|Posted by Maddalena Frau on March 25, 2014 at 1:35 AM||comments (0)|
Although the cause of hives is not always known, they are often a response to the body releasing histamines, which it does when we have an allergic reaction to food, medicine or other allergens. Histamine is also sometimes the body's response to infections, stress, sunlight and changes in temperature, among other things. Hives typically manifest as small, swollen, itchy, red areas on the skin that may occur singularly or in clusters.
Left untreated, hives usually fade within a few hours, but new ones may appear in their place. Most hive outbreaks resolve themselves completely within a few days. You can treat hives naturally to get relief from the symptoms.
Apply a wet, cold compress to the hives to reduce the swelling and cool the inflamed skin.
|Posted by Maddalena Frau on January 17, 2014 at 1:20 AM||comments (0)|
By Amit Goswami, Ph. D.
The actress Angelina Jolie, by her radical mastectomy because of a high probability for contracting breast cancer, has increased our awareness of the suffering that this tragic disease brings to women worldwide. The truth is, every year roughly 3 million people contract this disease, and thousands die.
Angelina’s case was special because her situation was hereditary. But many cases of breast cancer are not hereditary, (due to any genetic abnormality), and the question arises, could it be that in these cases the physical symptoms—cancerous growths—are not due to any physical cause at all? If there is a nonphysical cause, and we can understand it, can we treat the disease at the root and heal it? Furthermore, if we can understand the cause of these cases of cancer, could we prevent the cancer by eliminating or minimizing the cause in the first place?
Conventional medicine practitioners are not very friendly to such questions because of their “everything is matter” and “genetic abnormalities cause most disease” philosophy.
Quantum physics leads us to a different philosophy: Consciousness is the ground of being in which there are four worlds of quantum possibilities: material, vital, mental, and archetypal (which I call supramental). Choice by consciousness from material possibilities gives us material objects of sensing. When consciousness chooses from the possibility-movements of the vital world, we experience vital energy movements of feeling. Choice from the mental world (mind) gives us meaningful objects of thought. And choice from the supramental gives us the archetypal objects of intuition such as love.
The individual manifest worlds of our experience do not interact directly but only through the intermediary of consciousness with nonlocal, signnalless communication (quantum nonlocality).
This scientific validation of our subtle experiences of feeling, thinking, and intuition, opens the door for the validation of alternative practices of medicine that postulate an important disease-causing role to imbalances of the subtle movements of our experience. (Read my book The Quantum Doctor.) For example, vital body medicine practices such as Traditional Chinese Medicine [TCM], the Indian Ayurveda, and homeopathy claim that many diseases are caused by imbalances or blocks of vital energy movements associated with our organs and their interactions. Mind-body medicine practices hold that imbalances and blocks in our processing of mental meaning cause some of our diseases. And so forth.
TCM and What Quantum Physics and Avant-garde Biology Add to TCM Model of Breast Cancer Treatment and Prevention
Now back to breast cancer. According to TCM, breast cancer is caused by imbalances in the movement of vital energy in the breasts and in the related organs of importance to healthy breast functioning. Also of importance in TCM is the movement of vital energy in the channels called meridians that connect interacting organs.
In the early days of medicine, when Traditional Chinese medicine was formulated, very little was known about the vital body. Boldly, the Chinese thinkers used a modified version of the five-elements theory of matter and space (the classification in terms of earth, water, air, fire, and vacuum or empty space) to get a grip. But being good empiricists, they also took into account what they empirically knew about the organs. They discovered that organs affect organs in two ways, either in a supportive role or in a controlling role. Accordingly, they renamed the corresponding vital energy elements as: earth, water, wood, fire, and metal. Earth nourishes metal in a supporting role, but metal cuts wood in a controlling role.
In this way, TCM practitioners would say that the female breasts, liver, and stomach are connected by support and control. Therefore, they emphasize the importance of keeping the flow of vital energy in these organs and between these organs unblocked and balanced. This means we pay special attention to the flow of vital energy in their channels of communication, namely, the liver meridian and the stomach meridian. Balance in the conceptualization of TCM means a balance between the complementary aspects—yin and yang—of vital energy (chi).
TCM is especially effective as a preventive medicine. If we keep the vital energy balanced and unblocked in the way described above, we can prevent cancer, is their point. Empirical data supports their view.
