Soothe & Relaxx™ Soft Tissue & Stress Support
Has anybody tried this? My doctor put me on this for Lyme disease and it works great for me. It also works great for the fibromyalgia symptoms and anything to do with soft tissue pain, stress and relaxation. Thought I would share the information with you.
Product Description
Soft tissue, joint & muscle support with Relaxx™ Complex to calm the mind. (180 capsules)
Special Dietary Usefulness:
Under a physician’s direction, Soothe & Relaxx™ may have special dietary usefulness for individuals suffering from fibromyalgia and other chronic illnesses with soft tissue, joint and muscle pain.
Soothe & Relaxx™ was developed to meet the combination of needs that many chronically ill patients experience: pain and anxiety. The product addresses pain as a result of soft tissue or joint injury and the concomitant anxiety often associated with long-term health issues. The Relaxx™ Complex is designed to take the edge off versus being a sedating micro-formula. This is a favorite of patients who feel the benefit fairly quickly.
Each bottle provides a one month supply of the following complexes and health benefits:
Pro Joint Soothers™:
Proprietary blend of glucosamine sulfate, MSM, chrondroitin sulfate, hyaluronic acid which supports connective tissue, lubricates joints, promotes joint resilience, elasticity and overall strength.
ExInflame™ Complex:
Proprietary blend of White Willow Bark, Boswellin, Curcumin Extract, Holy Basil which promotes a healthy inflammation response.
Muscle & Leg Calmer™:
Proprietary blend of magnesium hydroxide and malic acid which calms muscle contractions and relaxes the body's muscles.
Relaxx™ Complex:
Proprietary blend of 5HTP, Valerian, Lemon Balm, Passion Flower, German Chamomile which relaxes & calms the mind, and promotes healthy sleep patterns.
Suggested Use:
As a dietary supplement, take two capsules three times per day or as directed by your health care professional.
Friday, June 4, 2010
Thursday, June 3, 2010
Lyme Disease & Common Co-Infections
Lyme Disease & Common Co-Infections
Short Symptom List
Borrelia, Babesia, Bartonella, and Ehrlichia
The following symptoms were excerpted from Diagnostic Hints And Treatment
Guidelines For Lyme And Other Tick Borne Illnesses, by Joseph J. Burrascano Jr.,M.D. (Fourteenth Edition, November, 2002). Available online at www.ilads.org/burrascano_1102.html
Borrelia
(Borreliosis, neuroborreliosis; also known as Lyme Disease)
Spread primarily though the bite of infected ticks that live on a wide range of mammalian species; secondary human-to-human transmission through semen, breast milk, and possibly in utero.
**Bladder dysfunction
**Burning or stabbing sensations
**Cardiac impairment
**Change in bowel function
**Chest pain
**Confusion
**Depression
**Difficulty thinking
**Difficulty with concentration and reading
**Difficulty with speech, writing
**Difficulty finding words; name blocking
**Disorientation: getting lost, going to wrong places
**Disturbed sleep: too much, too little, fractionated, early awakening
**Ears/Hearing: buzzing, ringing, ear pain, sound sensitivity
**Exaggerated symptoms or worse hangover from alcohol
**Eyes/Vision: double, blurry, increased floaters, light sensitivity
**Facial paralysis (Bell's palsy)
**Fatigue, tiredness, poor stamina
**Forgetfulness
**Headache
**Heart block
**Heart murmur
**Heart palpitations
**Heart valve prolapse
**Increased motion sickness
**Irritability
**Irritable bladder
**Joint pain or swelling
**Lightheadedness
**Mood swings
**Muscle pain or cramps
**Neck creaks & cracks
**Neck stiffness, pain
**Numbness
**Pelvic pain
**Poor attention
**Poor balance
**Poor short-term memory
**Problem absorbing new information
**Pulse skips
**Rib soreness
**Sexual dysfunction or loss of libido
**Shooting pains
**Shortness of breath; cough
**Skin hypersensitivity
**Sore throat
**Stiffness of the joints or back
**Swollen glands
**Testicular pain
**Tingling
**Tremor
**Twitching of the face or other muscles
**Unavoidable need to sit or lay down
**Unexplained breast pain
**Unexplained fevers, sweats, chills or flushing
**Unexplained hair loss
**Unexplained menstrual irregularity'
**Unexplained milk production
**Unexplained weight loss or gain
**Upset Stomach or abdominal pain
**Vertigo
**Wooziness
Babesia Babesiosis)
Babesia is a protozoan spread by ticks, blood transfusion, and in utero. Despite there being 13 known forms to date, current testing only looks for two of them.
**Air hunger
**Cough
**Fatigue
**Fevers
**Headache
**Hemolysis
**Imbalance without true vertigo
**Mild encephalopathy
**Shaking chills
**Sweats
Bartonella (Bartonellosis, also known as cat scratch fever)
Spread by bites from infected ticks and in utero
**abnormal liver enzymes
**encephalopathy
**endocarditis
**flu-like malaise
**headache
**hemolysis with anemia
**hepatomegaly
**high fever
**immune deficiency
**jaundice
**lymphadenopathy
**myalgias
**myocarditis
**papular or angiomatous rash
**somnolence
**sore throat
**splenomegaly
**weakened immune response
Ehrlichia (Ehrlichiosis)
Bites from infected ticks
**elevated liver enzymes
**headaches
**myalgias
**ongoing fatigue
**persistent leukopenia
**thrombocytopenia
Printed from www.anapsid.org/lyme/symptoms/tbi-symptoms.html
More information on Lyme and other tickborne diseases:
www.calda.intranets.com
www.ilads.org
www.lymenet.org
Short Symptom List
Borrelia, Babesia, Bartonella, and Ehrlichia
The following symptoms were excerpted from Diagnostic Hints And Treatment
Guidelines For Lyme And Other Tick Borne Illnesses, by Joseph J. Burrascano Jr.,M.D. (Fourteenth Edition, November, 2002). Available online at www.ilads.org/burrascano_1102.html
Borrelia
(Borreliosis, neuroborreliosis; also known as Lyme Disease)
Spread primarily though the bite of infected ticks that live on a wide range of mammalian species; secondary human-to-human transmission through semen, breast milk, and possibly in utero.
**Bladder dysfunction
**Burning or stabbing sensations
**Cardiac impairment
**Change in bowel function
**Chest pain
**Confusion
**Depression
**Difficulty thinking
**Difficulty with concentration and reading
**Difficulty with speech, writing
**Difficulty finding words; name blocking
**Disorientation: getting lost, going to wrong places
**Disturbed sleep: too much, too little, fractionated, early awakening
**Ears/Hearing: buzzing, ringing, ear pain, sound sensitivity
**Exaggerated symptoms or worse hangover from alcohol
**Eyes/Vision: double, blurry, increased floaters, light sensitivity
**Facial paralysis (Bell's palsy)
**Fatigue, tiredness, poor stamina
**Forgetfulness
**Headache
**Heart block
**Heart murmur
**Heart palpitations
**Heart valve prolapse
**Increased motion sickness
**Irritability
**Irritable bladder
**Joint pain or swelling
**Lightheadedness
**Mood swings
**Muscle pain or cramps
**Neck creaks & cracks
**Neck stiffness, pain
**Numbness
**Pelvic pain
**Poor attention
**Poor balance
**Poor short-term memory
**Problem absorbing new information
**Pulse skips
**Rib soreness
**Sexual dysfunction or loss of libido
**Shooting pains
**Shortness of breath; cough
**Skin hypersensitivity
**Sore throat
**Stiffness of the joints or back
**Swollen glands
**Testicular pain
**Tingling
**Tremor
**Twitching of the face or other muscles
**Unavoidable need to sit or lay down
**Unexplained breast pain
**Unexplained fevers, sweats, chills or flushing
**Unexplained hair loss
**Unexplained menstrual irregularity'
**Unexplained milk production
**Unexplained weight loss or gain
**Upset Stomach or abdominal pain
**Vertigo
**Wooziness
Babesia Babesiosis)
Babesia is a protozoan spread by ticks, blood transfusion, and in utero. Despite there being 13 known forms to date, current testing only looks for two of them.
