Ketamine and Psychedelic Drugs Change Structure of Neurons

Ketamine and Psychedelic Drugs Change Structure of Neurons

Summary: A new study reveals psychedelics increase dendrites, dendritic spines and synapses, while ketamine may promote neuroplasticity. The findings could help develop new treatments for anxiety, depression and other related disorders.

Source: UC Davis.

A team of scientists at the University of California, Davis is exploring how hallucinogenic drugs impact the structure and function of neurons — research that could lead to new treatments for depression, anxiety, and related disorders. In a paper published on June 12 in the journal Cell Reports, they demonstrate that a wide range of psychedelic drugs, including well-known compounds such as LSD and MDMA, increase the number of neuronal branches (dendrites), the density of small protrusions on these branches (dendritic spines), and the number of connections between neurons (synapses). These structural changes suggest that psychedelics are capable of repairing the circuits that are malfunctioning in mood and anxiety disorders.

“People have long assumed that psychedelics are capable of altering neuronal structure, but this is the first study that clearly and unambiguously supports that hypothesis. What is really exciting is that psychedelics seem to mirror the effects produced by ketamine,” said David Olson, assistant professor in the Departments of Chemistry and of Biochemistry and Molecular Medicine, who leads the research team.

Ketamine, an anesthetic, has been receiving a lot of attention lately because it produces rapid antidepressant effects in treatment-resistant populations, leading the U.S. Food and Drug Administration to fast-track clinical trials of two antidepressant drugs based on ketamine. The antidepressant properties of ketamine may stem from its tendency to promote neural plasticity — the ability of neurons to rewire their connections.

“The rapid effects of ketamine on mood and plasticity are truly astounding. The big question we were trying to answer was whether or not other compounds are capable of doing what ketamine does,” Olson said.

Psychedelics show similar effects to ketamine

Olson’s group has demonstrated that psychedelics mimic the effects of ketamine on neurons grown in a dish, and that these results extend to structural and electrical properties of neurons in animals. Rats treated with a single dose of DMT — a psychedelic compound found in the Amazonian herbal tea known as ayahuasca — showed an increase in the number of dendritic spines, similar to that seen with ketamine treatment. DMT itself is very short-lived in the rat: Most of the drug is eliminated within an hour. But the “rewiring” effects on the brain could be seen 24 hours later, demonstrating that these effects last for some time.

image shows neurons under psychedelics and ketamine

Behavioral studies also hint at the similarities between psychedelics and ketamine. In another recent paper published in ACS Chemical Neuroscience, Olson’s group showed that DMT treatment enabled rats to overcome a “fear response” to the memory of a mild electric shock. This test is considered to be a model of post-traumatic stress disorder (PTSD), and interestingly, ketamine produces the same effect. Recent clinical trials have shown that like ketamine, DMT-containing ayahuasca might have fast-acting effects in people with recurrent depression, Olson said.

These discoveries potentially open doors for the development of novel drugs to treat mood and anxiety disorders, Olson said. His team has proposed the term “psychoplastogen” to describe this new class of “plasticity-promoting” compounds.

“Ketamine is no longer our only option. Our work demonstrates that there are a number of distinct chemical scaffolds capable of promoting plasticity like ketamine, providing additional opportunities for medicinal chemists to develop safer and more effective alternatives,” Olson said.


Additional coauthors on the Cell Reports study are Calvin Ly, Alexandra Greb, Sina Soltanzadeh Zarandi, Lindsay Cameron, Jonathon Wong, Eden Barragan, Paige Wilson, Michael Paddy, Kassandra Ori-McKinney, Kyle Burbach, Megan Dennis, Alexander Sood, Whitney Duim, Kimberley McAllister, and John Gray.

Olson and Cameron were coauthors on the ACS Chemical Neuroscience paper along with Charlie Benson and Lee Dunlap.

Funding: The work was partly supported by grants from the National Institutes of Health.

Source: Andy Fell – UC Davis 
Publisher: Organized by
Image Source: image is credited to Calvin and Joanne Ly.
Original Research: Open access research for “Psychedelics Promote Structural and Functional Neural Plasticity” by Calvin Ly, Alexandra C. Greb, Lindsay P. Cameron, Jonathan M. Wong, Eden V. Barragan, Paige C. Wilson, Kyle F. Burbach, Sina Soltanzadeh Zarandi, Alexander Sood, Michael R. Paddy, Whitney C. Duim, Megan Y. Dennis, A. Kimberley McAllister, Kassandra M. Ori-McKenney, John A. Gray, and David E. Olson in Current Biology. Published April 6 2018

UC Davis “Ketamine and Psychedelic Drugs Change Structure of Neurons.” NeuroscienceNews. NeuroscienceNews, 12 June 2018.


