Parkinson’s disease (paralysis agitans, shaking palsy) was first described in 1817. It is now increasingly clear not only what causes Parkinson’s, but also how it can be prevented and its relentless progress slowed down.
Incidence and Symptoms
With no known cause, Parkinson’s disease affects about 1% of the population over the age of 60 years in the United States. It is more common among men than women and also seems to be more widespread in northern countries. The incidence of the disease increases with age although aging itself is not believed to be a causative factor. Parkinson’s disease is rarely inherited and less than 1% of all cases are thought to have a genetic component. At this time there is no medical cure for the condition, but drugs that alleviate the symptoms and slow the progress of the disease are available. L-dopa, the mainstay of current drug therapy, was introduced in 1970 and since then hundreds of research papers have been published on the disease.
The main symptom of Parkinson’s disease is a pronounced tremor affecting the extremities – notably the hands, chin or lips. The tremor is most evident at rest and disappears with movement and sleep. Other characteristic symptoms of Parkinson’s disease are stiffness or slowness of movement, a shuffling walk, stooped posture, and difficulties in performing simple tasks. Memory impairment and cognitive dysfunction are rarely encountered in early stage Parkinson’s disease. Depression is, however, a common feature and about 30% of Parkinson’s disease victims eventually develop Alzheimer’s disease or other forms of dementia.
Environmental and Dietary Factors
Parkinson-like symptoms can also occur as a result of head injuries, carbon monoxide poisoning or poisoning by pharmaceutical or other drugs. Certain diuretics (reserpine), antipsychotics (chlorpromazine), and heart drugs (verapamil) have all been implicated in causing or worsening Parkinson’s disease symptoms as has the “designer drug” MPTP (methylphenyl-tetrahydropyridine). In some cases, drug-induced Parkinson’s disease may be halted or reversed if the drug is promptly withdrawn. Naproxen and other NSAIDs may also exacerbate Parkinson’s disease.
Recent research carried out in Iceland, which has a very high incidence of Parkinson’s disease, has shown that children born during or after a whooping cough (pertussis) epidemic are particularly vulnerable to Parkinson’s disease in later life. This finding supports the idea that Parkinson’s disease may develop later in life as a result of a neurotoxic event that occurred at an early age.
The main pathological feature of Parkinson’s disease is the progressive destruction of dopamine-producing cells in the substantia nigra region of the brain stem. The loss of dopamine production affects the balance between dopamine and acetylcholine in the brain with the result that messages to the muscles become garbled. It is estimated that the characteristic Parkinson’s disease symptoms develop once 70% of the dopaminergic neurons in the substantia nigra have been destroyed.
The question as to what causes the destruction of the dopamine-producing cells has puzzled researchers for years but a consensus is now emerging that Parkinson’s disease is caused by oxidative stress and metal toxicity. The idea that oxidative stress, i.e. an excess of free radicals in the body, can cause disease was first brought forward in 1983. Numerous studies have shown that Parkinson’s disease victims have low levels of natural antioxidants (glutathione and superoxide dismutase) and high levels of iron in the substantia nigra areas of their brains. It is believed that iron helps catalyze the free radical reactions that destroy the dopamine-producing cells. Other metals, notably manganese, cadmium, copper, and mercury (from dental amalgams) have also been implicated as causative factors in the development of Parkinson’s disease.
Until recently there were few alternative treatments available for Parkinson’s disease patients. This is now changing. The finding that Parkinson’s disease is almost certainly caused by oxidative stress aggravated by metal toxicity is a major step forward in understanding and eventually conquering the disease.
The fact that antioxidants retard the development and slow the progression of existing Parkinson’s disease was demonstrated in 1991 in a pilot study carried out by Dr. Stanley Fahn of Columbia University. The overall conclusion of this research is that one can lower one’s risk of developing Parkinson’s disease by reducing one’s intake of animal fats and sugar, avoiding excessive exposure to metals such as aluminum, iron, manganese, mercury, cadmium and copper, and by ensuring an adequate intake of antioxidants. These preventive measures may also be useful in slowing down the progression of the disease.