**Air hunger
**Cough
**Fatigue
**Fevers
**Headache
**Hemolysis
**Imbalance without true vertigo
**Mild encephalopathy
**Shaking chills
**Sweats
Bartonella (Bartonellosis, also known as cat scratch fever)
Spread by bites from infected ticks and in utero
**abnormal liver enzymes
**encephalopathy
**endocarditis
**flu-like malaise
**headache
**hemolysis with anemia
**hepatomegaly
**high fever
**immune deficiency
**jaundice
**lymphadenopathy
**myalgias
**myocarditis
**papular or angiomatous rash
**somnolence
**sore throat
**splenomegaly
**weakened immune response
Ehrlichia (Ehrlichiosis)
Bites from infected ticks
**elevated liver enzymes
**headaches
**myalgias
**ongoing fatigue
**persistent leukopenia
**thrombocytopenia
Printed from www.anapsid.org/lyme/symptoms/tbi-symptoms.html
More information on Lyme and other tickborne diseases:
www.calda.intranets.com
www.ilads.org
www.lymenet.org
Basic Information about Lyme Disease
If you have been diagnosed with fibromyalgia, chronic fatigue syndrome, MS, early Alzheimers or early dementia, parkinson's disease or Lou Gerhig's disease, it is recommended that you get tested for Lyme disease. Lyme disease is the great pretender and can mimic these other diseases. Lyme disease is hard to diagnose and lab testing is not reliable. Your best bet for lab testing is IgeneX labs (tick speciality lab).
Basic Information about Lyme Disease
by The International Lyme and Associated Diseases Society
1. Lyme disease is transmitted by the bite of a tick, and the disease is prevalent across the United States and throughout the world. Ticks know no borders and respect no boundaries. A patient's county of residence does not accurately reflect his or her Lyme disease risk because people travel, pets travel, and ticks travel. This creates a dynamic situation with many opportunities for exposure to Lyme disease for each individual.
2. Lyme disease is a clinical diagnosis. The disease is caused by a spiral-shaped bacteria (spirochete) called Borrelia burgdorferi. The Lyme spirochete can cause infection of multiple organs and produce a wide range of symptoms. Case reports in the medical literature document the protean manifestations of Lyme disease, and familiarity with its varied presentations is key to recognizing disseminated disease.
3. Fewer than 50% of patients with Lyme disease recall a tick bite. In some studies this number is as low as 15% in culture-proven infection with the Lyme spirochete.
4. Fewer than 50% of patients with Lyme disease recall any rash. Although the erythema migrans (EM) or “bull’s-eye” rash is considered classic, it is not the most common dermatologic manifestation of early-localized Lyme infection. Atypical forms of this rash are seen far more commonly. It is important to know that the EM rash is pathognomonic of Lyme disease and requires no further verification prior to starting an appropriate course of antibiotic therapy.
5. The Centers for Disease Control and Prevention (CDC) surveillance criteria for Lyme disease were devised to track a narrow band of cases for epidemiologic purposes. As stated on the CDC website, the surveillance criteria were never intended to be used as diagnostic criteria, nor were they meant to define the entire scope of Lyme disease.
6. The ELISA screening test is unreliable. The test misses 35% of culture proven Lyme disease (only 65% sensitivity) and is unacceptable as the first step of a two-step screening protocol. By definition, a screening test should have at least 95% sensitivity.
7. Of patients with acute culture-proven Lyme disease, 20–30% remain seronegative on serial Western Blot sampling. Antibody titers also appear to decline over time; thus while the Western Blot may remain positive for months, it may not always be sensitive enough to detect chronic infection with the Lyme spirochete. For “epidemiological purposes” the CDC eliminated from the Western Blot analysis the reading of bands 31 and 34. These bands are so specific to Borrelia burgdorferi that they were chosen for vaccine development. Since a vaccine for Lyme disease is currently unavailable, however, a positive 31 or 34 band is highly indicative of Borrelia burgdorferi exposure. Yet these bands are not reported in commercial Lyme tests.
8. When used as part of a diagnostic evaluation for Lyme disease, the Western Blot should be performed by a laboratory that reads and reports all of the bands related to Borrelia burgdorferi. Laboratories that use FDA approved kits (for instance, the Mardx Marblot®) are restricted from reporting all of the bands, as they must abide by the rules of the manufacturer. These rules are set up in accordance with the CDCs surveillance criteria and increase the risk of false-negative results. The commercial kits may be useful for surveillance purposes, but they offer too little information to be useful in patient management.
9. There are 5 subspecies of Borrelia burgdorferi, over 100 strains in the US, and 300 strains worldwide. This diversity is thought to contribute to the antigenic variability of the spirochete and its ability to evade the immune system and antibiotic therapy, leading to chronic infection.
10. Testing for Babesia, Anaplasma, Ehrlichia and Bartonella (other tick-transmitted organisms) should be performed. The presence of co-infection with these organisms points to probable infection with the Lyme spirochete as well. If these coinfections are left untreated, their continued presence increases morbidity and prevents successful treatment of Lyme disease.
11. A preponderance of evidence indicates that active ongoing spirochetal infection with or without other tick-borne coinfections is the cause of the persistent symptoms in chronic Lyme disease.
12. There has never been a study demonstrating that 30 days of antibiotic treatment cures chronic Lyme disease. However there is a plethora of documentation in the US and European medical literature demonstrating by histology and culture techniques that short courses of antibiotic treatment fail to eradicate the Lyme spirochete. Short treatment courses have resulted in upwards of a 40% relapse rate, especially if treatment is delayed.
13. Most cases of chronic Lyme disease require an extended course of antibiotic therapy to achieve symptomatic relief. The return of symptoms and evidence of the continued presence of Borrelia burgdorferi indicates the need for further treatment. The very real consequences of untreated chronic persistent Lyme infection far outweigh the potential consequences of long-term antibiotic therapy.
14. Many patients with chronic Lyme disease require prolonged treatment until the patient is symptom-free. Relapses occur and retreatment may be required. There are no tests currently available to prove that the organism is eradicated or that the patient with chronic Lyme disease is cured.
15. Like syphilis in the 19th century, Lyme disease has been called the great imitator and should be considered in the differential diagnosis of rheumatologic and neurologic conditions, as well as chronic fatigue syndrome, fibromyalgia, somatization disorder and any difficult-to-diagnose multi-system illness.
Disclaimer: The foregoing information is for educational purposes only. It is not intended to replace or supersede patient care by a healthcare provider. If an individual suspects the presence of a tick-borne illness, that individual should consult a healthcare provider who is familiar with the diagnosis and treatment of tick-borne diseases.
Basic Information about Lyme Disease
by The International Lyme and Associated Diseases Society
1. Lyme disease is transmitted by the bite of a tick, and the disease is prevalent across the United States and throughout the world. Ticks know no borders and respect no boundaries. A patient's county of residence does not accurately reflect his or her Lyme disease risk because people travel, pets travel, and ticks travel. This creates a dynamic situation with many opportunities for exposure to Lyme disease for each individual.
2. Lyme disease is a clinical diagnosis. The disease is caused by a spiral-shaped bacteria (spirochete) called Borrelia burgdorferi. The Lyme spirochete can cause infection of multiple organs and produce a wide range of symptoms. Case reports in the medical literature document the protean manifestations of Lyme disease, and familiarity with its varied presentations is key to recognizing disseminated disease.
3. Fewer than 50% of patients with Lyme disease recall a tick bite. In some studies this number is as low as 15% in culture-proven infection with the Lyme spirochete.
4. Fewer than 50% of patients with Lyme disease recall any rash. Although the erythema migrans (EM) or “bull’s-eye” rash is considered classic, it is not the most common dermatologic manifestation of early-localized Lyme infection. Atypical forms of this rash are seen far more commonly. It is important to know that the EM rash is pathognomonic of Lyme disease and requires no further verification prior to starting an appropriate course of antibiotic therapy.
5. The Centers for Disease Control and Prevention (CDC) surveillance criteria for Lyme disease were devised to track a narrow band of cases for epidemiologic purposes. As stated on the CDC website, the surveillance criteria were never intended to be used as diagnostic criteria, nor were they meant to define the entire scope of Lyme disease.
6. The ELISA screening test is unreliable. The test misses 35% of culture proven Lyme disease (only 65% sensitivity) and is unacceptable as the first step of a two-step screening protocol. By definition, a screening test should have at least 95% sensitivity.
