Parasites and groin pain

What are parasites?

Parasites are animals or plants which must live on or in another plant or animal to survive (go on living). There are several parasites in the environment and when they get into a person’s body, his/her health can be affected. Some parasites enter the body by way of contaminated food or water and some live on the skin and the hair. Examples of parasites include:

  • stomach and gut worms (threadworm, hookworm)
  • skin mites (scabies)
  • hair and body lice (head lice and crab lice)
  • protozoa (Giardia)

Most of these parasites cannot be seen without the help of a magnifying glass. Like a microscope, this is another kind of special instrument which makes things look bigger than they really are. Some adult worms are big enough to see without the help of a magnifying glass.
It is often easy to see where parasites have been, such as when they cause rashes on the skin.

Protozoa

Protozoa are tiny single-celled animals which can move about on their own. Protozoa are so small they can only be seen with the help of a microscope and only some of them cause disease in humans. An example of one of these is Giardia lamblia.
Fig.  1.10: Giardia, a disease-causing protozoan
Fig. 1.10: Giardia, a disease-causing protozoan.

Worms

Parasitic worms are small animals which can live inside the body. Their eggs are taken into the body, usually by swallowing. The worms then hatch out of the eggs and live in the body. Some types of worm larvae (young worms) can also burrow their way into the body through the skin.
When the worms live in the body they can cause sickness. They may get into the stomach and gut and eat the food before the body has digested it. This means that the body does not get enough nourishment. Sometimes the worms will find their way into other parts of the body, such as the blood or liver. When this happens these parts of the body may not work properly.
Fig.  1.11: Worms
Fig. 1.11: Worms

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Mites and lice

These are small animals which affect the skin and hair of the body. They cause the skin, especially the scalp, to become very itchy.
Fig.  1.12: Lice
Fig. 1.12: Lice.

5.2 Diseases caused by parasites

Common diseases in Indigenous communities which are caused by parasites are described below.

Giardiasis

This is a parasitic infection caused by the protozoan Giardia lamblia getting into the small intestine. Giardia is a single celled animal which is so small it can only be seen with the help of a microscope.

This disease can occur anywhere in Australia and is very common in Indigenous communities. The symptoms (signs) of this disease are:

  • very severe or chronic (long-lasting) diarrhoea
  • stomach cramps and pain
  • fatigue (tiredness)
  • weakness
  • weight loss

There is special medicine which can be taken to get rid of Giardia from the body.

Hookworm infection

This is a widespread disease in warm, tropical and sub-tropical places, especially where sewage disposal is inadequate. It is common in the Kimberley and other parts of tropical northern Australia.

Hookworm is a parasitic worm. The adult worm is about 1 cm in length and is about the thickness of a pin.
The worms suck blood from the human host. The disease becomes serious when there are many worms in the intestine sucking blood from the host. When this happens, the host loses too much blood which contains the body’s important nutrients (nourishing food).

This can cause:

  • the body to become anaemic (pale and weak)
  • fever
  • diarrhoea or constipation

In extreme cases hookworm infestation can stop the person from thinking and moving properly. It can also slow down children’s growth.

To get rid of these worms from the body, the person must be treated with special medicine.

Threadworm (or pinworm) infection

This is a disease which can occur in any part of Australia. It is another disease which is caused by a parasitic worm which lives in large numbers in the human intestine.

Threadworm causes anal (bum hole) itching. This can lead to disturbed sleep and can cause people to become grumpy. Excessive scratching can lead to broken skin which may become infected (pus sores).

Threadworms are easily passed from one person to another and frequently whole families or groups become infected.

There is also special medicine to get rid of these worms from the body.

Dwarf tapeworm infection

Dwarf tapeworm is the most common human tapeworm in Australia. It is a parasitic infection of the stomach and intestine.
Infection with this tapeworm can cause:

  • diarrhoea
  • stomach pain
  • weight loss
  • weakness

There is special medicine which will get rid of these worms from the body.

Scabies infection

This is a skin disease caused by a tiny animal which is called a mite. It is usually about 0.3 mm long. The female burrows into the skin to lay her eggs and this irritates the skin and makes it very itchy. As a result, the person scratches the skin a lot.
If the skin breaks as a result of the scratching, germs can enter the break in the skin and cause an infection. When treating the infection it is important to also get rid of the mites or lice; otherwise the irritations will continue and cause more infections.
To get rid of scabies a specially medicated lotion is used.