Australian researchers have found that broad beans (Vicia faba) are an extremely good source of l-dopa and can, in some cases, actually replace l-dopa. A 100gm serving of broad beans (including the pods) provides about 250mg of l-dopa and in addition a significant amount of proanthocyanidins. The broad beans remain effective even if canned or frozen, but should always be consumed whole as the pod has been found to have the highest concentration of l-dopa. Medication dosage may have to be adjusted if broad beans are consumed on a regular basis.
Signs, symptoms & indicators of Parkinson's Disease / Risk
Slow/heavy physical motions
Symptoms of Parkinson’s disease include stiffness or slowness of movement, a shuffling walk, stooped posture, and difficulties in performing simple tasks.
Poor bodily coordination
Characteristic symptoms of Parkinson’s disease include stiffness or slowness of movement, a shuffling walk, stooped posture, and difficulties in performing simple tasks.
The main symptom of Parkinson’s disease is a pronounced tremor affecting the extremities – notably the hands, chin or lips. The tremor is most evident at rest and disappears with movement and sleep.
Slow reaction time
Signs of Parkinson’s disease include stiffness or slowness of movement, a shuffling walk, stooped posture, and difficulties in performing simple tasks.
Conditions that suggest Parkinson's Disease / Risk
Depression is a common feature amongst Parkinson’s disease victims. Depression may be difficult to diagnose in patients with Parkinson’s because the signs of these two disorders overlap. In addition, patients with atypical Parkinson’s more often have depression than patients with classical Parkinson’s.
Risk factors for Parkinson's Disease / Risk
Researchers from Mayo Clinic have discovered that allergic rhinitis is associated with the development of Parkinson’s disease later in life. Findings will be published in the Aug. 8, 2006 issue of the journal Neurology.
“The association with Parkinson’s disease is increased to almost three times that of someone who does not have allergic rhinitis,” says James Bower, M.D., Mayo Clinic neurologist and lead study investigator. “That’s actually a pretty high elevation.”
Previous studies had shown that people who regularly take nonsteroidal anti-inflammatory drugs, such as ibuprofen, are less likely to develop Parkinson’s disease. These results prompted the Mayo Clinic investigators to look further into the links between diseases characterized by inflammation and Parkinson’s. They studied 196 people who developed Parkinson’s disease, matched with people of similar age and gender who did not develop Parkinson’s. The study was conducted in Olmsted County, Minn., home of Mayo Clinic, over a 20-year period.
The researchers examined these groups to determine if those who developed Parkinson’s disease had more inflammatory diseases. They found that those with allergic rhinitis were 2.9 times more likely to develop Parkinson’s. They did not find a similar association between inflammatory diseases such as lupus, rheumatoid arthritis, pernicious anemia or vitiligo and Parkinson’s disease. The researchers hypothesize that they may not have found significant links between these diseases and Parkinson’s disease due to the relatively small number of those in the population who have these diseases, and thus the small number with these diseases in their population sample study. They also did not find the same association with Parkinson’s disease in patients with asthma that they discovered in those with allergic rhinitis.
Dr. Bower says that this study did not examine patients’ types of allergies or when they developed allergies. The investigators theorize that a tendency toward inflammation is the key link between the diseases.
Men with LDL cholesterol levels between 91 and 135 had 6 times the likelihood of having Parkinson’s as those with LDL levels above 135, and those with LDL levels below 91 had 4 times the likelihood.
One possibility is that cholesterol may help rid the body of environmental toxins that could trigger Parkinson’s. Another is that cholesterol could be a precursor for hormones involved in nervous system function.
It is unknown why the same association does not hold true for women. It may be connected with that fact that LDL cholesterol levels increase with age in men until they are 65 years old, but in women until they are 75. The lifetime risk of Parkinson’s disease is about twice as high for men as it is for women. [MSNBC September 29, 2005]
Optimal (?) LDL
LDL stands for low-density lipoprotein cholesterol; low levels of LDL cholesterol are considered an indicator of good cardiovascular health. Earlier studies have found intriguing correlations between Parkinson’s disease, heart attacks, stroke and smoking.