7. Of patients with acute culture-proven Lyme disease, 20–30% remain seronegative on serial Western Blot sampling. Antibody titers also appear to decline over time; thus while the Western Blot may remain positive for months, it may not always be sensitive enough to detect chronic infection with the Lyme spirochete. For “epidemiological purposes” the CDC eliminated from the Western Blot analysis the reading of bands 31 and 34. These bands are so specific to Borrelia burgdorferi that they were chosen for vaccine development. Since a vaccine for Lyme disease is currently unavailable, however, a positive 31 or 34 band is highly indicative of Borrelia burgdorferi exposure. Yet these bands are not reported in commercial Lyme tests.
8. When used as part of a diagnostic evaluation for Lyme disease, the Western Blot should be performed by a laboratory that reads and reports all of the bands related to Borrelia burgdorferi. Laboratories that use FDA approved kits (for instance, the Mardx Marblot®) are restricted from reporting all of the bands, as they must abide by the rules of the manufacturer. These rules are set up in accordance with the CDCs surveillance criteria and increase the risk of false-negative results. The commercial kits may be useful for surveillance purposes, but they offer too little information to be useful in patient management.
9. There are 5 subspecies of Borrelia burgdorferi, over 100 strains in the US, and 300 strains worldwide. This diversity is thought to contribute to the antigenic variability of the spirochete and its ability to evade the immune system and antibiotic therapy, leading to chronic infection.
10. Testing for Babesia, Anaplasma, Ehrlichia and Bartonella (other tick-transmitted organisms) should be performed. The presence of co-infection with these organisms points to probable infection with the Lyme spirochete as well. If these coinfections are left untreated, their continued presence increases morbidity and prevents successful treatment of Lyme disease.
11. A preponderance of evidence indicates that active ongoing spirochetal infection with or without other tick-borne coinfections is the cause of the persistent symptoms in chronic Lyme disease.
12. There has never been a study demonstrating that 30 days of antibiotic treatment cures chronic Lyme disease. However there is a plethora of documentation in the US and European medical literature demonstrating by histology and culture techniques that short courses of antibiotic treatment fail to eradicate the Lyme spirochete. Short treatment courses have resulted in upwards of a 40% relapse rate, especially if treatment is delayed.
13. Most cases of chronic Lyme disease require an extended course of antibiotic therapy to achieve symptomatic relief. The return of symptoms and evidence of the continued presence of Borrelia burgdorferi indicates the need for further treatment. The very real consequences of untreated chronic persistent Lyme infection far outweigh the potential consequences of long-term antibiotic therapy.
14. Many patients with chronic Lyme disease require prolonged treatment until the patient is symptom-free. Relapses occur and retreatment may be required. There are no tests currently available to prove that the organism is eradicated or that the patient with chronic Lyme disease is cured.
15. Like syphilis in the 19th century, Lyme disease has been called the great imitator and should be considered in the differential diagnosis of rheumatologic and neurologic conditions, as well as chronic fatigue syndrome, fibromyalgia, somatization disorder and any difficult-to-diagnose multi-system illness.
Disclaimer: The foregoing information is for educational purposes only. It is not intended to replace or supersede patient care by a healthcare provider. If an individual suspects the presence of a tick-borne illness, that individual should consult a healthcare provider who is familiar with the diagnosis and treatment of tick-borne diseases.
Distinct pattern of cognitive impairment noted in study of Lyme patients
Distinct pattern of cognitive impairment noted in study of Lyme patients
by Marian Rissenberg, Ph.D. & Susan Chambers, M.D.
the Lyme Times, Vol. 20, January-March 1998, pp. 29 -32
1) Cognitive Characteristics of Chronic Lyme Encephalopathy
On the basis of both a formal neuropsychological study of 49 patients (APA 5/96) and on clinical observation and comprehensive neuropsychological examination of well over 100 patients, a distinct pattern of cognitive impairment occurring chronic Lyme disease can be described. These patients consistently demonstrate deficits in directed, sustained and divided attention, planning and organization of responses, temporal ordering, verbal fluency, abstract reasoning, speed of processing, and motor programming. The overall pattern of intellectual impairment is not unlike that seen with diffuse brain injury, and it most often results in some degree of work-related disability.
Although performance is impaired on measures of cognitive functions associated with specific brain regions -- receptive and expressive language, visuospatial problem solving and memory -- the quality of performance is not suggestive of focal lesions in these areas. Rather, deficits are secondary to impairment of higher level integrative functions, likely mediated by complex neuronal systems. Specifically, the receptive language deficit is secondary to impaired auditory tracking and slowing of mental processing. The expressive language deficit is secondary to impaired word retrieval and response planning, The visuospatial problem solving deficit is secondary to impairment of mental flexibility, conceptualization and the ability to compare and contrast necessary in decision making. Finally, deficits on test of memory function are most often secondary to impairment of the encoding or initial processing of information, which depends on attention, and the retrieval of stored information. The storage of new information, or memory per se, is rarely impaired.
This pattern suggests that cognitive dysfunction in chronic Lyme, while expressed variably across individual patients, results from a common factor -- the breakdown of diffusely represented processes involving both integration and activation, and impacting primarily on attention and reasoning. The fluctuation of impairment over short periods of time suggest that a physiologic rather than a structural mechanism is responsible.
2) Neuropsychological deficits in chronic Lyme disease (A study presented at the annual meeting of The American Psychiatric Association , May 1996)
The neuro-psychological characteristics of 49 patients with Lyme disease were examined. The study set out to answer three questions:
1) Do all patients with subjectively perceived cognitive dysfunction have measurable intellectual impairment on objective testing?
2) In those without measurable impairment, does depression account for the perception of cognitive dysfunction?
3) What is the nature of the cognitive impairment in Lyme disease when it does occur?
Subjects were patients seen consecutively between 1990 and 1994 in a private neuropsycological practice with complaints of cognitive dysfunction and a symptom complex consistent with Lyme disease. Diagnosis was based on former CDC criteria. Mean duration of illness, defined as the time from the onset of general symptoms to the neuro-psychological exam, was 4.7 years (range: 3.3 to 14 years). Mean age was 39.9 years (range: 21 to 58 years) from 18 to 60 years. Mean level of education was 15.3 years (range 12 to 20 years).
Subjects were interviewed and administered a comprehensive battery of tests, including the complete WAIS-R and WMS-R, and additional test of language, attention, reasoning, visuospatial processing and complex motor function. They also completed the Beck Depression Inventory and a symptom checklist. Tests were divided into seven groups based on the cognitive functions they are presumed to measure: Attention, Memory, Language, Visuospatial Processing, Reasoning, Verbal Fluency and Motor programming.
Subjects were grouped into three levels of impairment based on their neuropsychological performance: Intact (N=11; 22%), with no functions impaired, Moderate (N=31; 63%) with two functions impaired, and Severe (N=7; 14%) with three or more functions impaired. Subjects in the Severe group met diagnostic criteria for dementia. The correlation between depression and cognitive impairment was nonsignificant, but the trend was positive, rather that negative. Anxiety by self report was significantly greater in the impaired groups that the Intact group. Duration of illness was greater in the Severe group (nonsignificant).
Of the 38 subjects with cognitive impairment, deficits of attention were most common, occurring in 26 subjects (68%) Deficits of memory storage were least common, occurring in 8 subjects (21%), Motor, Verbal Fluency, Visuospatial, Language and Reasoning deficits occurred in 24, 26, 29, 36 and 36% of the subjects respectively.
3) Possible Pathophysiologic Mechanisms of Cognitive Impairment in Lyme Disease
Based on these findings and on patients' reports, two characteristics of Lyme Encephalopathy arise which provide insight as to possible neurophysiologic mechanisms:
One, the nonfocal nature of the cognitive functions affected, and
Two, the subtle fluctuations and reportedly abrupt and global shifts in cognitive function from one day to another in a given patient.
Four broad categories of possible neurophysiologic mechanisms might be compatible with this pattern:
1) Diffuse cerebral diffusion abnormalities -- Single photon emission computerized tomography (SPECT) scans of the brain in Lyme disease often display a diffuse pattern consistent with heterogeneous areas of hyperfusion and/or diminished neuronal metabolism. While vasodilators are often capable of reversing these abnormal patterns on SPECT scan, this reversal does not consistently correlate with a symptomatic improvement in cognitive function.
2) Alterations in cellular metabolism at the cortical level -- Evidence of alterations in neurotransmitter function is suggested by clinical evidence of cognitive improvement following treatment with selective serotonin reuptake inhibitors (SSRI's) which appears to be independent of their antidepressant effect. Systematic studies of the impact of SSRI's on cognitive function, as well as the role of other transmitters, are required.
