica, 14(Suppl 46), 1-129.

Moon, J., Prasad, R., & Mercer, J. F. B. (2008). Molecular genetics of iron metabolism in mammals: Implications for disease. Annual Review of Genomics and Human Genetics, 9, 455-486.

Scheinberg, I. H., & Gitlin, D. (1952). Deficiency of ceruloplasmin in patients with hepatolenticular degeneration (Wilson’s disease). Science, 116(3018), 484-485.

Sternlieb, I., & Scheinberg, I. H. (1963). The role of radiocopper in the diagnosis of Wilson’s disease. Gastroenterology, 44, 550-553.

Wilson, S. A. K. (1912). Progressive lenticular degeneration: a familial nervous disease associated with cirrhosis of the liver. Brain, 34(4), 295-507.

Wilson, D. C., & Matthews, D. M. (1966). Metabolic inter-relationships between copper, zinc, and iron. Proceedings of the Nutrition Society, 25(1), 62-66.

Share This Post

More To Explore

Contact Me