Psychedelics Promote Structural and Functional Neural Plasticity

•Serotonergic psychedelics increase neuritogenesis, spinogenesis, and synaptogenesis
•Psychedelics promote plasticity via an evolutionarily conserved mechanism
•TrkB, mTOR, and 5-HT2A signaling underlie psychedelic-induced plasticity
•Noribogaine, but not ibogaine, is capable of promoting structural neural plasticity

Atrophy of neurons in the prefrontal cortex (PFC) plays a key role in the pathophysiology of depression and related disorders. The ability to promote both structural and functional plasticity in the PFC has been hypothesized to underlie the fast-acting antidepressant properties of the dissociative anesthetic ketamine. Here, we report that, like ketamine, serotonergic psychedelics are capable of robustly increasing neuritogenesis and/or spinogenesis both in vitro and in vivo. These changes in neuronal structure are accompanied by increased synapse number and function, as measured by fluorescence microscopy and electrophysiology. The structural changes induced by psychedelics appear to result from stimulation of the TrkB, mTOR, and 5-HT2A signaling pathways and could possibly explain the clinical effectiveness of these compounds. Our results underscore the therapeutic potential of psychedelics and, importantly, identify several lead scaffolds for medicinal chemistry efforts focused on developing plasticity-promoting compounds as safe, effective, and fast-acting treatments for depression and related disorders.

Domino Effect: Individual Damaged Neuron Types Cause Neurodegenerative Diseases

Domino Effect: Individual Damaged Neuron Types Cause Neurodegenerative Diseases

Summary: Age related neurodegeneration may be delayed by preventing oxidative damage in a few neuron types, researchers report.

Source: TUM.

If the sense of smell disappears, this can indicate a disease such as Alzheimer’s or Parkinson’s disease. However, unlike previously assumed, general degenerations in the nervous system do not play a leading role in the loss of the sense of smell with increasing age, but individual nerve cells or classes of nerves are decisive.

Some nerve cells (neurons) or neuron classes in the brain seem to age faster than others. For example, the loss of the sense of smell is one of the first clinical signs of natural aging. This can be accompanied by a neurodegenerative disease such as Alzheimer’s.

“Age is the major risk factor as to why people suffer from Alzheimer’s or Parkinson’s disease,” says Prof. Ilona Grunwald Kadow from the School of Life Sciences at the Technical University of Munich (TUM) – “only a small proportion of these diseases are due to known genetic reasons”. The question is why do some neurons age faster than others? Why are some more sensitive? And is the damage to certain types of neurons the reason why whole nerve networks no longer function properly?

A new study conducted under the direction of Prof. Grunwald Kadow (TUM) in collaboration with the groups of Prof. Julien Gagneur (TUM), Prof. Stephan Sigrist (Free University of Berlin) and Prof. Nicolas Gompel (LMU) using the genetic model organism of the fruit fly now shows how the olfactory capacity of these animals ages and how much this resembles the aging process in the human olfactory system. Like humans, the fruit fly loses its powers of smell as it ages. Several key genes and mechanisms were identified that contribute to this aging – associated degeneration.

Which neurons are affected?

In the next step, the scientists examined whether all or only specific neurons of the olfactory circuit are affected. The team found that some neurons are more sensitive than others and decline faster during aging.

They determined that oxidative stress alters primarily specific neuron types, causing the functioning of the entire neural network to gradually collapse. Oxidative stress results in too many reactive oxygen compounds in the cell or tissue, which can cause temporary or permanent damage and accelerated aging.

Interestingly, if the formation of these reactive oxygen compounds in only this type of neurons is prevented, this completely stopped the loss of sense of smell: Old flies sense odors just like their young conspecifics again. This suggests that age-related degeneration could be significantly delayed by preventing oxidative damage in only one or a few neuron types.

But what can reduce oxidative stress in its effect?

A trial with an antioxidant in the form of several weeks of resveratrol administration in younger flies showed that it can counteract oxidative stress, which develops during aging. This treatment appeared to protect the particularly sensitive neurons and thereby contributed to maintaining the function of the neurons connected to them within the neural network. In the elderly, such treatments might help to delay the onset of neurodegenerative diseases associated with ageing.

fruit fly

Another possible factor that could play a role in the aging process is the intestinal microbiome. It could be involved in the progression of Parkinson’s disease. Grunwald Kadow and her team have therefore also tested the effect of specific microbiota on olfactory ageing in fruit flies with the result that certain bacteria have a positive effect and slow down olfactory neurodegeneration.