“People with Parkinson’s disease have a lower occurrence of heart attack and stroke than people who do not have the disease,” said Dr. Xuemei Huang, medical director of the Movement Disorder Clinic at UNC Hospitals and an assistant professor of neurology in the UNC School of Medicine. “Parkinson’s patients are also more likely to carry the gene APOE-2, which is linked with lower LDL cholesterol.” And for more than a decade, researchers have known that smoking, which increases a person’s risk for cardiovascular disease, is also associated with a decreased risk of Parkinson’s disease.
These findings led Huang to examine whether higher LDL cholesterol might be associated with a decreased occurrence for Parkinson’s disease, and vice versa. “If my hypothesis was correct,” she said, “lower LDL-C, something that is linked to healthy hearts, would be associated with a higher occurrence of Parkinson’s.” The results of Huang’s study, published online by the journal Movement Disorders, confirmed her hypothesis. “We found that lower LDL concentrations were indeed associated with a higher occurrence of Parkinson’s disease,” Huang said. Participants with lower LDL levels (less than 114 milligrams per deciliter) had a 3.5-fold higher occurrence of Parkinson’s than the participants with higher LDL levels (more than 138 milligrams per deciliter).
Suspected/possible Parkinson's disease
Hysterectomy with one ovary or hysterectomy with both ovaries
Women may be stuck in a rock and a hard place when it comes to removing their ovaries: This new study reveals that women who have had both their ovaries removed are at twice the normal risk of developing Parkinson’s disease.
This is because significant amounts of the hormone estrogen, which has been found to protect certain types of nerve cells, are produced by women’s ovaries. Among the nerve cells estrogen helps are those found in the substantia nigra (a sector of the brain that controls voluntary movements). Parkinson’s patients show degeneration in this region of the brain, resulting in shaking and unsteadiness, both characteristic of the condition.
In order to understand how surgical removal of the ovaries influences a woman’s chance of developing Parkinson’s disease or its symptoms, researchers searched through medical records that dated from 1950-1987. The team also conducted thousands of medical checks over the past five years to follow up patients among the 5,000 women involved in the study.
1. About half of the women surveyed had at least one ovary removed and some 1,200 had both of them removed.
2. Of those who had the procedure (either one or both ovaries removed), 43 women showed Parkinson’s-like symptoms, and 25 of them developed the full-stage disease.
3. Only 18 of the roughly 2,500 women whose ovaries were not removed contracted Parkinson’s; 29 developed symptoms.
4. Getting both ovaries removed placed women at a higher risk of developing Parkinson’s. [Nature April 14, 2005]
Recommendations for Parkinson's Disease / Risk
Raising glutathione levels (a potent antioxidant and detoxifier) will provide a protective effect.
Both cysteine and NAC increase glutathione levels.
D-phenylalanine (DPA) may be helpful for some individuals with Parkinson’s disease. [Arzneimittelforsch 26: pp.577-9, 1976]
Flavonoids, and in particular the proanthocyanidins (grape seed and pine bark extracts) should also be excellent candidates as Parkinson’s disease preventers and retarders. Proanthocyanidins are water-soluble antioxidants that are stronger than vitamin C and which readily cross into the brain fluid. Clinical trials are, however, still required to support this hypothesis.
Parkinson’s disease is almost certainly caused by oxidative stress aggravated by metal toxicity. People who live in areas where the aluminum content of the drinking water is high have an excessive risk of developing Parkinson’s disease. Recent research has linked high aluminum levels in drinking water to acid rain that leaches the aluminum out of the soil and transfers it to the ground water. Other metals are also implicated.
People with a high intake of sugar (mono- and disaccharides) increase their risk of developing Parkinson’s disease by a factor of three as compared to people with a more moderate intake.
Diets high in vitamin C and beta-carotene provide significant protection against Parkinson’s disease. American researchers have concluded that a high intake of animal fats is associated with a five-fold increase risk.
American researchers have concluded that a high intake of animal fats is associated with a five-fold increase in the risk of developing Parkinson’s disease.
Fruit is a good source of antioxidants.
Parkinson’s disease can be triggered or worsened by ingesting aspartame according to researchers studying its possible adverse effects.