Modern science improves the theory quite a bit. I have already spoken of how quantum physics and the concept of psycho-physical parallelism make the concept of vital energy scientific. Balance in this approach means a balance between particle and wave modality of the flow of vital energy, a balance of what is and what is possible, in other words, a balance between conditioning and creativity in the mode of movement.
Now add new insights in the biological theory of form-making, morphogenesis. The biologist Rupert Sheldrake noted that morphogenesis (how a one-celled embryo, through cell division that creates identical replicas, can grow all the different organs of the body with differentiated functions depending on where in the body the organ lies) gives rise to a paradoxical question—how does the cell know where it is in the body? Accordingly, there must be new nonlocal, and therefore nonphysical, organizing principles, call them morphogenetic fields, that are instrumental in biological cell-differentiation and form-making.
When we combine the lesson of quantum psychophysical parallelism with Sheldrake’s morphogenetic fields, we can see clearly that the morphogenetic fields are the blueprints of biological form that consciousness uses to make organs. Each organ then has a “correlated” (through consciousness and quantum nonlocality) morphogenetic blueprint in the vital body. The conglomerate of these morphogenetic fields associated with all our organs is what we call the vital body.
As the physical body grows through childhood and early adulthood, the movements of these associated morphogenetic fields become conditioned to act in a certain predictable way. These are yin movements of vital energy. But the cells die and are replaced from food molecules, disease comes from various sources, environmental changes with seasons and places; in this way, the movements of the morphogenetic fields has to have creative dynamism, a balance of the yang component of chi.
The most serious situation, of course, is created when certain movements of vital energy are entirely blocked; in quantum parlance, these movements are never actualized or collapsed. We can see, that such blocks of vital energy movement that prevent the functioning of organs would have grave disease-producing consequences.
Now add another relatively new insight of modern biology and medicine, the discovery of the immune system that keeps the body healthy by killing off intruders. Naturally, modern medicine recognizes the importance of keeping the immune system functioning normally. Because of occasional mistakes in cell division mechanism, the body is always creating abnormal cells that the immune system kills off routinely as intruders. But if the immune system does not function properly, these abnormal cells can grow and become malignant causing cancer.
However, modern medicine has only a few legitimate scientific mechanisms for immune system malfunctioning. The principal one is genetic; if there is a defect in the gene structure, the immune system will go awry with high probability. This was suspected to be the case with actress Angelina Jolie.
Another mechanism sometimes suggested is the action of a bacteria or a virus that trips off the immune system. However, there is no concrete case of this happening. Recently, a red flag was raised in proposing that oral sex can lead to throat cancer through bacterial infection. The actor Michael Douglas made himself the butt of many jokes when he claimed that his throat cancer was caused by HPV contracted through cunnilingus.
Vital energy medicine can do better. Blocking of the vital energies associated with the immune system is a likely mechanism for immune system malfunctioning. What can produce a vital energy block of this kind.
What feelings are associated with immune system functioning? The job of the immune system in the form of the thymus gland –- its geographical location roughly the same as the female breasts — is to distinguish between “me and not me”. When we fall in love with someone, the movement of the morphogenetic field associated with our immune system is temporarily suspended, suspending immune system functioning as well. This is experienced as an intense yearning for physical union, a part of all episodes of romantic love. When the union is achieved, movement of the morphogenetic field (vital energy) resumes, and the immune system functioning returns to normal.
In this way, certain situations in women’s lives can lead to prolonged suspension of immune system functioning, such as a woman in grief from bereavement. This then can produce breast cancer.
In Eastern psychology, the presence of certain feeling centers along the spine was discovered long ago. These points are called chakra points. Notice that the location of the thymus gland is roughly in the same area as the heart. The corresponding chakra point where we feel romantic love is called the heart chakra. There are seven such major chakra points.
The identification of unfulfilled romantic love as the source of immune system malfunctioning gives us an extra handle. It brings to the fore the role of the mind in causing vital energy blocks. To starve the heart chakra of romantic love until fulfillment is achieved with only the desired partner is often a mental decision that suppresses the feeling of love towards others. Thus, certain types of cancer, breast cancer in particular, can be recognized as a mind-body disease.