3) Neuro transmitter abnormalities (imbalances of synthesis and/or receptor activity) -- Neurotoxic substances may well play a role in Lyme Encephalopathy. given the neurotropic nature to Treponema pallidim , and the close parallel between syphilis and Lyme disease, it is possible that Borrelia burgdorferi could produce intracellular or extracellular neurotoxins which we have yet to identify.
4) Neurotoxic substances produced endogenously or possibly exogenously -- Endogenous neurotoxins have been identified as by-products of the humoral immune response. Among these is quinolinic acid, a product of the interleukin cascade system, which accumulates as a result of the humoral response to acute infectious agents and functions as a neuronal excitotoxin. As there are many similarities between Lyme Encephalopathy and the nonspecific mental dysfunction of acute systemic infections, such as influenza, it is quite possible that continue stimulation of production of quinolinic acid and other cytokines plays a role in the pathophysiology of Lyme encephalopathy.
4) Clinical Impressions and Implications for Diagnosis and Treatment in Chronic Lyme Disease
This study demonstrates that for the majority of chronic Lyme patients with cognitive complaints, there is in fact a measurable and significant decline in intellectual acuity. The nature and severity of the cognitive impairment is such that it interferes with all aspects of normal functioning: employment, home, marriage, social interactions, and general emotional well-being. Rather than the cognitive complaints being secondary to anxiety or depression, as is sometimes suspected, depression and anxiety increase with, and are apparently secondary to, cognitive impairment and the emotional and practical impact of a loss of competence. Thus, while patients with chronic Lyme disease can present a confusing and "psychiatric" picture to the clinician, it is important that their concerns be properly investigated and addressed.
Patients with Lyme encephalopathy complain of problems with memory and concentration, word retrieval, confusion, problems with thinking, "mental fogginess", a decline in job performance, difficulty with calculations, directions, and judgment. Decreased initiative, manifest as difficulty getting started with or following through with projects is often noted. Mood disturbance is common with complaints of irritability, explosiveness or "a short fuse," sadness, hopelessness or guilt, increased anxiety or mood swings. Sleep disturbance is also common, and can present as initial, middle or terminal insomnia or some combination of these. Fatigue is universal. Headache is common, and of course joint and muscle pain. Increased sensitivity to light and noise, visual disturbance, and tingling in the extremities are also common.
On interview patients with Lyme encephalopathy tend to be vague and disorganized in the presentation of the history of their illness. This is despite their close attention to their symptoms and having recounted them many times before. Although in most cases memory of discreet events - tests, dates, diagnoses, responses to medications -- is intact, the patient is unable to recall them spontaneously or organize them in temporal order. They may be unclear as to their chief complaint. They may completely lose track of what they were saying, sometimes repeatedly, or of what the question was. They may get off on a tangent and have trouble re-orienting themselves. Frequent prompting and refocusing will be necessary. beginning the interview with an open-ended question like "Tell me what the problem is" will allow these qualities to become clear.
Often patients with chronic Lyme disease will seem overly focused on their illness, or overly concerned with convincing the clinician that they are ill. The clinician may be tempted to interpret this as evidence of a primary psychiatric disorder. It is important to understand that the frustration many of these patients experience is real, and results from the general attitude of doubt toward Lyme disease as a serious and chronic illness, the invisibility of their symptoms, the difficulty in getting a definitive diagnosis and getting approval for extended treatment from insurance carries. Many have been accused of hypochondriasis or malingering. As with head injury, the patient may "look fin" though they are having difficulty with very basic work, social and day to day functioning.
The cognitive deficits in chronic Lyme disease involve primarily attention and arousal mechanisms. Patients have difficulty keeping track of external and internal events, retrieval of information from memory and with planning and sequencing, as occurs in attention deficit disorder. However their experience is different from that of ADD, in that rather than having the experience that there are many thoughts competing for attention, the Lyme patient has difficulty bringing any thought into clear focus. They experience difficulty thinking. One patient described it as the universe ending six inches from his face. He can't process information that is not immediately apparent, immediately experienced. Another said that when he tries to think about something, or figure something out, all he can do is repeat the question -- he can't get to the meaning. This is like the idea of "surface" versus "deep" processing in cognitive psychology. Reading a passage for typing errors would be surface processing, while reading for meaning is deep processing. One patient, a physician, described it as a "mental intention tremor" -- the more she tries to focus on something the more out of focus it becomes.
The clinician should proceed with empathy and reason. Specific cognitive complaints in previously high functioning individuals are unusual and indicative of serious illness, either psychiatric or neurologic. Comprehensive neuropsychological evaluation will most often differentiate the two.
Where the neuropsychological exam is normal or there is a significant psychiatric component, a psychiatric evaluation is advised. Psychiatric symptomatology is not uncommon in Lyme and the presence of depression, anxiety, obsessive compulsive symptoms, flat affect and so on may cloud the issue of significant cognitive decline. Both the cognitive and psychiatric symptoms would be expected to improve with antibiotic treatment in Lyme encephalopathy. However sometimes concurrent treatment with psychotropic medication is necessary.
Unfortunately for some patients significant cognitive impairment persists even after years of antibiotic treatment. These patients may never be able to return to their premorbid level of employment, or be gainfully employed at all. Cognitive remediation can help them learn strategies for improving memory and concentration and relieving stress. Support and advice in regard to living with a chronic condition is equally important. Strategies include reducing work hours when possible, taking regular rest periods during the day, limiting the number of outings in a week, and using a calendar to stay organized and structure their time.
5) Cognitive impairment in Lyme disease: specific functions and the impact or deficits
1. Attention and mental tracking: includes directed and sustained attention: the ability to direct and maintain one's focus on a particular event or idea, whether in the environment or internally; and divided attention: the ability to simultaneously attend to two events, or dot two or more things at a time, or to retain awareness of one thing while doing another.
Impact: difficulty functioning effectively in many situations, remembering what one was doing before a distraction, keeping track of conversation, taking notes while someone is speaking, remembering that someone is on hold or what you were about to say.
2. Memory: Retaining new information.
Impact: secondary to impaired attention, slowing of processing and the retrieval of stored information, but not storage per se, a tendency to lose or forget things, miss appointments, repeat oneself.
3. Receptive language: understanding spoken or written language
Impact: secondary to impaired attention and speed of processing, difficulty participating in meetings or social conversation, difficulty with reading comprehension.
4. Expressive language: Using spoken or written language to express ideas
Impact: difficulty finding the right word, using the wrong word and not noticing, not being able to express oneself or communicate
5. Visuospatial Processing: Efficient scanning of the visual field, making sense of how things are related in space, visuospatial conceptualization and problem solving.
Impact: a tendency to get lost, difficulty with reading comprehension.
6. Abstract reasoning: The ability to generalize from the particular, to identify the common factor between related concepts, to compare and contrast two things or ideas, to see the "big picture", to identify the critical factor in a situation, to anticipate consequences and make inferences regarding cause and effect.
Impact: difficulty with decision making, planning, and problem solving.
7. Speed of mental and motor processing: the ability to think and respond quickly, critical to understanding speech which occurs at a fairly constant rate.
Impact: difficulty understanding or keeping up a conversation, functioning in a timely manner in day to day situations, meeting deadlines.
by Marian Rissenberg, Ph.D. & Susan Chambers, M.D.
the Lyme Times, Vol. 20, January-March 1998, pp. 29 -32
1) Cognitive Characteristics of Chronic Lyme Encephalopathy
On the basis of both a formal neuropsychological study of 49 patients (APA 5/96) and on clinical observation and comprehensive neuropsychological examination of well over 100 patients, a distinct pattern of cognitive impairment occurring chronic Lyme disease can be described. These patients consistently demonstrate deficits in directed, sustained and divided attention, planning and organization of responses, temporal ordering, verbal fluency, abstract reasoning, speed of processing, and motor programming. The overall pattern of intellectual impairment is not unlike that seen with diffuse brain injury, and it most often results in some degree of work-related disability.
