If copper is associated with Alzheimer’s disease, what about healthy, whole plant food sources such as nuts, seeds, beans, and whole grains?
Alzheimer’s Disease, Copper, and Saturated Fat
Though the underlying cause of Alzheimer’s disease has yet to be found, there is an increasing burden of proof on the role of metals in the development of the disease. Iron and copper, for example, are strongly concentrated within the plaques and tangles that represent the hallmarks of the Alzheimer’s brain.
Alzheimer’s disease victims have higher levels of copper in their blood and in the fluid that surrounds their brain, and inside their brain. Here’s a slice of Alzheimer’s diseased brain tissue showing the amyloid plaques, corresponding to copper hotspots. Copper may then make these amyloid plaques more toxic, leading to increased oxidative stress. Free copper is extremely efficient in the generation of free radicals, and when copper is removed with a chelating drug, the free radical oxidation drops.
Unfortunately, when researchers tried giving that drug to nine Alzheimer’s patients in a pilot study, it did not seem to have any effect on slowing the clinical progression of the disease; so, maybe we need to prevent the copper buildup in the first place.
Organ meats and shellfish are the richest food sources of copper. But should we also consider cutting down on plant sources, such as nuts, seeds, legumes, and whole grains? Copper intake only seems to be a problem when consumed with saturated fat or transfat.
In the Chicago Health and Aging Project, thousands of elderly Chicagoans were followed for six years. Those who were getting the highest copper doses, largely from multivitamin supplements, combined with a diet high in saturated fats, lost cognition as if they had aged 19 years in a period of six years, tripling their rate of cognitive decline. But copper intake was not associated with cognitive change when the diet was not also high in saturated fats.
Diet-induced high cholesterol has been shown to increase the formation and progression of amyloid plaques in the brain. And dietary copper may interfere with clearance of amyloid from the brain, and may further promote the plaque accumulation that results from elevated cholesterol levels. Copper has been shown to interact badly with amyloid, causing its clumping and the production of hydrogen peroxide, a potent pro-oxidant neurotoxin.
This may help explain why the higher the levels of copper, the quicker Alzheimer’s disease may progress, particularly among people with high cholesterol levels.
This is what we think may be happening. As cholesterol and copper levels rise, cholesterol is incorporated into the nerve cell membrane, causing it to stiffen. The amyloid protein in the membrane detaches to form plaques, at which point, iron and copper generate neurotoxic free radicals. Inside the cell, similar havoc is created, and finally cholesterol-enriched diets can lead to nerve cell death, DNA damage, and blood-brain barrier disruption.
In conclusion, the present systematic review suggests that a diet rich in copper and iron might aggravate the detrimental effects of a high intake of cholesterol and saturated fat on the risk of developing Alzheimer’s disease. So, diets rich in saturated fat and deficient in antioxidants appear to promote the onset of the disease, while more plant-based diets would likely suppress its onset. There are compounds in plant foods that not only scavenge free radicals and prevent oxidative damage, but are also known to chelate, or bind up, metals, potentially making them additionally be protective against the onset of Alzheimer’s. Therefore, the practical implications could be to eat lots of fruits and vegetables, avoid copper-containing supplements, and avoid high intakes of saturated fat and excessive iron intake.
To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video. This is just an approximation of the audio contributed by Katie Schloer.
Please consider volunteering to help out on the site.
- M C Morris, D A Evans, C C Tangney, J L Bienias, J A Schneider, R S Wilson, P A Scherr. Dietary copper and high saturated and trans fat intakes associated with cognitive decline. Arch Neurol. 2006 Aug;63(8):1085-8.
- B N Ramesh, T S Rao, A Prakasam, K Sambamurti, K S Rao. Neuronutrition and Alzheimer's disease. J Alzheimers Dis. 2010;19(4):1123-39.
- R Squitti, F Bressi, P Pasqualetti, C Bonomini, R Ghidoni, G Binetti, E Cassetta, F Moffa, M Ventriglia, F Vernieri, P M Rossini. Longitudinal prognostic value of serum "free" copper in patients with Alzheimer disease. Neurology. 2009 Jan 6;72(1):50-5.