Again, from the perspective of mind-body disease, prevention is the best policy to deal with the problem. In the olden days, people were encouraged to grieve more than they naturally would. Now with a cancer-prone environment and an exponential increase of mental stress, we should do the opposite and discourage prolonged mourning.
Is there any healing along these lines once one has contracted breast cancer? The best results are achieved if we try changing the context of the mental thought that contributes to the negative emotion of grief.
The physician Deepak Chopra discovered the phenomenon of quantum healing as an explanation of many cases of spontaneous healing without medical intervention. Quantum healing occurs as a discontinuous transition of the mind to the archetypal world to discover a new context for mental thinking that is causing the vital energy block. Such quantum leaps are part of the creative process. In the case of mind-caused breast cancer, the quantum leap will let you love again.
The quantum leaps of quantum healing of cancer bring about the normal functioning of the immune system back with such fury that overnight all the cancerous mass is destroyed.
Can we do even better, life-long prevention, once we have rediscovered love? In TCM, it is recognized that the vital blueprints of the three organs of the lung, liver, and stomach form a special trio of circular hierarchy: the liver blueprint controls the stomach; the stomach blueprint does not control the liver back directly; instead, the stomach blueprint supports the lung blueprint, and the lung blueprint controls the liver blueprint. Thus the vital blueprints of the three organs form a causal circularity, a situation called tangled hierarchy which produces self-identity. What this means is that when consciousness collapses the possibility waves of these organs and their associated blueprints (morphogenetic fields), it identifies with the trio as a whole giving the system apparent autonomy. There is no evidence for any autonomous functioning of the lung, but there is such evidence for the immune system. Clearly, ancient Chinese thought has validity if we substitute immune system for the lung. In other words, the immune system, the liver, and the stomach form one autonomous system of identification for consciousness. And it is important to keep each member of the trio and their vital connections healthy to ensure proper immune system functioning.
So the quantum recipe for forever healthy living: discover love and expand your center of functioning from your neocortex to include the heart (immune system) center also. As John Lennon wrote, “all you need is love”.
|Posted by Maddalena Frau on January 16, 2014 at 11:40 PM||comments (0)|
To discuss challenges concerning treatment for chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) and review complementary and alternative medical (CAM) therapies being evaluated for this condition, we performed a comprehensive search of articles published from 1990–2005 using the PubMed, Medline databases. Data from the articles were abstracted and pooled by subject. Keywords cross-searched with CP/CPPS included: complementary, alternative, integrative, therapies, interventions, nutrition, antioxidants, herbs, supplements, biofeedback and acupuncture. Listed articles with no abstracts were not included. Various CAM therapies for CP/CPPS exist including biofeedback, acupuncture, hyperthermia and electrostimulation. Additionally, a variety of in vitro and in vivo studies testing herbal and nutritional supplements were found. Saw palmetto, cernilton and quercetin were the most frequently tested supplements for CP/CPPS. Although many CAM therapies demonstrate positive preliminary observations as prospective treatments for CP/CPPS, further exploratory studies including more randomized, controlled trials are necessary for significant validation as treatment options for this complex disorder.
Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is of significant interest in urology and accounts for up to 2 million office visits per year . Currently, there are multiple approaches to the management of CP/CPPS depending on the classification of the related symptoms. However, there are no absolute findings or laboratory tests employed and diagnosis is often one of exclusion.
In 1995, the National Institutes of Health established an International Prostatitis Collaborative Network in order to construct a new classification of prostatitis syndromes and better define chronic prostatitis. The categories are now documented as follows:
While most patients report a primary subjective symptom of local pain and/or dysuria, the clinical presentation of acute versus chronic prostatitis varies. Laboratory cultures are standardly employed to detect bacterial involvement and this testing along with other diagnostic criteria determines each classification. Men with Category 1, acute prostatitis, frequently present with dysuria, fever, malaise, myalgia (non-specific) and positive culture analysis that often reveals coliform bacteria. This imparts to standard antibiotic treatment with good prognosis for recovery and minimal recurrence.
Patients with Category 2, chronic bacterial prostatitis, present with similar symptoms as those with acute prostatitis. However, the frequency of symptoms (duration >3 months), recurrent urinary tract infections and additional diagnostic tests including analysis of lower urinary tract cultures contribute to its diagnosis as Category 2 prostatitis.