A team of researchers examined the relationship between coffee intake and the incidence of Parkinson’s disease among 8,004 Japanese-American men over a 30 year period. Of these men, 102 developed Parkinson’s disease. The incidence of Parkinson’s disease was found to be lower in those who drank coffee. In fact, the men who drank the most coffee were the least likely to get Parkinson’s disease. Men who did not drink any coffee were five times more likely to exhibit symptoms of Parkinson’s disease than men who drank more than 28 ounces of coffee each day. Caffeine from other sources such as green tea, black tea, chocolate and soda was also associated with a lower risk of Parkinson’s disease.
Caffeine belongs to the xanthine chemical group. A naturally occurring xanthine in the brain called adenosine is used as a neurotransmitter at some synapses. When adenosine receptors are blocked, levels of the neurotransmitter dopamine increase. Caffeine may protect against Parkinson’s disease by blocking adenosine receptors, thus increasing the amount of dopamine in the brain.
Although the new research is suggestive of a link between caffeine and Parkinson’s disease, it is too early to say that caffeine will prevent Parkinson’s disease. Perhaps the brains of people who like and dislike coffee are different, with differing rates of Parkinson’s. Also, the study included older, Japanese-American men. It is unknown if this caffeine/Parkinson disease relationship holds for other ethnic groups, women and younger people.
The timing of protein intake can markedly increase the effectiveness of l-dopa and thereby lead to reduced dosage requirements. Researchers now recommend that protein intake be kept as low as possible and that protein be included primarily in the evening meal.
Conventional medical treatment relies heavily on l-dopa (levo-dihydroxy-phenylalanine), a dopamine precursor that can cross the blood-brain barrier and is converted to dopamine in the brain. L-dopa is now rarely used by itself, but rather in combination with carbidopa (Sinemet) or benserazide (Madopar) that protects it from breaking down before it reaches the brain tissue. As l-dopa must compete with other amino acids in crossing both from the gut to the blood stream and from the blood stream to the brain it is usually recommended that it be taken between meals rather than with meals.
Although l-dopa medications can bring significant relief from Parkinson’s disease symptoms they become less effective with time. After four or five years of increasing dosages their effect becomes sporadic and unpredictable (the “on-off syndrome”) and patients become increasingly helpless and depressed. There is also evidence that the use of l-dopa medications may lead to a deficiency of B-vitamins, especially niacin and vitamin B-6. Most Parkinson’s disease experts now recommend that l-dopa therapy be started as late as possible after diagnosis of Parkinson’s disease so as to postpone the day when it no longer works and to limit its many serious adverse effects.
Selegiline (Deprenyl, Eldepryl) is another drug used in Parkinson’s disease therapy. It works by blocking the breakdown of dopamine in the brain. Trials have shown that starting Parkinson’s disease patients on selegiline can extend the time period before they need l-dopa by about nine months. Combinations of l-dopa medications and selegiline have also been tried in early stage Parkinson’s disease patients, but were found to have no advantage. A study concluded that the combination therapy increased mortality by about 50% when compared to Parkinson’s disease patients treated with l-dopa medications alone.
However, a subsequent study found that Eldepryl (Selegiline, Deprenyl) can slow Parkinson’s Disease safely. In patients with early Parkinson’s disease, selegiline and other drugs in a class called monoamine oxidase type B inhibitors are cheap and effective treatments that reduce disability and the need for levodopa, researchers reported in the British Medical Journal. Their study findings also show that the drugs are not associated with increased mortality, as had been reported in an earlier study. [British Medical Journal, August 14, 2004]
Anticholinergenic drugs work by reducing the amount of acetylcholine produced in the brain and thereby redressing the imbalance between dopamine and acetylcholine. They are no longer recommended for older patients as they have serious neuropsychiatric side-effects.
2009 (Ames, Iowa) – Anumantha Kanthasamy and W. Eugene and Linda R. Lloyd, researchers at Iowa State University, have reportedly found an essential key to possibly cure Parkinson’s disease.
Kanthasamy discovered that the protein kinase-C (specifically PKCd) is killing the dopamine-producing cells which Parkinson’s sufferers lack and he, and his research staff, discovered a compound that neutralizes the cell-killing kinase-C and allows the dopamine-producing cells to survive and function.
As reported in an Iowa State University publication, Kanthasamy’s group is now looking for additional compounds that also can serve to neutralize protein kinase-C. By identifying more compounds that perform the function of neutralizing kinase-C, notes the report, researchers are more likely to locate one that works well and has few side effects.