Although performance is impaired on measures of cognitive functions associated with specific brain regions -- receptive and expressive language, visuospatial problem solving and memory -- the quality of performance is not suggestive of focal lesions in these areas. Rather, deficits are secondary to impairment of higher level integrative functions, likely mediated by complex neuronal systems. Specifically, the receptive language deficit is secondary to impaired auditory tracking and slowing of mental processing. The expressive language deficit is secondary to impaired word retrieval and response planning, The visuospatial problem solving deficit is secondary to impairment of mental flexibility, conceptualization and the ability to compare and contrast necessary in decision making. Finally, deficits on test of memory function are most often secondary to impairment of the encoding or initial processing of information, which depends on attention, and the retrieval of stored information. The storage of new information, or memory per se, is rarely impaired.
This pattern suggests that cognitive dysfunction in chronic Lyme, while expressed variably across individual patients, results from a common factor -- the breakdown of diffusely represented processes involving both integration and activation, and impacting primarily on attention and reasoning. The fluctuation of impairment over short periods of time suggest that a physiologic rather than a structural mechanism is responsible.
2) Neuropsychological deficits in chronic Lyme disease (A study presented at the annual meeting of The American Psychiatric Association , May 1996)
The neuro-psychological characteristics of 49 patients with Lyme disease were examined. The study set out to answer three questions:
1) Do all patients with subjectively perceived cognitive dysfunction have measurable intellectual impairment on objective testing?
2) In those without measurable impairment, does depression account for the perception of cognitive dysfunction?
3) What is the nature of the cognitive impairment in Lyme disease when it does occur?
Subjects were patients seen consecutively between 1990 and 1994 in a private neuropsycological practice with complaints of cognitive dysfunction and a symptom complex consistent with Lyme disease. Diagnosis was based on former CDC criteria. Mean duration of illness, defined as the time from the onset of general symptoms to the neuro-psychological exam, was 4.7 years (range: 3.3 to 14 years). Mean age was 39.9 years (range: 21 to 58 years) from 18 to 60 years. Mean level of education was 15.3 years (range 12 to 20 years).
Subjects were interviewed and administered a comprehensive battery of tests, including the complete WAIS-R and WMS-R, and additional test of language, attention, reasoning, visuospatial processing and complex motor function. They also completed the Beck Depression Inventory and a symptom checklist. Tests were divided into seven groups based on the cognitive functions they are presumed to measure: Attention, Memory, Language, Visuospatial Processing, Reasoning, Verbal Fluency and Motor programming.
Subjects were grouped into three levels of impairment based on their neuropsychological performance: Intact (N=11; 22%), with no functions impaired, Moderate (N=31; 63%) with two functions impaired, and Severe (N=7; 14%) with three or more functions impaired. Subjects in the Severe group met diagnostic criteria for dementia. The correlation between depression and cognitive impairment was nonsignificant, but the trend was positive, rather that negative. Anxiety by self report was significantly greater in the impaired groups that the Intact group. Duration of illness was greater in the Severe group (nonsignificant).
Of the 38 subjects with cognitive impairment, deficits of attention were most common, occurring in 26 subjects (68%) Deficits of memory storage were least common, occurring in 8 subjects (21%), Motor, Verbal Fluency, Visuospatial, Language and Reasoning deficits occurred in 24, 26, 29, 36 and 36% of the subjects respectively.
3) Possible Pathophysiologic Mechanisms of Cognitive Impairment in Lyme Disease
Based on these findings and on patients' reports, two characteristics of Lyme Encephalopathy arise which provide insight as to possible neurophysiologic mechanisms:
One, the nonfocal nature of the cognitive functions affected, and
Two, the subtle fluctuations and reportedly abrupt and global shifts in cognitive function from one day to another in a given patient.
Four broad categories of possible neurophysiologic mechanisms might be compatible with this pattern:
1) Diffuse cerebral diffusion abnormalities -- Single photon emission computerized tomography (SPECT) scans of the brain in Lyme disease often display a diffuse pattern consistent with heterogeneous areas of hyperfusion and/or diminished neuronal metabolism. While vasodilators are often capable of reversing these abnormal patterns on SPECT scan, this reversal does not consistently correlate with a symptomatic improvement in cognitive function.
2) Alterations in cellular metabolism at the cortical level -- Evidence of alterations in neurotransmitter function is suggested by clinical evidence of cognitive improvement following treatment with selective serotonin reuptake inhibitors (SSRI's) which appears to be independent of their antidepressant effect. Systematic studies of the impact of SSRI's on cognitive function, as well as the role of other transmitters, are required.
3) Neuro transmitter abnormalities (imbalances of synthesis and/or receptor activity) -- Neurotoxic substances may well play a role in Lyme Encephalopathy. given the neurotropic nature to Treponema pallidim , and the close parallel between syphilis and Lyme disease, it is possible that Borrelia burgdorferi could produce intracellular or extracellular neurotoxins which we have yet to identify.
4) Neurotoxic substances produced endogenously or possibly exogenously -- Endogenous neurotoxins have been identified as by-products of the humoral immune response. Among these is quinolinic acid, a product of the interleukin cascade system, which accumulates as a result of the humoral response to acute infectious agents and functions as a neuronal excitotoxin. As there are many similarities between Lyme Encephalopathy and the nonspecific mental dysfunction of acute systemic infections, such as influenza, it is quite possible that continue stimulation of production of quinolinic acid and other cytokines plays a role in the pathophysiology of Lyme encephalopathy.
4) Clinical Impressions and Implications for Diagnosis and Treatment in Chronic Lyme Disease
This study demonstrates that for the majority of chronic Lyme patients with cognitive complaints, there is in fact a measurable and significant decline in intellectual acuity. The nature and severity of the cognitive impairment is such that it interferes with all aspects of normal functioning: employment, home, marriage, social interactions, and general emotional well-being. Rather than the cognitive complaints being secondary to anxiety or depression, as is sometimes suspected, depression and anxiety increase with, and are apparently secondary to, cognitive impairment and the emotional and practical impact of a loss of competence. Thus, while patients with chronic Lyme disease can present a confusing and "psychiatric" picture to the clinician, it is important that their concerns be properly investigated and addressed.
Patients with Lyme encephalopathy complain of problems with memory and concentration, word retrieval, confusion, problems with thinking, "mental fogginess", a decline in job performance, difficulty with calculations, directions, and judgment. Decreased initiative, manifest as difficulty getting started with or following through with projects is often noted. Mood disturbance is common with complaints of irritability, explosiveness or "a short fuse," sadness, hopelessness or guilt, increased anxiety or mood swings. Sleep disturbance is also common, and can present as initial, middle or terminal insomnia or some combination of these. Fatigue is universal. Headache is common, and of course joint and muscle pain. Increased sensitivity to light and noise, visual disturbance, and tingling in the extremities are also common.
On interview patients with Lyme encephalopathy tend to be vague and disorganized in the presentation of the history of their illness. This is despite their close attention to their symptoms and having recounted them many times before. Although in most cases memory of discreet events - tests, dates, diagnoses, responses to medications -- is intact, the patient is unable to recall them spontaneously or organize them in temporal order. They may be unclear as to their chief complaint. They may completely lose track of what they were saying, sometimes repeatedly, or of what the question was. They may get off on a tangent and have trouble re-orienting themselves. Frequent prompting and refocusing will be necessary. beginning the interview with an open-ended question like "Tell me what the problem is" will allow these qualities to become clear.
Often patients with chronic Lyme disease will seem overly focused on their illness, or overly concerned with convincing the clinician that they are ill. The clinician may be tempted to interpret this as evidence of a primary psychiatric disorder. It is important to understand that the frustration many of these patients experience is real, and results from the general attitude of doubt toward Lyme disease as a serious and chronic illness, the invisibility of their symptoms, the difficulty in getting a definitive diagnosis and getting approval for extended treatment from insurance carries. Many have been accused of hypochondriasis or malingering. As with head injury, the patient may "look fin" though they are having difficulty with very basic work, social and day to day functioning.
The cognitive deficits in chronic Lyme disease involve primarily attention and arousal mechanisms. Patients have difficulty keeping track of external and internal events, retrieval of information from memory and with planning and sequencing, as occurs in attention deficit disorder. However their experience is different from that of ADD, in that rather than having the experience that there are many thoughts competing for attention, the Lyme patient has difficulty bringing any thought into clear focus. They experience difficulty thinking. One patient described it as the universe ending six inches from his face. He can't process information that is not immediately apparent, immediately experienced. Another said that when he tries to think about something, or figure something out, all he can do is repeat the question -- he can't get to the meaning. This is like the idea of "surface" versus "deep" processing in cognitive psychology. Reading a passage for typing errors would be surface processing, while reading for meaning is deep processing. One patient, a physician, described it as a "mental intention tremor" -- the more she tries to focus on something the more out of focus it becomes.