According to Prof. Grunwald Kadow, these findings and further ongoing experiments in the fruit fly model can help to pave the way for more targeted and new treatments and therapy routes, in which, among other things, drug or microbiota administration would be combined with each other.


Source: Ilona Grunwald Kadow – TUM
Publisher: Organized by
Image Source: image is credited to Ariane Böhm / TUM.
Original Research: Open access research in eLife.

TUM “Domino Effect: Individual Damaged Neuron Types Cause Neurodegenerative Diseases.” NeuroscienceNews. NeuroscienceNews, 1 March 2018.


Inhibition of oxidative stress in cholinergic projection neurons fully rescues aging-associated olfactory circuit degeneration in Drosophila

Loss of the sense of smell is among the first signs of natural aging and neurodegenerative diseases such as Alzheimer’s and Parkinson’s. Cellular and molecular mechanisms promoting this smell loss are not understood. Here, we show that Drosophila melanogaster also loses olfaction before vision with age. Within the olfactory circuit, cholinergic projection neurons show a reduced odor response accompanied by a defect in axonal integrity and reduction in synaptic marker proteins. Using behavioral functional screening, we pinpoint that expression of the mitochondrial reactive oxygen scavenger SOD2 in cholinergic projection neurons is necessary and sufficient to prevent smell degeneration in aging flies. Together, our data suggest that oxidative stress induced axonal degeneration in a single class of neurons drives the functional decline of an entire neural network and the behavior it controls. Given the important role of the cholinergic system in neurodegeneration, the fly olfactory system could be a useful model for the identification of drug targets.

Sugar , transfat and poor lifestyle – causes of American death in last 35 years

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Smoking , alcohol, meds/drugs and poor lifestyle (absence of exercise, clean water, air and whole foods) contributed to poor health in the southern part of the United States.

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Caring for clients with anxiety disorders, the brain in the gut


Most geriatric and family practice doctors prescribe anti-anxiety and anti-depressent meds from Gabapentin to other narcotics with serious side effects as exhibit more Parkinson’s and Alzheimer’s disease.

One client of mine told her doctor that she does not need anti-depressant med and only need to sleep more or a low dose of a sleeping aid pill. She took melatonin from her own research, an anti-aging supplement.

Many seniors in care homes or living alone in bay area homes are set on their ways. They use the same recliner chair, bed, watch the same TV classic show, listen to the same music and so on. They do not want a lot of changes in their daily routines.

At times, when they could not sleep, they may have constipation and disturbed digestive system (see the section below on – The brain in the gut).

So when caring for seniors, ensure that changes are introduced slowly in their daily routines only when necessary and with their full cooperation and approval. Ensure that they are in a warm environment, cared for with proper meals and changed dry clothes, fed warm food, and just observing their daily needs and assist them with care and love.

Most of my caregivers at Motherhealth caregivers do bring love and care to be effective in their caregiving. They take these seniors as if they are part of their family.

The Enteric Nervous System – The Brain in the Gut

The gut has a mind of its own, the “enteric nervous system”. Just like the larger brain in the head, researchers say, this system sends and receives impulses, records experiences and respond to emotions. Its nerve cells are bathed and influenced by the same neurotransmitters. The gut can upset the brain just as the brain can upset the gut.

The gut’s brain or the “enteric nervous system” is located in the sheaths of tissue lining the esophagus, stomach, small intestine and colon. Considered a single entity, it is a network of neurons, neurotransmitters and proteins that zap messages between neurons, support cells like those found in the brain proper and a complex circuitry that enables it to act independently, learn, remember and, as the saying goes, produce gut feelings.

The gut’s brain is reported to play a major role in human happiness and misery. Many gastrointestinal disorders like colitis and irritable bowel syndrome originate from problems within the gut’s brain. Also, it is now known that most ulcers are caused by a bacterium not by hidden anger at one’s mother.

Details of how the enteric nervous system mirrors the central nervous system have been emerging in recent years, according to Dr. Michael Gershon, professor of anatomy and cell biology at Columbia-Presbyterian Medical Center in New York. He is one of the founders of a new field of medicine called “neurogastroenterology.”

The gut contains 100 million neurons – more than the spinal cord. Major neurotransmitters like serotonin, dopamine, glutamate, norephinephrine and nitric oxide are in the gut. Also two dozen small brain proteins, called neuropeptides are there along with the major cells of the immune system. Enkephalins (a member of the endorphins family) are also in the gut. The gut also is a rich source of benzodiazepines – the family of psychoactive chemicals that includes such ever popular drugs as valium and xanax.