Pediculosis (head lice infection)

These tiny bloodsucking animals live their whole life on a person’s head. The lice stab an opening through the skin and suck up blood from the host. This causes irritation. The resulting scratching can lead to broken skin which can become infected.
Special shampoos are used to get rid of head lice. The eggs which are stuck to the hair need to be removed with a special fine-toothed comb.

5.3 Methods on how some important parasites are spread

Giardia

Giardia occur in the intestines of humans. When Giardia are inside the body they can move about quite easily, but they often leave the body as tiny egg-like cysts in faeces.

Infection happens when these cysts are taken back into the body of someone who does not have Giardia in their intestines. Once inside the intestine they become mobile (able to move) again and start to reproduce themselves by dividing and redividing.

Giardia cysts can be passed:

  • directly by the faecal/oral route from an infected person to one who is not infected
  • indirectly by taking in the cysts in contaminated water or food when eating or drinking

Hookworm

When hookworms get inside people, they lay their eggs inside the person’s intestines. These eggs get into the soil or water when infected human faeces has been left on the ground or from faulty or broken sewage systems.

Tiny larvae (young worms) will hatch out. If the soil is wet the larvae will develop to a stage where they can infect people. They can survive in wet soil for several weeks and are able to burrow through unbroken skin. This happens when people’s skin comes into contact with water, soil or faeces which is infected with hookworm larvae.

People can become infected with hookworm directly by the ingestion of larvae or by larvae burrowing through the skin.

People in the tropical parts of northern Australia who walk around in contaminated wet places without shoes are very likely to get infected.

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Inside the body the larvae travel through the blood stream to the lungs where they are coughed up and then swallowed. They finally reach the intestines where they develop into adult worms. Adult worms are able to attach themselves to the walls of the intestines. They have hooks around the mouth which allow them to do this. They live there and suck blood from the human host.
Fig.  1.14: How hookworm gets into the body and where it lives in the body
Fig. 1.14: How hookworm gets into the body and where it lives in the body.

Threadworm (or pinworm)

These worms look like tiny white threads and live in the intestine. The female worm will travel to the anal opening to lay its eggs on the skin around the anus. It is this activity which causes the itching. The eggs and the worms leave the body in faeces. The eggs hatch when they are taken into the same or another person’s intestine.

The worms or their eggs can be passed from one person to another:

  • directly through the faecal/oral route from an infected person to one who is not infected
  • indirectly through contact with contaminated clothing, bedding or food

Dwarf tapeworm

The dwarf tapeworm occurs in the stomach and intestines of humans. The adult tapeworm lays its eggs in the body. The eggs are passed out of the body in the faeces. If these eggs are ingested by other people indirectly or directly, the eggs will hatch in the intestine. The immature worm goes through two further stages of development before it becomes an adult.

Humans become infected with dwarf tapeworms:

  • directly by touching the mouth with fingers which are contaminated with faeces containing the egg
  • indirectly by ingesting eggs in contaminated food or water, or by swallowing an insect which has ingested eggs which have then hatched into larvae inside the insect

Roundworms

Roundworms are nematodes and are found in northern parts of Australia and in many tropical countries. Strongyloides stercoralis is a roundworm which causes a life threatening disease called Strongyloidiasis.

People can become infected through contact with soil contaminated by faeces containing the parasite.

People can often get sick where hygiene and sanitation are poor. Infection can be detected with a special blood test and people can be cured with special tablets.

Scabies

These small animals are a type of mite. The female burrows into the skin where it lays its eggs. When the mites hatch they climb out onto the surface of the skin and then enter hair follicles. These are the small openings in the skin which hold the hair roots. The young mites grow into adults in the hair follicles. They then climb out and mate and start the process all over again. It is the burrowing activity of the mites which causes the skin irritation associated with scabies.
Fig.  1.15: Scabies' life cycle
Fig. 1.15: Scabies’ life cycle.

Scabies prefer to live in certain places in the body. These are body creases such as the backs of the knee and elbow and in the armpit and groin.
Fig.  1.16: Scabies rash on the body
Fig. 1.16: Scabies rash on the body.

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Scabies can be passed from an infected person to an uninfected person by:

  • direct contact; or
  • indirect contact with contaminated clothing or bedding. Infection happens more frequently when people live in overcrowded conditions

 

Head lice

Adult lice live their whole lives in the hair of a person’s head. The lice stab openings in the skin to suck blood. The eggs of the head lice, which are also called nits, are glued to the hairs on the person’s head. The nits are about 1 mm in size and are whitish in colour. They take about a week to hatch.