According to the report, the discovery is expected to provide new treatment options to stop the progression of the disease or even cure it.
According to Dr. Bihari, LDN clearly halts progression in multiple sclerosis. As such its use has been more recently extended to other neurodegenerative diseases, such as Parkinson’s disease and amyotrophic lateral sclerosis (ALS or Lou Gehrig’s disease) whose etiology remains unknown but for which there is suggestive evidence of a possible autoimmune mechanism.
Naproxen and other NSAIDs may exacerbate Parkinson’s disease.
Occupational exposure to pesticides and herbicides has also been linked to a significantly higher risk of developing Parkinson’s disease.
C.A. Hackethal, M.D. has reported excellent success in treating Parkinson’s Disease by use of replacement therapy of DHEA. Apparently the bad side-effects of L-Dopa are avoided, and the Parkinsonian victim is restored to appropriate functioning. Until further confirmation, one should not expect miraculous results based upon this one reference.
Avoiding overexposure to some metals, especially iron, can reduce the risk of developing Parkinson’s disease.
Research has raised the possibility that people with Parkinson’s might have problems with structures called mitochondria, a spherical or elongated organelle in the cytoplasm of nearly all eukaryotic cells, containing genetic material and many enzymes important for cell metabolism, including those responsible for the conversion of food to usable energy. The researchers who performed this study found that Parkinson’s patients have reduced levels of coenzyme Q10 in their mitochondria. This led the researchers to investigate whether the antioxidant would be useful in treating the disease.
The study involved 80 people who had been diagnosed with Parkinson’s but had not yet received treatment. The participants were randomly assigned to take a daily dose of 300mg, 600mg or 1,200mg of coenzyme Q10 or an inactive pill called a placebo. Patients were evaluated at the start of the study and after one, four, eight, 12 and 16 months.
The progression of Parkinson’s disease was significantly slower in people taking the highest dose of coenzyme Q10. These patients experienced a slower decline in all areas measured by the researchers, including mental and motor skills, but the greatest effect was in the activities of daily living. Compared to placebo, the lower doses of the drug also seemed to slow Parkinson’s, but the differences were not statistically significant. [Archives of Neurology Oct 2002; 59: pp.1523,1541-1550] No currently used drugs slow the progression of Parkinson’s, but act by controlling the symptoms. This places CoQ10 in a unique position, as it appears to slow progression.
The compound 5-adenosylmethionine (SAMe), potentially produced through the demethylation of TMG, has been shown to improve Parkinson’s disease.
Stress aggravates Parkinson’s disease and relaxation therapy has been found useful in the treatment of the disease. A well thought-out program of rest, exercise and physiotherapy can also significantly ameliorate the symptoms of Parkinson’s disease.
In a Russian trial, 60 patients with Parkinsonism of various causes with pronounced tremor were effectively treated with intramuscular doses of vitamin B6. Single doses were as high as 400mg; the total doses were from 3000 to 6000mg. Changes in laboratory findings (EMG, tremorographic and myotonometric) correlated with the clinical picture. Vitamin B6 is recommended irrespective of the cause of the disease and of the patient’s age, and can be given either alone or in combination with anti-Parkinsonian drugs aside from DOPA. High doses of B6 are not recommended, however, for patients with angina or coronary insufficiency. [Sov Med (7): 14- 9, 1979 (in Russian)]
High dietary intake of vitamin E (from food only) was associated with a reduced risk of Parkinson disease in a study of over 124.000 men and women who were followed for at least 12 years. Vitamin E or vitamin C supplements were NOT associated with the risk of developing Parkinson’s. [Neurology 2002;59(8): pp.1161-9]
Supplementation with vitamin C and E markedly slows the progression of the disease in its early stages.