In evolutionary terms, it makes sense that the body has two brains, said Dr. David Wingate, a professor of gastrointestinal science at the University of London and a consultant at Royal London Hospital. “The first nervous systems were in tubular animals that stuck to rocks and waited for food to pass by,” according to Dr. Wingate. The limbic system is often referred to as the “reptile brain.” “As life evolved, animals needed a more complex brain for finding food and sex and so developed a central nervous system. But the gut’s nervous system was too important to put inside the newborn head with long connections going down to the body,” says Wingate. Offspring need to eat and digest food at birth. Therefore, nature seems to have preserved the enteric nervous system as an independent circuit inside higher animals. It is only loosely connected to the central nervous system and can mostly function alone, without instructions from topside.

This is indeed the picture seen by developmental biologists. A clump of tissue called the neural crest forms early in embryo genesis. One section turns into the central nervous system. Another piece migrates to become the enteric nervous system. According to Dr. Gershon, it is only later that the two systems are connected via a cable called the vagus nerve.

The brain sends signals to the gut by talking to a small number of “command neurons,” which in turn send signals to gut interneurons that carry messages up and down the pike. Both command neurons and interneurons are spread throughout two layers of gut tissue called the “myenteric plexus and the submuscosal plexus.” Command neurons control the pattern of activity in the gut. The vagus nerve only alters the volume by changing its rates of firing.

The plexuses also contain glial cells that nourish neurons, mast cells involved in immune responses, and a “blood brain barrier” that keeps harmful substances away from important neurons. They have sensors for sugar, protein, acidity and other chemical factors that might monitor the progress of digestions, determining how the gut mixes and propels its contents.

As light is shed on the circuitry between the two brains, researchers are beginning to understand why people act and feel the way they do. When the central brain encounters a frightening situation, it releases stress hormones that prepare the body to fight or flee. The stomach contains many sensory nerves that are stimulated by this chemical surge – hence the “butterflies.” On the battlefield, the higher brain tells the gut brain to shut down. A frightened running animal does not stop to defecate, according to Dr. Gershon.

Fear also causes the vagus nerve to “turn up the volume” on serotonin circuits in the gut. Thus over stimulated, the gut goes into higher gear and diarrhea results. Similarly, people sometimes “choke” with emotion. When nerves in the esophagus are highly stimulated, people have trouble swallowing.

Even the so-called “Maalox moment” of advertising can be explained by the interaction of the two brains, according to Dr. Jackie D. Wood, chairman of the department of physiology at Ohio State University in Columbus, Ohio. Stress signals from the head’s brain can alter nerve function between the stomach and esophagus, resulting in heartburn.

In cases of extreme stress, Dr. Wood say that the higher brain seems to protect the gut by sending signals to immunological mast cells in the plexus. The mast cells secrete histamine, prostaglandin and other agents that help produce inflammation. This is protective. By inflaming the gut, the brain is priming the gut for surveillance. If the barrier breaks then the gut is ready to do repairs. Unfortunately, the chemicals that get released also cause diarrhea and cramping.

There also is an interaction between the gut brain and drugs. According to Dr. Gershon, “when you make a drug to have psychic effects on the brain, it’s very likely to have an effect on the gut that you didn’t think about.” He also believes that some drugs developed for the brain could have uses in the gut. For example, the gut is loaded with the neurotransmitter serotonin. According to Gershon, when pressure receptors in the gut’s lining are stimulated, serotonin is released and starts the reflexive motion of peristalsis. A quarter of the people taking Prozac or similar antidepressants have gastrointestinal problems like nausea, diarrhea and constipation. These drugs act on serotonin, preventing its uptake by target cells so that it remains more abundant in the central nervous system.

Gershon also is conducting a study of the side effects of Prozac on the gut. Prozac in small doses can treat chronic constipation. Prozac in larger doses can cause constipation – where the colon actually freezes up. Moreover, because Prozac stimulates sensory nerves, it also can cause nausea.

Some antibiotics like erythromycin act on gut receptors to produce ascillations. People experience cramps and nausea. Drugs like morphine and heroin attach to the gut’s opiate receptors, producing constipation. Both brains can be addicted to opiates.

Victims of Alzheimer’s and Parkinson’s diseases suffer from constipation. The nerves in their gut are as sick as the nerve cells in their brains. Just as the central brain affects the gut, the gut’s brain can talk back to the head. Most of the gut sensations that enter conscious awareness are negative things like pain and bloatedness.