The lice can be passed:

  • directly from person-to-person, such as when small children play or sleep together; or
  • indirectly through the sharing of infected combs, brushes and hats

While head lice can be killed with special shampoos, the nits are difficult to kill in this way. For this reason, nits must be removed with a special fine toothed comb.

Vitamin A and zinc

Scientists found that vitamin A and zinc supplementation was associated with distinct parasite-specific health outcomes. Vitamin A plus zinc reduces G. lamblia incidence, whereas zinc supplementation increases A. lumbricoides incidence but decreases E. histolytica-associated diarrhea.

Supplementation of B-complex vitamins, vitamin C, vitamin E and selenium reduce the risk of infection by invasive diarrheal pathogens.

Supplementation of selenium and copper may help the control of H. contortus.

Zinc, copper and magnesium to fight diabetes and neurodegeneration

Dear GF with diabetes,

If you are not 12,000 miles away from me, I will bring sesame seeds, pumpkin seeds and cashew (raw and unsalted). I will massage you with special oils. Take care, I hope to see you soon.

Connie

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Zinc and Diabetes – Diabetes Self-Management

https://www.diabetesselfmanagement.com › Blog › Amy Campbell

Mar 26, 2007 – Zinc is also necessary for the formation of insulin in the pancreas’s beta cells. For these reasons, researchers have looked at the role of zinc supplementation in the prevention and treatment of Type 2 diabetes—unfortunately, without success. However, new light has been shed on the role of zinc indiabetes.

Effects of zinc supplementation on diabetes mellitus: a systematic …

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Apr 26, 2016 – Zinc Supplementation in Patients with Type 2 Diabetes. … To gauge the effects of zincsupplementation on patients’ fasting blood glucose levels, HbA1c, serum zinc concentration, and serum insulin levels, the researchers conducted a meta-analysis of randomized trials.

Take Zinc If Your Diabetes Is High – Diabetes Developments

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Sep 27, 2017 – Before I was diagnosed prediabetic, for at least a year I felt tired & sleepy after lunch. Like 6 months before my diagnosis, I was taking 50 mg zinc a day for a month to see if it helps me build muscle. It did help. Looking back, during that month of taking zinc, I had a lot more energy & I definitely didn’t feel …

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According to researchers, cellular changes in the brain caused by genetic mutations associated with Autism can be reversed with the help of zinc. READ MORE…

Toxic metals and BPA in babies and copper as culprit in Alzheimer’s brain

Image shows DNA strands.
The image shows the s1 of a mouse cerebral cortex.

Copper toxicity and mental diseases

Inflammation and damage to nerve cells in brain tissue

Iowa State University researchers have described with single-molecule precision how copper ions cause prion proteins to misfold and seed the misfolding and clumping of nearby prion proteins.

The researchers also found the copper-induced misfolding and clumping is associated with inflammation and damage to nerve cells in brain tissue from a mouse model.

Prions are abnormal, pathogenic agents that are transmissible and induce abnormal folding of a specific type of protein called prion proteins, according to the Centers for Disease Control and Prevention. Prion proteins are mostly found in the brain. The abnormal folding of prion proteins leads to brain damage and symptoms of neurodegenerative disease. A similar cycle of neuronal protein misfolding and clumping is observed in other neurodegenerative disorders, including Parkinson’s and Alzheimer’s diseases.

Copper exposure and prion protein neurotoxicity

“Our study establishes a direct link, at the molecular level, between copper exposure and prion protein neurotoxicity,” the researchers wrote in a summary of the paper.

The findings were published today in the journal Science Advances. The corresponding author is Sanjeevi Sivasankar, an Iowa State University associate professor of physics and astronomy; the first author is Chi-Fu Yen, an Iowa State doctoral student in electrical and computer engineering. Co-authors are Anumantha Kanthasamy, an Iowa State Clarence Hartley Covault Distinguished Professor in Veterinary Medicine, chair of biomedical sciences and director of the Iowa Center for Advanced Neurotoxicology; and Dilshan Harischandra, an Iowa State doctoral student in biomedical sciences.

Grants from the National Institute of Environmental Health Sciences at the National Institutes of Health supported the project, including one from the Virtual Consortium for Transdisciplinary Environmental Research.

Although this study determined that copper-induced misfolding and clumping of prion proteins is associated with the degeneration of nerve tissues, Sivasankar cautioned that the study does not directly address the infectivity of prion diseases.