Parkinson’s disease patients given large doses of oral vitamin C and synthetic vitamin E supplements (3000mg and 3200 IU daily respectively) delayed the progression of their disease to the point where they needed l-dopa 2.5 years later than a group of patients who were not taking supplements. Later research has shown that synthetic vitamin E in itself does not retard the progression of Parkinson’s disease. Thus it is likely that it was vitamin C by itself or its combination with vitamin E that was the active component in Dr. Fahn’s experiment. This fits with a later finding that vitamin E, a fat-soluble vitamin, does not readily cross the blood-brain barrier nor does it accumulate in the cerebrospinal fluid that bathes the brain. Vitamin C, on the other hand, while not crossing the blood-brain barrier does enter the cerebrospinal fluid and can be found there in concentrations proportional to dietary intake. Inasmuch as vitamin C is a highly effective antioxidant and is particularly adept in quenching hydroxyl radicals (the main culprits in the dopamine-cell destruction), it is becoming increasingly clear that this vitamin may be an excellent protector against Parkinson’s disease and can materially help in slowing down the progression of the disease.
Niacinamide (nicotinamide) enhances mitochondrial energy production and may help protect mitochondria from damage by toxic substances. A product derived from nicotinamide, called nicotinamide adenine dinucleotide (NADH), is essential for cell development and energy production.
Animal studies suggest that the protective effects from an oral nicotinamide supplement are greatest when given early in the course of Parkinson’s disease, before dopamine is severely depleted. The benefits of NADH in Parkinson’s disease may result from its ability to reduce inflammation within the brain and from its effect on the immune system.
Vitamin A works with other antioxidants to provide a protective effect.
Supplementation with vitamin B-complex may be necessary, especially for patients who take l-dopa medications.
|Weak or unproven link|
|Strong or generally accepted link|
|Proven definite or direct link|
|May do some good|
|Likely to help|
|May have adverse consequences|
|Reasonably likely to cause problems|
A chronic, slowly-progressing disease of the nervous system characterized clinically by the combination of tremor, rigidity, extreme slowness of movement, and stooped posture. It is characterized pathologically by loss of dopamine in the substantia nigra.
A progressive disease of the middle-aged and elderly, characterized by loss of function and death of nerve cells in several areas of the brain, leading to loss of mental functions such as memory and learning. Alzheimer's disease is the most common cause of dementia.
An acquired progressive impairment of intellectual function. Marked compromise exists in at least three of the following mental activity spheres: memory, language, personality, visuospatial skills, and cognition (i.e., abstraction and calculation).
An agent increasing urine flow, causing the kidneys to excrete more than the usual amount of sodium, potassium and water.
Non-steroidal anti-inflammatory drug.
Describes a disease occurring in extensive outbreaks, or with an unusually high incidence at certain times and places.
Poisonous to the nerves.
A neurohormone; precursor to norepinephrine which acts as a stimulant to the nervous system.
A neurotransmitter widely distributed in body tissues with a primary function of mediating synaptic activity of the nervous system and skeletal muscles.
A free radical is an atom or group of atoms that has at least one unpaired electron. Because another element can easily pick up this free electron and cause a chemical reaction, these free radicals can effect dramatic and destructive changes in the body. Free radicals are activated in heated and rancid oils and by radiation in the atmosphere, among other things.
A chemical compound that slows or prevents oxygen from reacting with other compounds. Some antioxidants have been shown to have cancer-protecting potential because they neutralize free radicals. Examples include vitamins C and E, alpha lipoic acid, beta carotene, the minerals selenium, zinc, and germanium, superoxide dismutase (SOD), coenzyme Q10, catalase, and some amino acids, like cystiene. Other nutrient sources include grape seed extract, curcumin, gingko, green tea, olive leaf, policosanol and pycnogenol.
A natural sulfur-bearing peptide formed from the linking of three amino acids: glutamic acid, cysteine and glycine. Glutathione acts as an antioxidant and detoxicant and is involved with the selenium-containing enzyme glutathione peroxidase. Glutathione is also involved in amino acid transport across cell membranes.
An essential mineral. Prevents anemia: as a constituent of hemoglobin, transports oxygen throughout the body. Virtually all of the oxygen used by cells in the life process are brought to the cells by the hemoglobin of red blood cells. Iron is a small but most vital, component of the hemoglobin in 20,000 billion red blood cells, of which 115 million are formed every minute. Heme iron (from meat) is absorbed 10 times more readily than the ferrous or ferric form.