The question has been raised: Why does the human gut contain receptors for benzodiazepine, a drug that relieves anxiety? This suggests that the body produces its own internal source of the drug. According to Dr. Anthony Basile, a neurochemist in the Neuroscience Laboratory at the National Institutes of Health in Bethesda, MD, an Italian scientist made a startling discovery. Patients with liver failure fall into a deep coma. The coma can be reversed, in minutes, by giving the patient a drug that blocks benzodiazepine. When the liver fails, substances usually broken down by the liver get to the brain. Some are bad, like ammonia and mercaptan, which are “smelly compounds that skunks spray on you,” says Dr. Basile. But a series of compounds are also identical to benzodiazepine. “We don’t know if they come from the gut itself, from bacteria in the gut or from food, but when the liver fails, the gut’s benzodiazepine goes straight to the brain, knocking the patient unconscious, says Dr. Basile.

The payoff for exploring gut and head brain interactions is enormous, according to Dr. Wood. Many people are allergic to certain foods like shellfish. This is because mast cells in the gut mysteriously become sensitized to antigens in the food. The next time the antigen shows up in the gut, the mast cells call up a program, releasing chemical modulators that try to eliminate the threat. The allergic person gets diarrhea and cramps.

Many autoimmune diseases like Krohn’s disease and ulcerative colitis may involve the gut’s brain, according to Dr. Wood. The consequences can be horrible, as in “Chagas disease,” which is caused by a parasite found in South America. Those infected develop an autoimmune response to neurons in their gut. Their immune systems slowly destroy their own gut neurons. When enough neurons die, the intestines literally explode.

A big question remains. Can the gut’s brain learn? Does it “think” for itself? Dr. Gershon tells a story about an old Army sergeant, a male nurse in charge of a group of paraplegics. With their lower spinal cords destroyed, the patients would get impacted. “At 10am every morning, the patients got enemas. Then the sergeant was rotated off the ward. His replacement decided to give enemas only after compactions occurred. But at 10 the next morning everyone on the ward had a bowel movement at the same time, without enemas.” Had the sergeant trained those colons?

The human gut has long been seen as a repository of good and bad feelings. Perhaps emotional states from the head’s brain are mirrored in the gut’s brain, where they are felt by those who pay attention to them.
Reference: Taken from “A contemporary view of selected subjects from the pages of The New York Times, January 23, 1996. Printed in Themes of the Times: General Psychology, Fall 1996. Distributed Exclusively by Prentice-Hall Publishing Company.


Motherhealth Inc Caregivers for bay area homebound seniors 408-854-1883



General Comments:

Since older adults are set on their ways, it is also difficult to change their perspectives and political views. For Bernie Sanders to win, all those 18 to 35 yrs old must vote with full research of political issues and truthful news.



Copper Deficiency May Underlie Osteoporosis, Anemia and Neurodegenerative Disorders

Despite their obviously different appearances, osteoporosis, anemia, neurodegenerative disorders, cardiovascular disease, and impaired cellular immunity may all be manifestations of chronic copper deficiency, an often-overlooked nutritional problem that is more common than many doctors realize.

Copper plays a key role in myelination of neurons, neutrophil activation, collagen synthesis, hemoglobin formation, and endogenous antioxidant synthesis. “It is a mineral that is greatly under-recognized and under-utilized,” said Ron Grabowski, RD, DC, Professor of Clinical Practice at Texas Chiropractic College, Houston, and Director of Research for the American Chiropractic Association’s Council on Nutrition.

Deficiency can manifest in many different ways including seizures and neurological problems, poor temperature control, connective tissue degeneration, bone mineral loss, pallor, anemia, and poor hair and skin quality. Several recent studies suggest that in addition to the well-recognized neural and hematologic sequelae, copper deficiency also has a role in diabetes and cardiovascular disease.

Copper excess can be problematic too, causing liver damage, neruologic problems, chondroplasia and skeletal abnormalities. But given the way most Americans eat, and the wide use of medications that interfere with copper uptake, deficiency is vastly more common than excess.

Dr. Grabowski contends that many patients diagnosed with iron-deficiency anemia, early-stage multiple sclerosis, and various immunodeficiency disorders actually have unrecognized copper deficiency. Fortunately, this is correctable via supplementation. It may take time, and it requires careful monitoring, but restoring healthy copper levels can greatly improve patients’ health status.

Modest Requirements, Often Unmet

“Our daily need for copper is actually quite modest. For most adults, 1.5–3.0 mg/d is sufficient for good health. That doesn’t sound like much, but more than 30% of people on a typical American diet are not even getting 1 mg per day. Another third of the population is not even reaching the minimum daily allowance (900 mcg),” said Dr. Grabowski.