The clinician should proceed with empathy and reason. Specific cognitive complaints in previously high functioning individuals are unusual and indicative of serious illness, either psychiatric or neurologic. Comprehensive neuropsychological evaluation will most often differentiate the two.
Where the neuropsychological exam is normal or there is a significant psychiatric component, a psychiatric evaluation is advised. Psychiatric symptomatology is not uncommon in Lyme and the presence of depression, anxiety, obsessive compulsive symptoms, flat affect and so on may cloud the issue of significant cognitive decline. Both the cognitive and psychiatric symptoms would be expected to improve with antibiotic treatment in Lyme encephalopathy. However sometimes concurrent treatment with psychotropic medication is necessary.
Unfortunately for some patients significant cognitive impairment persists even after years of antibiotic treatment. These patients may never be able to return to their premorbid level of employment, or be gainfully employed at all. Cognitive remediation can help them learn strategies for improving memory and concentration and relieving stress. Support and advice in regard to living with a chronic condition is equally important. Strategies include reducing work hours when possible, taking regular rest periods during the day, limiting the number of outings in a week, and using a calendar to stay organized and structure their time.
5) Cognitive impairment in Lyme disease: specific functions and the impact or deficits
1. Attention and mental tracking: includes directed and sustained attention: the ability to direct and maintain one's focus on a particular event or idea, whether in the environment or internally; and divided attention: the ability to simultaneously attend to two events, or dot two or more things at a time, or to retain awareness of one thing while doing another.
Impact: difficulty functioning effectively in many situations, remembering what one was doing before a distraction, keeping track of conversation, taking notes while someone is speaking, remembering that someone is on hold or what you were about to say.
2. Memory: Retaining new information.
Impact: secondary to impaired attention, slowing of processing and the retrieval of stored information, but not storage per se, a tendency to lose or forget things, miss appointments, repeat oneself.
3. Receptive language: understanding spoken or written language
Impact: secondary to impaired attention and speed of processing, difficulty participating in meetings or social conversation, difficulty with reading comprehension.
4. Expressive language: Using spoken or written language to express ideas
Impact: difficulty finding the right word, using the wrong word and not noticing, not being able to express oneself or communicate
5. Visuospatial Processing: Efficient scanning of the visual field, making sense of how things are related in space, visuospatial conceptualization and problem solving.
Impact: a tendency to get lost, difficulty with reading comprehension.
6. Abstract reasoning: The ability to generalize from the particular, to identify the common factor between related concepts, to compare and contrast two things or ideas, to see the "big picture", to identify the critical factor in a situation, to anticipate consequences and make inferences regarding cause and effect.
Impact: difficulty with decision making, planning, and problem solving.
7. Speed of mental and motor processing: the ability to think and respond quickly, critical to understanding speech which occurs at a fairly constant rate.
Impact: difficulty understanding or keeping up a conversation, functioning in a timely manner in day to day situations, meeting deadlines.
Saturday, May 29, 2010
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All of our products are free of artificial colors, perfumes, fragrances, sulfates or preservatives. We use Rosemary Extract as a natural preservative. No animal products (except honey soap), animal by-products or animal testing.
USDA Approved, Certified Organic alternatives to the often irritating, chemical and detergent based personal care products now in general use. Handmade cold process bar soaps for sensitive skin. Master Soapmakers blend organic food grade ingredients into soap products the old fashioned way. Our special bar soap process removes excess alkali from the soap, creating a super mild bar for the most sensitive skin.
These organic handcrafted soaps produce a rich moisturizing lather to thoroughly cleanse and can be used by anyone even those with sensitive skin. Many soaps are just plain boring. Enjoy your experience each time with unique soap blends for every mood, season and person.
It takes nearly a month to handcraft a bar of Soap. Only this 200 year old process yields a bar of soap suitable for the most sensitive skin.
Always gentle, hypoallergenic and completely natural. No wonder they call it the mildest soap on Earth!
10 Choices of Natural Organic Handcrafted Soaps to choose from.
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Measuring the Pollution in People
Measuring the Pollution in People
A number of striking studies (i) have shown that the man-made chemicals in our environment and in consumer products—including cosmetics—make their way into our bodies. Many of the chemicals found in cosmetics are absorbed by the skin into the body, and can be detected in blood or urine.
The length of time chemicals remain in the body varies from chemical to chemical and ranges from hours to decades. For chemicals that are excreted quickly, the fact that we can so consistently measure them indicates continual exposures that may have long-term effects on health.
Body Burden and Biomonitoring (Buy natural organic products)
Body burden refers to the levels of man-made chemicals in an individual’s body, generally measured through blood or urine. Large-scale biomonitoring programs that assess the levels of chemicals in a population or subset of a population would greatly support the ability of researchers to explore the links between exposures and disease. A gap in determining the long-term effects of chemical exposures upon disease has long been a lack of knowledge about chemical exposures and the intake of environmental toxins into the body. Ongoing biomonitoring programs would fill this vital data gap.
The Pollution in People (Buy natural organic products)
The largest U.S. body burden study to date measured the levels of 148 chemicals in approximately 3,000 people of varying ages, ethnicities and geographical locations (ii). This study, by the U.S. Centers for Disease Control, detected a common sunscreen ingredient, benzophenone-3 (BP-3) in 96.8 percent of individuals (iii), and triclosan, an antibacterial agent often used in antibacterial soaps, in 74.6 percent of individuals (iv). A CDC study found residues of four different phthalates in more than 75 percent of subjects (v). Phthalates are found in numerous cosmetics, often as a constituent ingredient of fragrances. A 2008 study of teen girls by the Environmental Working Group revealed 16 hormone-altering cosmetics chemicals in their young test subjects (vi).
The CDC tests of 148 chemicals represents a very small percentage of the over 80,000 chemicals manufactured and the approximately 10,000 chemicals used in cosmetic products. The next edition of the CDC report, anticipated in 2009, will include measurements of 250 chemicals, an increase that still doesn't approach the total number of chemicals in commerce. Nevertheless, this and other studies illustrate that chemicals we use in an array of consumer products make their way into our bodies (vii). This knowledge also furthers our understanding of the links between the chemicals we use, the absorption of these chemicals into our bodies, and the known and probable health effects of these chemicals.
More Information (Buy natural organic products)
Report: "Earliest Exposures" biomonitoring study of pregnant women (2009)
Report: "Hazardous Chemicals in Health Care: A Snapshot of Chemicals in Doctors and Nurses" (2009)
Report: "Teen Girls' Body Burden of Hormone-Altering Cosmetics Chemicals" (2008)
i Commonweal Biomonitoring Resource Center (2005). Taking It All In: Documenting Chemical Pollution in Californians through Biomonitoring. Available online at http://www.commonweal.org/programs/download/TIAI_1205.pdf. Accessed August 19, 2008.
Environmental Working Group (2006). Across Generations: Industrial Chemicals in Mothers and Daughters: The pollution we share and inherit. Available online at http://www.ewg.org/reports/generations/. Accessed August 19, 2008.
Environmental Working Group (2005). Body Burden: The Pollution in Newborns. Available online at: http://www.ewg.org/node/17686. Accessed August 19, 2008.
Environmental Working Group (2003). Body Burden: The Pollution in People. Available online at: http://archive.ewg.org/reports/bodyburden1/. Accessed August 19, 2008.
ii Centers for Disease Control and Prevention (CDC) (2005). Third National Report on Human Exposure to Environmental Chemicals. Available online at http://www.cdc.gov/exposurereport/. Accessed December 23, 2008.
iii Calafat AM, Wong LY, Ye X, Reidy JA, Needham LL. Concentrations of the Sunscreen Agent, Benzophenone-3, in Residents of the United States: National Health and Nutrition Examination Survey 2003-2004. Environ Health Perspect 116:893–897 (2008).
iv Calafat AM, Ye X, Wong LY, Reidy JA, Needham LL. Urinary Concentrations of Triclosan in the U.S. Population: 2003–2004. Environmental Health Perspectives, 116:303–307 (2008).
v Silva MJ, Barr DB, Reidy JA, Malek NA, Hodge CC, Caudill SP, Brock JW, Needham LL, Calafat AM. “Urinary Levels of Seven Phthalate Metabolites in the U.S. Population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000,” Environmental Health Perspectives, 112(3): 331-338 (2004).
vi Sutton, R (2008). Teen Girls' Body Burden of Hormone-Altering Cosmetics Chemicals. Available online at http://www.ewg.org/reports/teens. Accessed October 10, 2008.
vii Commonweal and Breast Cancer Fund (2005). Taking It All In: Documenting Chemical Pollution in Californians through Biomonitoring. Available online at http://www.commonweal.org/programs/download/TIAI_1205.pdf. Accessed August 19, 2008.