An essential mineral found in trace amounts in tissues of the body. Adults normally contain an average of 10 to 20mg of manganese in their bodies, most of which is contained in bone, the liver and the kidneys. Manganese is essential to several critical enzymes necessary for energy production, bone and blood formation, nerve function and protein metabolism. It is involved in the metabolism of fats and glucose, the production of cholesterol and it allows the body to use thiamine and Vitamin E. It is also involved in the building and degrading of proteins and nucleic acid, biogenic amine metabolism, which involves the transmitting of nerve impulses.
An essential mineral that is a component of several important enzymes in the body and is essential to good health. Copper is found in all body tissues. Copper deficiency leads to a variety of abnormalities, including anemia, skeletal defects, degeneration of the nervous system, reproductive failure, pronounced cardiovascular lesions, elevated blood cholesterol, impaired immunity and defects in the pigmentation and structure of hair. Copper is involved in iron incorporation into hemoglobin. It is also involved with vitamin C in the formation of collagen and the proper functioning in central nervous system. More than a dozen enzymes have been found to contain copper. The best studied are superoxide dismutase (SOD), cytochrome C oxidase, catalase, dopamine hydroxylase, uricase, tryptophan dioxygenase, lecithinase and other monoamine and diamine oxidases.
(gm): A metric unit of weight, there being approximately 28 grams in one ounce.
(mg): 1/1,000 of a gram by weight.
Also called procyanidin, it is a powerful antioxidant that chemically belongs to the class of bioflavonoids. Pycnogenol from grape seed and pine bark extracts is an example. Berries, such as hawthorn berries, cherries, blueberries, and blackberries and, to a lesser extent, red wine, are natural sources.
Also known as hay fever, this is an inflammation of the nasal mucous membranes that is caused by specific allergen(s). It is an allergy characterized by sneezing, itchy and watery eyes, a runny or stuffy nose, coughing and a burning/scratchy sensation of the palate and throat.
Reducing inflammation by acting on body mechanisms, without directly acting on the cause of inflammation, e.g., glucocorticoids, aspirin.
A long-term, destructive connective tissue disease that results from the body rejecting its own tissue cells (autoimmune reaction).
Anemia caused by a vitamin B12 deficiency.
A lung disorder marked by attacks of breathing difficulty, wheezing, coughing, and thick mucus coming from the lungs. The episodes may be triggered by breathing foreign substances (allergens) or pollutants, infection, vigorous exercise, or emotional stress.
Hypersensitivity caused by exposure to a particular antigen (allergen), resulting in an increased reactivity to that antigen on subsequent exposure, sometimes with harmful immunologic consequences.
(LDL): Also known as "bad" cholesterol, LDLs are large, dense, protein-fat particles composed of a moderate proportion of protein and a high proportion of cholesterol. Higher levels of LDLs are associated with a greater risk of cardiovascular disease.
A waxy, fat-like substance manufactured in the liver and found in all tissues, it facilitates the transport and absorption of fatty acids. In foods, only animal products contain cholesterol. An excess of cholesterol in the bloodstream can contribute to the development of atherosclerosis.
Chemical substances secreted by a variety of body organs that are carried by the bloodstream and usually influence cells some distance from the source of production. Hormones signal certain enzymes to perform their functions and, in this way, regulate such body functions as blood sugar levels, insulin levels, the menstrual cycle, and growth. These can be prescription, over-the-counter, synthetic or natural agents. Examples include adrenal hormones such as corticosteroids and aldosterone; glucagon, growth hormone, insulin, testosterone, estrogens, progestins, progesterone, DHEA, melatonin, and thyroid hormones such as thyroxine and calcitonin.
A system in the body that is comprised of the brain, spinal cord, nerves, ganglia and parts of the receptor organs that receive and interpret stimuli and transmit impulses to effector organs.
Pertaining to the heart and blood vessels.
A sudden loss of brain function caused by a blockage or rupture of a blood vessel that supplies the brain, characterized by loss of muscular control, complete or partial loss of sensation or consciousness, dizziness, slurred speech, or other symptoms that vary with the extent and severity of the damage to the brain. The most common manifestation is some degree of paralysis, but small strokes may occur without symptoms. Usually caused by arteriosclerosis, it often results in brain damage.
One of the female sex hormones produced by the ovaries.