The primary dietary sources of copper are shellfish (oysters, mussels, clams, lobster, crab, squid) and organ meats (beef liver, kidneys and heart). With a few exceptions like bananas, grapes, tomatoes, avocados and sweet potatoes, most produce lacks copper. Fortunately for vegetarians, nuts (cashews, filberts, macadamias, pecans, almonds, pistachios) and some legumes (peanuts, navy beans, lentils, soy) are good copper sources.

The rising prevalence of copper deficiency is due in part to the fact that many people are simply not eating as many copper-rich foods as they once did. The high prevalence of digestive disorders, and widespread use of drugs and supplements that deplete or interfere with copper are the other major factors.

Easily Absorbed, Easily Blocked

Copper absorption occurs in the upper portion of the small intestine. In people with a healthy digestive tract, it is absorbed very efficiently compared to other minerals. Any disease that affects digestion may interfere with copper absorption or promote copper loss in the lower GI tract. Think about deficiency in anyone with Crohn’s disease, irritable bowel or any other inflammatory GI problem.

Proper copper absorption requires ample stomach acid. Consequently, drugs that block acid secretion impede copper uptake. This includes all proton pump inhibitors and H2 blockers. “In my practice. I see so much copper deficiency and also B12 deficiency in people on these medications,” Dr. Grabowski told Holistic Primary Care.

High fructose consumption increases copper excretion in urine, and also increases demand for superoxide dismutase (SOD), an endogenous antioxidant the formation of which requires copper. “This is a big problem because high-fructose corn syrup is ubiquitous in the American food stream.”

Be aware that whole grains contain phytates that bind copper, zinc and other minerals. This is not to suggest that people shouldn’t eat whole grains, but they shouldn’t take minerals at the same time. “People often do not understand that it matters when and with what they take their supplements. Don’t take them with whole grain breads or brown rice; you won’t get the benefits of the minerals. We need to harmonize supplements with our diets.”

Copper & Zinc: A Dynamic Balance

Much like calcium and magnesium, copper and zinc have a sometimes synergistic, sometimes antagonistic relationship. Both are involved in a host of enzymatic and metabolic reactions. When the balance of zinc and copper is right, these processes proceed well. But, like calcium and magnesium, too much of one diminishes the other. Excesses of either zinc or copper can cause problems.

The first report of a pathologic zinc-induced copper deficiency came out 20 years ago. Mayo Clinic physicians described an individual who took high daily doses of zinc for 10 months. The patient presented with hypochromic-microcytic anemia, leukopenia and neutropenia. When iron failed to resolve the abnormalities, the physicians dug deeper and found extreme copper deficiency, correctable only with intravenous infusion of 10 mg cupric chloride for 5 days (Hoffman HH, 2nd, et al. Gastroenterology. 1988; 94(2): 508–512).

Zinc excess with copper deficiency is common, said Dr. Grabowski. “A zinc to copper ratio of 30:1 will really force people into serious copper deficiency. Some researchers say the problem begins at 10:1. When patients show me their multivitamins and I see 30 mg of zinc to 1 mg of copper, it makes me very, very nervous. The supplements they’re taking to improve their health may actually be inducing a copper deficiency that increases their risk of disease.”

Self-Induced Deficiencies

During the winter cold and flu season, many people unwittingly induce copper deficiency by gobbling zinc lozenges and heavy doses of vitamin C, believing this will enhance immunity and increase antioxidant capacity. But both zinc and vitamin C compete with or interfere with copper absorption. Because copper is essential for production and activation of neutrophils—the first line of defense against pathogens—excess zinc and vitamin C may actually render people more susceptible to the very ailments they’re seeking to avoid.

Two recent papers review the role of copper and other trace minerals in both cellular and humoral immunity. Maggini and colleagues illustrate the vicious cycle occurring when micronutrient deficiencies suppress T-cell mediated and adaptive antibody responses, thus increasing susceptibility to infection, which, in turn, increases micronutrient loss, interferes with metabolism of many nutrients, and reduces nutrient intake (Maggini S, et al. Br J Nutr. 2007; 98(Suppl 1): S29–S35).

In the same journal, Munoz and colleagues point out that careful micronutrient supplementation can boost immune function and reduce infection susceptibility. This is particularly important in the elderly, because vaccinations against respiratory infections are only partially effective (Munoz C, et al. Br J Nutr. 2007; 98(Suppl 1): S24–S28).