Environmental Working Group (2006). Across Generations: Industrial Chemicals in Mothers and Daughters: The pollution we share and inherit. Available online at http://www.ewg.org/reports/generations/. Accessed August 19, 2008.
Environmental Working Group (2005). Body Burden: The Pollution in Newborns. Available online at: http://www.ewg.org/node/17686. Accessed August 19, 2008.
Environmental Working Group (2003). Body Burden: The Pollution in People. Available online at: http://archive.ewg.org/reports/bodyburden1/. Accessed August 19, 2008.
(Read your ingredients and know what you are putting on your body - Buy natural organic products)
A number of striking studies (i) have shown that the man-made chemicals in our environment and in consumer products—including cosmetics—make their way into our bodies. Many of the chemicals found in cosmetics are absorbed by the skin into the body, and can be detected in blood or urine.
The length of time chemicals remain in the body varies from chemical to chemical and ranges from hours to decades. For chemicals that are excreted quickly, the fact that we can so consistently measure them indicates continual exposures that may have long-term effects on health.
Body Burden and Biomonitoring (Buy natural organic products)
Body burden refers to the levels of man-made chemicals in an individual’s body, generally measured through blood or urine. Large-scale biomonitoring programs that assess the levels of chemicals in a population or subset of a population would greatly support the ability of researchers to explore the links between exposures and disease. A gap in determining the long-term effects of chemical exposures upon disease has long been a lack of knowledge about chemical exposures and the intake of environmental toxins into the body. Ongoing biomonitoring programs would fill this vital data gap.
The Pollution in People (Buy natural organic products)
The largest U.S. body burden study to date measured the levels of 148 chemicals in approximately 3,000 people of varying ages, ethnicities and geographical locations (ii). This study, by the U.S. Centers for Disease Control, detected a common sunscreen ingredient, benzophenone-3 (BP-3) in 96.8 percent of individuals (iii), and triclosan, an antibacterial agent often used in antibacterial soaps, in 74.6 percent of individuals (iv). A CDC study found residues of four different phthalates in more than 75 percent of subjects (v). Phthalates are found in numerous cosmetics, often as a constituent ingredient of fragrances. A 2008 study of teen girls by the Environmental Working Group revealed 16 hormone-altering cosmetics chemicals in their young test subjects (vi).
The CDC tests of 148 chemicals represents a very small percentage of the over 80,000 chemicals manufactured and the approximately 10,000 chemicals used in cosmetic products. The next edition of the CDC report, anticipated in 2009, will include measurements of 250 chemicals, an increase that still doesn't approach the total number of chemicals in commerce. Nevertheless, this and other studies illustrate that chemicals we use in an array of consumer products make their way into our bodies (vii). This knowledge also furthers our understanding of the links between the chemicals we use, the absorption of these chemicals into our bodies, and the known and probable health effects of these chemicals.
More Information (Buy natural organic products)
Report: "Earliest Exposures" biomonitoring study of pregnant women (2009)
Report: "Hazardous Chemicals in Health Care: A Snapshot of Chemicals in Doctors and Nurses" (2009)
Report: "Teen Girls' Body Burden of Hormone-Altering Cosmetics Chemicals" (2008)
i Commonweal Biomonitoring Resource Center (2005). Taking It All In: Documenting Chemical Pollution in Californians through Biomonitoring. Available online at http://www.commonweal.org/programs/download/TIAI_1205.pdf. Accessed August 19, 2008.
Environmental Working Group (2006). Across Generations: Industrial Chemicals in Mothers and Daughters: The pollution we share and inherit. Available online at http://www.ewg.org/reports/generations/. Accessed August 19, 2008.
Environmental Working Group (2005). Body Burden: The Pollution in Newborns. Available online at: http://www.ewg.org/node/17686. Accessed August 19, 2008.
Environmental Working Group (2003). Body Burden: The Pollution in People. Available online at: http://archive.ewg.org/reports/bodyburden1/. Accessed August 19, 2008.
ii Centers for Disease Control and Prevention (CDC) (2005). Third National Report on Human Exposure to Environmental Chemicals. Available online at http://www.cdc.gov/exposurereport/. Accessed December 23, 2008.
iii Calafat AM, Wong LY, Ye X, Reidy JA, Needham LL. Concentrations of the Sunscreen Agent, Benzophenone-3, in Residents of the United States: National Health and Nutrition Examination Survey 2003-2004. Environ Health Perspect 116:893–897 (2008).
iv Calafat AM, Ye X, Wong LY, Reidy JA, Needham LL. Urinary Concentrations of Triclosan in the U.S. Population: 2003–2004. Environmental Health Perspectives, 116:303–307 (2008).
v Silva MJ, Barr DB, Reidy JA, Malek NA, Hodge CC, Caudill SP, Brock JW, Needham LL, Calafat AM. “Urinary Levels of Seven Phthalate Metabolites in the U.S. Population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000,” Environmental Health Perspectives, 112(3): 331-338 (2004).
vi Sutton, R (2008). Teen Girls' Body Burden of Hormone-Altering Cosmetics Chemicals. Available online at http://www.ewg.org/reports/teens. Accessed October 10, 2008.
vii Commonweal and Breast Cancer Fund (2005). Taking It All In: Documenting Chemical Pollution in Californians through Biomonitoring. Available online at http://www.commonweal.org/programs/download/TIAI_1205.pdf. Accessed August 19, 2008.
Environmental Working Group (2006). Across Generations: Industrial Chemicals in Mothers and Daughters: The pollution we share and inherit. Available online at http://www.ewg.org/reports/generations/. Accessed August 19, 2008.
Environmental Working Group (2005). Body Burden: The Pollution in Newborns. Available online at: http://www.ewg.org/node/17686. Accessed August 19, 2008.
Environmental Working Group (2003). Body Burden: The Pollution in People. Available online at: http://archive.ewg.org/reports/bodyburden1/. Accessed August 19, 2008.
(Read your ingredients and know what you are putting on your body - Buy natural organic products)
Parabens
Parabens
Parabens are used to prevent the growth of microbes in cosmetic products and can be absorbed through the skin, blood and digestive system (i). They have been found in biopsies from breast tumors (ii) at concentrations similar to those found in consumer products (iii). Parabens are found in nearly all urine samples from U.S. adults of a variety of ethnic, socioeconomic and geographic backgrounds (iv).
Products That May Contain Parabens (Buy Paraben FREE Products)
Parabens are several distinct chemicals with similar a molecular structure. Four of these occur frequently in cosmetics: ethylparaben, butylparaben, methylparaben and propylparaben. Methylparaben and propylparaben are the most common of these, each appearing in well over 10,000 of the 25,000 products in the Environmental Working Group's Skin Deep database.
Parabens appear mostly in personal care products that contain significant amounts of water, such as shampoos, conditioners, lotions and facial and shower cleansers and scrubs. While concentration limits are recommended for each paraben, these recommendations do not account for the use of multiple parabens in a single product or for exposure to parabens from several products by a single individual.
Health Concerns (Buy Paraben FREE Products)
EWG's Skin Deep database, which compares cosmetic ingredients to over 50 international toxicity databases, indicates that parabens are linked to cancer, endocrine disruption, reproductive toxicity, immunotoxicity, neurotoxicity and skin irritation (v). Since parabens are used to kill bacteria in water-based solutions, they inherently have some toxicity to cells (vi).
A 2004 UK study detected traces of five parabens in the breast cancer tumors of 19 out of 20 women studied (vii). This small study does not prove a causal relationship between parabens and breast cancer, but it is important because it detected the presence of intact parabens – unaltered by the body’s metabolism – which is an indication of the chemicals' ability to penetrate skin and remain in breast tissue.
Of greatest concern is that parabens are known to disrupt hormone function, an effect that is linked to increased risk of breast cancer and reproductive toxicity. Parabens mimic estrogen by binding to estrogen receptors on cells. They also increase the expression of genes usually regulated by estradiol (a form of estrogen); these genes cause human breast tumor cells to grow and multiply in cellular studies (viii).