- M Ventriglia, S Bucossi, V Panetta, R Squitti. Copper in Alzheimer's disease: a meta-analysis of serum, plasma, and cerebrospinal fluid studies. J Alzheimers Dis. 2012;30(4):981-4.
- M Loef, H Walach. Copper and iron in Alzheimer's disease: a systematic review and its dietary implications. Br J Nutr. 2012 Jan;107(1):7-19.
- M A Lovell, J D Robertson, W J Teesdale, J L Campbell, W R Markesbery. Copper, iron and zinc in Alzheimer's disease senile plaques. J Neurol Sci. 1998 Jun 11;158(1):47-52.
- L M Sayre, G Perry, P L Harris, Y Liu, K A Schubert, M A Smith. In situ oxidative catalysis by neurofibrillary tangles and senile plaques in Alzheimer's disease: a central role for bound transition metals. J Neurochem. 2000 Jan;74(1):270-9.
- Y Manso, G Comes, J Hidalgo, A I Bush, P A Adlard. Copper modulation as a therapy for Alzheimer's disease? Int J Alzheimers Dis. 2011;2011:370345.
- L M Miller, Q Wang, T P Telivala, R J Smith, A Lanzirotti, J Miklossy. Synchrotron-based infrared and X-ray imaging shows focalized accumulation of Cu and Zn co-localized with beta-amyloid deposits in Alzheimer's disease. J Struct Biol. 2006 Jul;155(1):30-7.
- R Squitt, P M Rossini, E Cassetta, F Moffa, P Pasqualetti, M Cortesi, A Colloca, L Rossi, A Finazzi-Agró. d-penicillamine reduces serum oxidative stress in Alzheimer's disease patients. Eur J Clin Invest. 2002 Jan;32(1):51-9.
Images thanks to Geralt via Pixabay.
Though the underlying cause of Alzheimer’s disease has yet to be found, there is an increasing burden of proof on the role of metals in the development of the disease. Iron and copper, for example, are strongly concentrated within the plaques and tangles that represent the hallmarks of the Alzheimer’s brain.
Alzheimer’s disease victims have higher levels of copper in their blood and in the fluid that surrounds their brain, and inside their brain. Here’s a slice of Alzheimer’s diseased brain tissue showing the amyloid plaques, corresponding to copper hotspots. Copper may then make these amyloid plaques more toxic, leading to increased oxidative stress. Free copper is extremely efficient in the generation of free radicals, and when copper is removed with a chelating drug, the free radical oxidation drops.
Unfortunately, when researchers tried giving that drug to nine Alzheimer’s patients in a pilot study, it did not seem to have any effect on slowing the clinical progression of the disease; so, maybe we need to prevent the copper buildup in the first place.
Organ meats and shellfish are the richest food sources of copper. But should we also consider cutting down on plant sources, such as nuts, seeds, legumes, and whole grains? Copper intake only seems to be a problem when consumed with saturated fat or transfat.
In the Chicago Health and Aging Project, thousands of elderly Chicagoans were followed for six years. Those who were getting the highest copper doses, largely from multivitamin supplements, combined with a diet high in saturated fats, lost cognition as if they had aged 19 years in a period of six years, tripling their rate of cognitive decline. But copper intake was not associated with cognitive change when the diet was not also high in saturated fats.
Diet-induced high cholesterol has been shown to increase the formation and progression of amyloid plaques in the brain. And dietary copper may interfere with clearance of amyloid from the brain, and may further promote the plaque accumulation that results from elevated cholesterol levels. Copper has been shown to interact badly with amyloid, causing its clumping and the production of hydrogen peroxide, a potent pro-oxidant neurotoxin.
This may help explain why the higher the levels of copper, the quicker Alzheimer’s disease may progress, particularly among people with high cholesterol levels.
This is what we think may be happening. As cholesterol and copper levels rise, cholesterol is incorporated into the nerve cell membrane, causing it to stiffen. The amyloid protein in the membrane detaches to form plaques, at which point, iron and copper generate neurotoxic free radicals. Inside the cell, similar havoc is created, and finally cholesterol-enriched diets can lead to nerve cell death, DNA damage, and blood-brain barrier disruption.