Copper is essential for synthesis of one form of superoxide dismutase (SOD), and anything that reduces copper also reduces SOD, diminishing overall antioxidant capacity. People who take high dose vitamin C to boost their antioxidants may be surprised to learn they’re actually inducing the opposite effect. Anything over 1,000 mg of vitamin C per day interferes with copper.

The best way to increase overall antioxidant capacity is by increasing intake of antioxidant rich foods, rather than amplifying one antioxidant vitamin out of the many, said Dr. Grabowski.

Iron, Copper & Anemia

Many doctors reflexively prescribe iron to any patient with signs and symptoms of anemia without actually testing to see if iron is deficient. According to Dr. Grabowski, many cases of alleged iron-deficiency anemia are actually due to copper deficiency. Like iron, copper is involved in hemoglobin formation. Suspect low copper if a patient’s anemia does not resolve with additional iron.

“Copper deficiency can present exactly like iron deficiency and you’ll never know the difference unless you test for it,” he said. There is one other give-away, though: low neutrophil count. Copper is essential for neutrophil production and phagocytic activation. Copper-deficient people show low neutrophil counts, a feature not seen in iron deficiency anemia.

Of course, someone may be deficient in both iron and copper. “Copper has a part to play in iron uptake in the GI tract. If copper is low, iron absorption tends to be low as well.”

In a just-published paper, Cleveland Clinic hematologists show hypocupremia as a cause in 3 cases of cytopenia and bone marrow failure, and suggest it should be added to the differential diagnosis of bone marrow failure syndromes, including myelodysplasia (Haddad AS, et al. Haematologica. 2008; 93(1): 1–5).

This corroborates a 5-case series from Washington University a few months earlier that also points to copper deficiency as a cause of myelodysplasia. In all 5 cases, the problem resolved with copper supplementation (Fong T, et al. Haematologica. 2007; 92(10): 1429–1430).

Copper & CVD

Several recent papers point to lack of copper as a risk factor for cardiovascular disease, but the picture is complex. University of Turin researchers looked at the relationship of dietary copper to a host of metabolic variables in 1,197 individuals. They found clear inverse relationships between copper and diastolic blood pressure, total cholesterol, LDL, blood glucose, uric acid, and total antioxidant status, a clearly high-risk profile. There were linear correlations between copper and both C-reactive protein and nitrotyrosine, a marker of oxidative stress (Bo S, et al. J Nutr. 2008; 138(2): 305–310).

The authors note that, “Marginal copper deficiency is associated with an unfavorable metabolic pattern, but copper supplementation might not be recommended in view of its association with inflammation and markers of oxidative stress.”

In a new review article, Dr. Hamid Aliabadi of the Duke University Department of Neurosurgery notes that, “Dietary copper deficiency has been shown to cause a variety of metabolic changes, including hypercholesterolemia, hypertriglyceridemia, hypertension, and glucose intolerance” (Alibadi H. Med Hypotheses. 2008; epub ahead of print).

At the other end of the spectrum, excess copper and iron may contribute to acute myocardial infarction. Researchers at the University of Sindh, Pakistan studied serum and hair levels of zinc, copper and iron in samples from 130 MI patients and 61 healthy age-matched controls. They found consistently low zinc but high iron and copper in the MI patients, particularly those with second and third MIs, and those who died from MI versus those who survived (Kazi TG, et al. Clin Chim Acta. 2008; 389(1–2): 114–119).

Of Copper & Collagen

When people think about osteoporosis, they immediately think of calcium and vitamin D. Both are important for healthy bone. But copper is just as important, said Dr. Grabowski. It is essential for formation of the collagen component in bone, which is necessary for maintaining bone mineral density (BMD).

“I’ve had people come to me and say that they just had a BMD test done and they were surprised it was low, because they’re taking vitamin D and calcium/magnesium. I’ll do the tests, and yes, vitamin D, calcium and magnesium are fine. But then we look at copper, and it is very low. By supplementing with copper we may be able to improve BMD by improving bone collagen formation.”

As a chiropractor, Dr. Grabowski sees many patients with musculoskeletal injuries. “They’re taking all sorts of things: ibuprofen, Aleve (naproxen), high-dose vitamin C. None of these things will help create new collagen. But copper will.”

Some people take high-dose vitamin C following physical injuries, believing it speeds tissue healing. But because copper is a key factor in collagen and elastin formation, and vitamin C interferes with copper, the excess vitamin may impede rather than facilitate wound healing.

Copper Deficiency & Demyelination: An MS Mimic?

