Low-copper diet as a preventive strategy for Alzheimer’s disease

 

Neurobiology of Aging

2014 epub

 

Rosanna Squitti, Mariacristina Siotto, Renato Polimanti This article has 82 references.

 

[Low molecular-weight copper, also known as “free,” labile, or non-ceruloplasmin

(non-Cp)]

 

KEY POINTS FROM THIS ARTICLE:

 

 

  • Alzheimer’s disease (AD) is the most common form of dementia, and its prevalence is increasing.

     

  • “A large portion of the world’s public health expenditures is AD related.”

     

  • “Effective strategies to prevent or to postpone AD onset are clearly needed.”

     

  • “Copper is an essential element, and either a copper deficiency or excess can be life threatening.”

     

  • Alteration of copper metabolism is one of the pathogenetic mechanisms of Alzheimer’s disease (AD). 

     

  • “A low-copper diet can reduce the risk of AD in individuals with an altered copper metabolism.” 

     

  • “Deficiencies of some micronutrients, especially those related to antioxidant and amino acid metabolism mechanisms (e.g., vitamins B1, B2, B6, B12, C, and folate), have been associated with cognitive impairment in elderly people.”

     

  • Excess metals are neurotoxic.

     

  • Aluminum in the diet may increase AD risk.

     

  • “One of the most recent concepts in AD pathogenesis is that alterations of copper metabolism associated with genetic defects are associated with a ‘copper phenotype’ in a large percentage of AD patients.”

     

  • “The amount of literature available on dysfunction of copper metabolism has reached such a critical mass that dietary changes may be justified. In fact, these changes may be justified not only in cases in which available evidence demonstrates risk beyond any doubt but also in cases in which evidence of risk is substantial.”

  • The minimal acceptable intake of copper is about 0.9-1.3 mg per day, whereas, the average person consumes about 2 mg per day. Ingesting 2-3 mg per day of copper is safe and adequately prevents copper deficiency. 

     

  • Ingesting >5 mg per day is considered toxic. 

     

  • Once in the cell, copper is carried by cytochrome C oxidase assembly to the mitochondria. [Key to Low Level Laser Therapy]

     

  • Defects in copper homeostasis result in serious health consequences,

    “specifically for brain health and development.” 

     

  • Menke’s disease is a copper deficiency caused by genetic mutations. Signs include weak muscle tone, sagging facial features, seizures, mental retardation, blue sclera, and developmental delay. Disease onset begins during infancy.  Early diagnosis and treatment with copper intravenous infusion increase the likelihood of the survival.

     

  • Wilson disease is caused by a defect in copper excretion with copper accumulation, adversely affecting the liver and brain. The overload of non-Cp copper in systemic circulation causes brain copper deposits.

     

  • Oxidative stress “is one of the most relevant processes” driving Alzheimer’s disease (AD). “Studies indicate that copper can play a key role in these [AD] pathogenic processes.” 

     

  • “Non-Cp copper in the brain can likely overwhelm homeostatic processes and trigger the activation of the previously described copper-related amyloid cascade.”

     

  • “An increase in copper levels is established in specific cancers (i.e., breast, cervical, ovarian, lung, prostate, stomach, and leukemia).” The association between increased copper and cancer is likely because of increased oxidative stress causing tumor onset and progression and mitochondrial mutations.

     

  • Elevated copper may also be associated with epigenetic changes.

     

  • Diabetic patients have higher plasma copper concentrations.

     

  • Elevated copper can interact with glycated proteins in the formation of free radicals and increase oxidative stress. 

     

  • Elevated copper may be linked to atherosclerosis. “The interaction between copper and homocysteine generates free radicals and, consequently, leads to oxidized low-density lipoprotein.”

  • Since 2002, studies have linked elevated copper to the increased risk of developing AD. “An increase of 1 mmol/L in total serum copper accounted for 80% of the risk of having AD.” “The risk doubles [100% increased risk] if the comparison is made between AD patients and subjects affected by vascular dementia.”

  • In Alzheimer’s disease, copper absorption is normal, but there is a failure in its incorporation into ceruloplasmin (Cp). “This causes an overflow of non-Cp copper sufficiently to be detected in general circulation.” When values of non-Cp copper exceed 1.6 mmol/L, it crosses the brain blood barrier (BBB), producing amyloidbeta (Ab) increasing and Ab-plaque deposition. 

     

  • “For humans, the main sources of environmental copper are food and drinking water.” Drinking water encompasses 20%-25% of the copper ingested by most humans globally. Some authors believe that the copper present in drinking water because of leaching from copper plumbing can increase the risk for AD.

     

  • “The most relevant sources of dietary copper include seafood (especially shellfish), organ meats, grains, and legumes.” “Nuts and certain fruits (e.g., lemons, raisins, coconuts, papaya, and apples) are also rich in copper. Other copper sources include cereals, potatoes, red meat, and mushrooms.”

     

  • The top 10 foods with the highest content in copper are:

    Animal liver (veal) 

    Oysters

    Sesame seeds

    Cocoa 

    Nuts (cashew) 

    Seafood (calamari) 

    Sunflower seeds 

    Sun dried tomatoes 

    Pumpkin

    Dried herbs (basil) 

     

  • “Low copper foods include tea, rice, and chicken.”

     

  • “In individuals with copper metabolism defects, high dietary copper intake can be harmful.”

     

  • The identification of individuals with a higher AD copper risk can be performed by 1 of 2 approaches: 

     

  • A biochemical method based on the analysis of serum non-Cp copper, looking for values greater than the normal reference value of 1.6 mmol/L. 

     

  • The sequence analysis of genes involved in copper metabolism (e.g., ATP7B, ATOX1, and COMMD1).

  • Zinc ingestion reduces the body’s capacity to absorb copper.

     

  • Zinc therapy may have some efficacy for AD. But the use of oral zinc supplements has been associated with copper deficiency myelopathy, which is an irreversible neurologic syndrome.

     

  • This study “strongly support the hypothesis that copper balance is a modifiable factor that could reduce AD risk in certain individuals who can implement a low-copper diet.”

     

  • Healthful and inexpensive dietary precautions, monitored by medical professionals are fully justified.

     

  • “We suggest that individuals with high copper-related AD risk should adopt a low copper diet, that is, increase the quantity of low-copper foods, whereas reducing the quantity of high-copper foods, fatty foods, and alcohol consumption

    (that affects liver functionality). These individuals should also take zinc supplements, provided this can be done under medical supervision.”  

     

    COMMENTS

     

    We have seen this copper link to Alzheimer’s several times before. The basic premise is that excess copper, especially in individuals with genetic copper problems, have increased risk for dementia. The copper crosses the blood-brain barrier where it generates excess levels of free radicals, damaging the brain.

     

    The sources of excess copper include drinking water, food, and nutritional supplements. Following the advice of other authors on the topic, I suggest reverse osmosis for consumed water (to remove the copper) and avoiding supplements with copper, unless advised otherwise by a health care professional.

     

    Article Review 49-11: The Risks of Copper Toxicity Contributing to Cognitive Decline in the Aging Population and to Alzheimer's Disease; Journal of the American College of Nutrition; 2009.

     

    Article Review 3-12: Risks of Copper and Iron Toxicity during Aging in Humans; Chemical Research in Toxicology; 2010.

     

    Article Review 34-13: Oxidative Stress in Alzheimer’s Disease and Mild Cognitive Impairment; Journal of Alzheimer’s Disease; 2012.

     

     

     

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