Men with Category 4, asymptomatic inflammatory prostatitis, do not present with subjective symptoms. This diagnosis is often discovered via laboratory findings such as the positive presence of white blood cells in prostatic secretions or in prostate tissue during routine evaluation for other disorders.
Comparative to the total number of prostatitis cases reported, the majority of representative cases are Category 3, CP/CPPS. This diagnosis is usually one of exclusion, as bacterial etiology acute or chronic is ruled out. Other exclusion criteria include urogenital cancer, urethral stricture and neurologic disease affecting the bladder. However, the patient may still present with polyuria, dysuria, generalized myalgia or specific pelvic pain, urethral discharge, voiding dysfunction, sexual dysfunction and negative impact on quality-of-life (QOL). The presentation of this symptom set is now termed Category 3, CP/CPPS. Categories 3A and 3B are further differentiated by the presence or absence of inflammatory blood cells in prostatic secretions and seminal fluid, respectively further outlines the characteristics and treatment options of Category 3 prostatitis.
Due to the complexity in diagnosing CP/CPPS, the National Institutes of Diabetes and Digestive and Kidney Diseases funded the Chronic Prostatitis Collaborative Research Network (CPCRN) in 1995 . This network was fundamental in the construction and validation of the National Institutes of Health Chronic Prostatitis Symptom Index (NIH-CPSI), which was implemented in 1999. The index has become a valid measure that quantifies the qualitative experience of men with CP/CPPS and addresses three different aspects of CP/CPPS: pain, function and QOL.
The formation of the CPCRN and the advent of the NIH-CPSI have better characterized diagnosis and treatment for CP/CPPS, but challenges still exist. While standard treatment options including anti-inflammatory agents, analgesics and alpha-blockers are often prescribed, impact on QOL is another factor often overlooked in the treatment and management of CP/CPPS . The focus on QOL, anecdotal data, epidemiological studies and the increased popularity and validation of herbal, complementary and alternative medicine (CAM) has led to exploration of the utility of CAM therapies as treatments for CP/CPPS. CAM therapies including biofeedback, acupuncture, heat therapy, electrostimulation, herbal and nutritional supplements will be discussed below.
CAM, as defined by the National Center for Complementary and Alternative Medicine (NCCAM), is a group of diverse medical and health care systems, practices and products that are not presently considered part of conventional medicine. Conventional medicine is further defined as medicine as practiced by holders of MD (medical doctor) or DO (doctor of osteopathy) degrees. Though the list of what therapies or practices considered to be CAM changes continually, the pool of both practitioners of CAM modalities and patients utilizing CAM services continues to grow within the United States and globally.
The inclusion of CAM practices in urology is also being implemented in the clinic. Many groups such as the Committee of Complementary and Alternative Medicine within the American Urological Association (AUA) recognize the integration of non-conventional therapies into urological clinical practice. Additionally, both public demand for CAM therapies and their testing and validation within health science research centers has increased . It has been suggested that many urological conditions possessing subjective and QOL components such as in benign prostatic hyperplasia (BPH), chronic prostatitis, voiding, erectile dysfunction and cancer prevention and survivorship might be particularly amenable to CAM treatment strategies. This review will focus on current CAM therapies found in the literature for CP/CPPS.
Biofeedback therapy is considered a mind–body technique that utilizes a monitoring machine to assist people in controlling bodily functions such as heart rate, blood pressure and muscle tension. This therapy has been studied for its efficacy in urological conditions such as incontinence, prolapse, pediatric voiding dysfunction and CP/CPPS . The hypothesis of biofeedback's mechanism of action in treating CP/CPPS is based on the principle that maximum muscle contraction prompts maximum muscle relaxation. This mechanism addresses the chronic pain aspect of CP/CPPS and focuses on muscular reeducation, which may ultimately provide symptom relief.
Two studies testing the value of biofeedback therapy for CP/CPPS yielded positive results. The first study assessed 62 patients who were refractory to conventional therapy (such as antibiotics and/or alpha-blockers) for greater than half a year. These patients were treated utilizing the Urostym Biofeedback equipment five times a week for 2 weeks with a stimulus intensity of 15–23 mA and duration of 20 min. The NIH-CPSI index noted a significant overall reduction in score (P < 0.01) and no side effects were reported during the trial.