Cosmetic manufacturers, particularly those in the natural/organic sector, are seeking effective alternatives to prevent microbial growth in personal care products. Another solution is to sell products with a shorter shelf life. Companies are testing new product formulations and have created preservative-free products with a shelf life of six months to one full year. For the products most people use daily – their favorite lotion, face wash or shampoo – products are likely to be used up before they would expire.
More Information
Skin Deep ingredient information: Parabens (Buy Paraben FREE Products)
i Gray, J (2008). State of the Evidence: The Connection between Breast Cancer and the Environment. San Francisco, CA: The Breast Cancer Fund.
ii Daubre PD, Aljarrah A, Miller WR, Coldham NG, Sauer MJ, Pope GS (2004). Concentrations of parabens in human breast tumours. Journal of Applied Toxicology 24:5-13.
iii Rastogi SC, Schouten A, Dekruijf N, Weijland JW (1995). Contents of methylparaben, ethylparaben, propylparaben, butylparaben and benzylparaben in cosmetic products. Contact Dermatits 32: 28-30.
iv Ye X, Bishop AM, Reidy JA, Needham LL, Calafat AM (2006). Parabens as urinary biomarkers of exposure in humans. Environmental Health Perspectives114: 1843-1846.
v Environmental Working Group. Skin Deep. Parabens. Available online: http://www.cosmeticsdatabase.com/ingredient.php?ingred06=704450&refurl=%2Fproduct.php%3Fprod_id%3D17311%26. Accessed December 9, 2008.
Environmental Working Group. Skin Deep. Methylparaben. Available online: Environmental Working Group. Skin Deep. Parabens. Available online: http://www.cosmeticsdatabase.com/ingredient.php?ingred06=704450&refurl=%2Fproduct.php%3Fprod_id%3D17311%26. Accessed December 9, 2008.
Environmental Working Group. Skin Deep. Butylparaben. Available online: http://www.cosmeticsdatabase.com/ingredient.php?ingred06=700868. Accessed December 9, 2008.
Environmental Working Group. Skin Deep. Propylparaben. Available online: http://www.cosmeticsdatabase.com/ingredient.php?ingred06=705335. Accessed December 9, 2008.
vi Ishiwatari S, Suzuki T, Hitomi T, Yoshino T, Matsukuma S, Tsuji T. (2006). Effects of methyl paraben on skin keratinocytes. Journal of Applied Toxicology 27:1-9.
Handa O, Kokura S, Adachi S, Takagi T, Naito Y, Tanigawa T, Yoshida N, Yoshikawa T. (2006). Methylparaben potentiates UV-induced damage on skin keratinocytes. Toxicology. 227: 62-72.
vii Darbre PD, Aljarrah A, Miller WR, Coldham NG, Sauer MJ, Pope GS (2004). Concentrations of parabens in human breast tumors. Journal of Applied Toxicology 24:5-13.
viiii Byford JR, Shaw LE, Drew MGB, Pope GS, Sauer MJ, Darbre PD (2002). Oestrogenic activity of parabens in MCF7 human breast cancer cells. Journal of Steroid Biochemistry & Molecular Biology 80:49-60.
Parabens are used to prevent the growth of microbes in cosmetic products and can be absorbed through the skin, blood and digestive system (i). They have been found in biopsies from breast tumors (ii) at concentrations similar to those found in consumer products (iii). Parabens are found in nearly all urine samples from U.S. adults of a variety of ethnic, socioeconomic and geographic backgrounds (iv).
Products That May Contain Parabens (Buy Paraben FREE Products)
Parabens are several distinct chemicals with similar a molecular structure. Four of these occur frequently in cosmetics: ethylparaben, butylparaben, methylparaben and propylparaben. Methylparaben and propylparaben are the most common of these, each appearing in well over 10,000 of the 25,000 products in the Environmental Working Group's Skin Deep database.
Parabens appear mostly in personal care products that contain significant amounts of water, such as shampoos, conditioners, lotions and facial and shower cleansers and scrubs. While concentration limits are recommended for each paraben, these recommendations do not account for the use of multiple parabens in a single product or for exposure to parabens from several products by a single individual.
Health Concerns (Buy Paraben FREE Products)
EWG's Skin Deep database, which compares cosmetic ingredients to over 50 international toxicity databases, indicates that parabens are linked to cancer, endocrine disruption, reproductive toxicity, immunotoxicity, neurotoxicity and skin irritation (v). Since parabens are used to kill bacteria in water-based solutions, they inherently have some toxicity to cells (vi).
A 2004 UK study detected traces of five parabens in the breast cancer tumors of 19 out of 20 women studied (vii). This small study does not prove a causal relationship between parabens and breast cancer, but it is important because it detected the presence of intact parabens – unaltered by the body’s metabolism – which is an indication of the chemicals' ability to penetrate skin and remain in breast tissue.
Of greatest concern is that parabens are known to disrupt hormone function, an effect that is linked to increased risk of breast cancer and reproductive toxicity. Parabens mimic estrogen by binding to estrogen receptors on cells. They also increase the expression of genes usually regulated by estradiol (a form of estrogen); these genes cause human breast tumor cells to grow and multiply in cellular studies (viii).
Cosmetic manufacturers, particularly those in the natural/organic sector, are seeking effective alternatives to prevent microbial growth in personal care products. Another solution is to sell products with a shorter shelf life. Companies are testing new product formulations and have created preservative-free products with a shelf life of six months to one full year. For the products most people use daily – their favorite lotion, face wash or shampoo – products are likely to be used up before they would expire.
More Information
Skin Deep ingredient information: Parabens (Buy Paraben FREE Products)
i Gray, J (2008). State of the Evidence: The Connection between Breast Cancer and the Environment. San Francisco, CA: The Breast Cancer Fund.
ii Daubre PD, Aljarrah A, Miller WR, Coldham NG, Sauer MJ, Pope GS (2004). Concentrations of parabens in human breast tumours. Journal of Applied Toxicology 24:5-13.
iii Rastogi SC, Schouten A, Dekruijf N, Weijland JW (1995). Contents of methylparaben, ethylparaben, propylparaben, butylparaben and benzylparaben in cosmetic products. Contact Dermatits 32: 28-30.
iv Ye X, Bishop AM, Reidy JA, Needham LL, Calafat AM (2006). Parabens as urinary biomarkers of exposure in humans. Environmental Health Perspectives114: 1843-1846.
v Environmental Working Group. Skin Deep. Parabens. Available online: http://www.cosmeticsdatabase.com/ingredient.php?ingred06=704450&refurl=%2Fproduct.php%3Fprod_id%3D17311%26. Accessed December 9, 2008.
Environmental Working Group. Skin Deep. Methylparaben. Available online: Environmental Working Group. Skin Deep. Parabens. Available online: http://www.cosmeticsdatabase.com/ingredient.php?ingred06=704450&refurl=%2Fproduct.php%3Fprod_id%3D17311%26. Accessed December 9, 2008.
Environmental Working Group. Skin Deep. Butylparaben. Available online: http://www.cosmeticsdatabase.com/ingredient.php?ingred06=700868. Accessed December 9, 2008.
Environmental Working Group. Skin Deep. Propylparaben. Available online: http://www.cosmeticsdatabase.com/ingredient.php?ingred06=705335. Accessed December 9, 2008.
vi Ishiwatari S, Suzuki T, Hitomi T, Yoshino T, Matsukuma S, Tsuji T. (2006). Effects of methyl paraben on skin keratinocytes. Journal of Applied Toxicology 27:1-9.
Handa O, Kokura S, Adachi S, Takagi T, Naito Y, Tanigawa T, Yoshida N, Yoshikawa T. (2006). Methylparaben potentiates UV-induced damage on skin keratinocytes. Toxicology. 227: 62-72.
vii Darbre PD, Aljarrah A, Miller WR, Coldham NG, Sauer MJ, Pope GS (2004). Concentrations of parabens in human breast tumors. Journal of Applied Toxicology 24:5-13.
viiii Byford JR, Shaw LE, Drew MGB, Pope GS, Sauer MJ, Darbre PD (2002). Oestrogenic activity of parabens in MCF7 human breast cancer cells. Journal of Steroid Biochemistry & Molecular Biology 80:49-60.
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