“There are different strains of misfolded prion proteins and not all of them are pathogenic,” Sivasankar said. “Although we do not show that the strains generated in our experiments are infectious, we do prove that copper ions trigger misfolding of prion proteins which causes toxicity in nerve cells.”

From Wiki:

Copper is essential in all plants and animals. Copper is carried mostly in the bloodstream on a plasma protein called ceruloplasmin. When copper is first absorbed in the gut it is transported to the liver bound to albumin. Copper is found in a variety of enzymes, including the copper centers of cytochrome c oxidase and the enzyme superoxide dismutase (containing copper and zinc). In addition to its enzymatic roles, copper is used for biological electron transport. The blue copper proteins that participate in electron transport include azurin and plastocyanin. The name “blue copper” comes from their intense blue color arising from a ligand-to-metal charge transfer (LMCT) absorption band around 600 nm.

Most molluscs and some arthropods such as the horseshoe crab use the copper-containing pigment hemocyanin rather than iron-containing hemoglobin for oxygen transport, so their blood is blue when oxygenated rather than red.[12]

It is believed that zinc and copper compete for absorption in the digestive tract so that a diet that is excessive in one of these minerals may result in a deficiency in the other. The RDA for copper in normal healthy adults is 0.9 mg/day. Because of its role in facilitating iron uptake, copper deficiency can often produce anemia-like symptoms.

Toxicity

All copper compounds, unless otherwise known, should be treated as if they were toxic. Thirty grams of copper sulfate is potentially lethal in humans. The suggested safe level of copper in drinking water for humans varies depending on the source, but tends to be pegged at 1.5 to 2 mg/L. The DRI Tolerable Upper Intake Level for adults of dietary copper from all sources is 10 mg/day. In toxicity, copper can inhibit the enzyme dihydrophil hydratase, an enzyme involved in haemopoiesis.

Symptoms of copper poisoning are very similar to those produced by arsenic. Fatal cases are generally terminated by convulsions, palsy, and insensibility.

In cases of suspected copper poisoning, Ovalbumin is to be administered in either of its forms which can be most readily obtained, as milk or whites of eggs. Vinegar should not be given. The inflammatory symptoms are to be treated on general principles, and so are the nervous.

A significant portion of the toxicity of copper comes from its ability to accept and donate single electrons as it changes oxidation state. This catalyzes the production of very reactive radical ions such as hydroxyl radical in a manner similar to fenton chemistry.[13] This catalytic activity of copper is used by the enzymes that it is associated with and is thus only toxic when unsequestered and unmediated. This increase in unmediated reactive radicals is generally termed oxidative stress and is an active area of research in a variety of diseases where copper may play an important but more subtle role than in acute toxicity.

An inherited condition called Wilson’s disease causes the body to retain copper, since it is not excreted by the liver into the bile. This disease, if untreated, can lead to brain and liver damage. In addition, studies have found that people with mental illnesses such as schizophrenia had heightened levels of copper in their systems. However it is unknown at this stage whether the copper contributes to the mental illness, whether the body attempts to store more copper in response to the illness, or whether the high levels of copper are the result of the mental illness.

Too much copper in water has also been found to damage marine life. The observed effect of these higher concentrations on fish and other creatures is damage to gills, liver, kidneys, and the nervous system. It also interferes with the sense of smell in fish, thus preventing them from choosing good mates or finding their way to mating areas.

Zinc can cancel Copper absorption

copper deficopper excess

Dopamine pathways and Parkinson

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Dopamine pathways is to Parkinson and Serotonin pathway is to Alzheimer’s

Dopaminergic pathways, sometimes called dopaminergic projections, are neural pathways in the brain that transmit the neurotransmitter dopamine from one region of the brain to another.[1][2]

The neurons of the dopaminergic pathways have axons that run the entire length of the pathway. The neurons’ somata produce the enzymes that synthesize dopamine, and they are then transmitted via the projecting axons to their synaptic destinations, where most of the dopamine is produced. Dopaminergic nerve cell bodies in such areas as the substantia nigra tend to be pigmented due to the presence of the black pigment melanin.

Serotonin pathways are pathways that help to regulate mood control.[1]

Dysregulation can be association with obsessive-compulsive disorder, anxiety disorders, and depression.[2

mesolimbicneuro

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 (www.Spectracell.com). 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.”

http://www.holisticprimarycare.net/topics/topics-o-z/vitamins-a-supplements/354-copper-deficiency-may-underlie-osteoporosis-anemia-and-neurodegenerative-disorders

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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