In addition to collagen formation, copper plays a central role in myelin formation. Prolonged deficiency can result in demyelination and neurodegeneration, which shows up as spastic gait, optic nerve inflammation, peripheral neuropathy, and fatigue. In many ways, it is a near-perfect mimic of multiple sclerosis.

According to Dr. Neeraj Kumar, of the Department of Neurology at the Mayo Clinic, Rochester, MN, unrecognized copper deficiency is a common cause of idiopathic myelopathy in adults. “The clinical picture bears striking similarities to the syndrome of subacute combined degeneration associated with vitamin B12 deficiency,” wrote Dr. Kumar, summing up a study of 13 Mayo Clinic patients (Kumar N, et al. Neurology. 2004; 13; 63(1): 33–39).

All had polyneuropathies, with pronounced gait difficulty and sensory ataxia. In addition to measurable copper deficiencies, 7 had high or high-normal zinc. Copper supplements restored circulating levels to normal or near normal in 7 of 12 evaluable patients; parenteral supplementation restored another 3. In all cases, repletion prevented further neurodegeneration; improvement of neurological function was variable.

Copper supplementation fairly easily reverses anemia and neutropenia, but neurologic deficits may be less responsive. “Improvement, when it occurs, is often subjective and preferentially involves sensory symptoms,” he noted (Kumar N. Mayo Clin Proc. 2006 Oct; 81(10): 1371–1384).

An earlier paper by University of Oklahoma neurologists details two cases of myelopathy, neutropenia and anemia linked to copper deficiency and zinc excess (Prodan CI, et al. Neurology. 2002; 12; 59(9): 1453–1456). In both cases, “Hematologic recovery followed copper supplementation, both initially and after relapse off copper therapy, while serum zinc levels remained high and the neurologic abnormalities only stabilized.”

Dr. Grabowski believes many patients diagnosed with MS actually have copper deficiencies. The idea is not so far-fetched. Neurologists have long recognized the value of vitamin B12 for MS, because the vitamin plays a key role in myelination. Most routinely check B12 in patients suspected of having MS. They tend to overlook copper, though it is just as important in myelination.

“It’s not that copper deficiency causes MS. It’s that copper deficiency causes demyelination, which can mimic or be mis-diagnosed as MS,” Dr. Grabowski explained. “We don’t really know if copper deficiency is involved in MS, or if giving copper to MS patients will help. But it is certainly worth thinking about.”

Testing for and Treating Copper Deficiency

Copper supplementation requires careful monitoring. Patients should not try it by themselves, as it is easy to over-do it on copper, thus interfering with zinc.

Dr. Grabowski has found that serum testing for copper is not very reliable. Methods and norms often vary from lab to lab, as was pointed out in a recent study from the University of Ipswitch, UK (Twomey PJ, et al. Int J Clin Pract. 2007; epub ahead of print). Further, serum measurements don’t show the extent to which copper is actually doing its job at the cellular level.

He told Holistic Primary Care that he much prefers the intracellular copper analysis recently introduced by SpectraCell Laboratories ( This test shows copper levels in lymphocytes, and gives a much more accurate picture of how the mineral is taken up and utilized by cells.

Like all of SpectraCell’s tests, the copper assay is based on the fact lymphocytes are the longest-lived cells in circulation, with a typical lifetime of 120 days or more. By way of comparison, neutrophils typically live for several hours to 13 days; platelets have a lifespan of 3–7 days; red blood cells live for 90–100 days. The nutrient content of lymphocytes provides a sort of time-elapsed composite picture of a patient’s nutritional status over the last several months.

SpectraCell incorporates the copper test into its comprehensive Functional Intracellular Assessment (FIA) panel, which gives a broad survey of micronutrients and trace minerals. The FIA enables doctors to detect both deficiencies and excesses of various nutrients, and to track them over time. One can use it to assess the impact of supplementation not only on the target nutrient but on all other nutrients with which it interacts. In the case of minerals, the FIA panel details copper levels as well as iron, zinc, and other trace minerals. So one can see whether increasing copper is changing these others.

“When dealing with copper deficiencies, you need to look very closely at zinc. If I give copper supplements to try and correct a deficiency, I can end up throwing the zinc level way off. I have to test them both periodically,” said Dr. Grabowski. “It’s a balancing act, and one can go back and forth for long periods of time, increasing copper but lowering zinc, then increasing zinc but lowering copper, before one gets it right.”

Connie’s comments: White hair may signify lack of copper. You find copper in iron-rich foods.  Up your zinc intake to increase absorption of copper. Add vinegar in salad to up mineral absorption. If you have genetic predisposition to the above, protect you and family with Index Universal Life Insurance with living benefits. Call 408-854-1883


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