In conclusion, the present systematic review suggests that a diet rich in copper and iron might aggravate the detrimental effects of a high intake of cholesterol and saturated fat on the risk of developing Alzheimer’s disease. So, diets rich in saturated fat and deficient in antioxidants appear to promote the onset of the disease, while more plant-based diets would likely suppress its onset. There are compounds in plant foods that not only scavenge free radicals and prevent oxidative damage, but are also known to chelate, or bind up, metals, potentially making them additionally be protective against the onset of Alzheimer’s. Therefore, the practical implications could be to eat lots of fruits and vegetables, avoid copper-containing supplements, and avoid high intakes of saturated fat and excessive iron intake.
To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video. This is just an approximation of the audio contributed by Katie Schloer.
Please consider volunteering to help out on the site.
- M C Morris, D A Evans, C C Tangney, J L Bienias, J A Schneider, R S Wilson, P A Scherr. Dietary copper and high saturated and trans fat intakes associated with cognitive decline. Arch Neurol. 2006 Aug;63(8):1085-8.
- B N Ramesh, T S Rao, A Prakasam, K Sambamurti, K S Rao. Neuronutrition and Alzheimer's disease. J Alzheimers Dis. 2010;19(4):1123-39.
- R Squitti, F Bressi, P Pasqualetti, C Bonomini, R Ghidoni, G Binetti, E Cassetta, F Moffa, M Ventriglia, F Vernieri, P M Rossini. Longitudinal prognostic value of serum "free" copper in patients with Alzheimer disease. Neurology. 2009 Jan 6;72(1):50-5.
- M Ventriglia, S Bucossi, V Panetta, R Squitti. Copper in Alzheimer's disease: a meta-analysis of serum, plasma, and cerebrospinal fluid studies. J Alzheimers Dis. 2012;30(4):981-4.
- M Loef, H Walach. Copper and iron in Alzheimer's disease: a systematic review and its dietary implications. Br J Nutr. 2012 Jan;107(1):7-19.
- M A Lovell, J D Robertson, W J Teesdale, J L Campbell, W R Markesbery. Copper, iron and zinc in Alzheimer's disease senile plaques. J Neurol Sci. 1998 Jun 11;158(1):47-52.
- L M Sayre, G Perry, P L Harris, Y Liu, K A Schubert, M A Smith. In situ oxidative catalysis by neurofibrillary tangles and senile plaques in Alzheimer's disease: a central role for bound transition metals. J Neurochem. 2000 Jan;74(1):270-9.
- Y Manso, G Comes, J Hidalgo, A I Bush, P A Adlard. Copper modulation as a therapy for Alzheimer's disease? Int J Alzheimers Dis. 2011;2011:370345.
- L M Miller, Q Wang, T P Telivala, R J Smith, A Lanzirotti, J Miklossy. Synchrotron-based infrared and X-ray imaging shows focalized accumulation of Cu and Zn co-localized with beta-amyloid deposits in Alzheimer's disease. J Struct Biol. 2006 Jul;155(1):30-7.
- R Squitt, P M Rossini, E Cassetta, F Moffa, P Pasqualetti, M Cortesi, A Colloca, L Rossi, A Finazzi-Agró. d-penicillamine reduces serum oxidative stress in Alzheimer's disease patients. Eur J Clin Invest. 2002 Jan;32(1):51-9.
Images thanks to Geralt via Pixabay.
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Alzheimer’s Disease, Copper, and Saturated Fat
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Content URLDoctor's Note
Isn’t Alzheimer’s genetic? What about the “Alzheimer’s gene”? Just because we’ve been dealt some bad genetic cards doesn’t mean we can’t reshuffle the deck with diet. See The Alzheimer’s Gene: Controlling ApoE.
If the relationship between cholesterol and dementia is new to you, see Alzheimer’s and Atherosclerosis of the Brain and Cholesterol and Alzheimer’s disease for more.
What else can we do to protect our brain? Check out:
- Preventing Alzheimer’s with Lifestyle Changes
- Preventing Alzheimer’s Disease with Diet
- Preventing Alzheimer’s Disease with Plants
- Reducing Glycotoxin Intake to Prevent Alzheimer’s
- Higher Blood Pressure May Lead to Brain Shrinkage
- Benefits of Rosemary for Brain Function
- Should Vegans Take DHA to Preserve Brain Function?
It’s never too early to start eating healthier, because Alzheimer’s May Start Decades Before Diagnosis.
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