A second pilot study evaluated biofeedback therapy in 19 men with pelvic floor tension and CP/CPPS. These results demonstrated significant improvement in pain scores as measured by the AUA symptom index (P = 0.001). While this study focused on testing the effect of biofeedback therapy in treating the symptoms associated with CP/CPPS, it also implicated the presence of pelvic floor tension contributing to pain and the paramount importance of muscular reeducation for its treatment. These initial, positive biofeedback studies may warrant larger randomized clinical trials to confirm safety and efficacy as well as explore the mechanism of action of biofeedback therapy.
Acupuncture is a traditional Chinese method of medical treatment involving the insertion of fine, single-use, sterile needles in acupoints according to a system of channels and meridians that was developed by early practitioners of Traditional Chinese Medicine (TCM) over 2000 years ago. The needles are stimulated by manual manipulation, electrical stimulation or heat. Currently, acupuncture is often used with TCM and it is a recognized health profession with strict licensure and regulatory status in 40 states. Common applications include acupuncture as a complementary therapy for cancer patients undergoing chemotherapy or radiotherapy, for conditions involving pain such as migraines and back pain, and for relieving the impact of stress among patients with chronic conditions. The precise physiological mechanism of action of acupuncture is unknown but a variety of hypotheses exist. For example, acupuncture analgesia is thought to be mediated by central nervous system (CNS) mechanisms of pain control via the release of specific neurotransmitters, such as endorphins. Additionally, there are significant data which suggest that acupuncture treatment can decrease inflammation and relieve pain.
Data suggesting the ability of acupuncture treatment to decrease pain, positively impact QOL and potentially modulate inflammation and/or affect the CNS has suggested it as potential therapeutic option for men with CP/CPPS. While a number of studies listed in other journals test the utility of acupuncture treatment for CP/CPPS only two medline listed pilot studies are shown testing acupuncture treatment in patients with CP/CPPS.
The first study examined whether acupuncture improved pain, voiding symptoms and QOL in 12 men with CP/CPPS. This study reported a significant decrease in total NIH-CPSI pain, urinary and QOL scores (P < 0.05) over 6 weeks of treatment and an average 33 weeks of follow-up. The mechanism of action addressed in this paper suggests a neuropathic model of CP/CPPS and the hypothesis that acupuncture, if considered a neuromodulatory therapy, may provide a therapeutic option for men with CP/CPPS.
A second study tested acupuncture treatment for CP/CPPS patients with intrapelvic venous congestion. This study of 10 patients receiving 5 weeks of acupuncture treatment also reported a significant decease in NIH-CPSI pain and QOL scores (P < 0.05, P < 0.01). While the study reported no serious adverse events, the mechanism of action was not addressed. The promising clinical outcome of both studies testing acupuncture for CP/CPPS implies that larger studies are required to confirm the utility of acupuncture in this patient population.
Only one study in English was found utilizing electrostimulation for chronic prostatitis. This study tested a new, high frequency, urethral–anal prototype stimulation device in men with CP/CPPS twice weekly for 5 weeks. The results demonstrated a significant decrease in the NIH-CPSI (P = 0.0002) with no urethral, anal complaints or other side effects. The authors suggest that due to the positive results, simple technology and ability to be self-administered, this new device may have utility in the treatment of CP/CPPS. However, further studies and standardization of the electrostimulation device are essential.
Anecdotal evidence and a few clinical trials have suggested heat therapy or hyperthermia as a treatment option for men with CP/CPPS. Its mechanism of action is based on the application of heat to the prostate to relieve pain. An excellent review by Zeitlin discusses the lack of literature concerning hyperthermia and CP/CPPS. The review notes a variety of pitfalls in hyperthermia research including variation and lack of standardization of treatment. These concerns are applicable to both the type of heat utilized such as interstitial heat or microwaves and variation in its application, either transrectally or transurethrally. The review also suggests that the hyperthermia instruments used were not validated and outcome measures were subjective. However, the review implies that utilization of a quantitative assessment tool, applied statistics and greater documentation of therapy type may offer hyperthermia a better opportunity to be evaluated as a potential therapy for CP/CPPS.
We also discovered the paucity of literature described by Zeitlin and only three listed clinical trials utilizing hyperthermia. The first study analyzed a group of 45 men with chronic abacterial prostatitis or prostadynia who underwent 6 weekly, 1 h sessions of local deep microwave hyperthermia (42.5 +/−0.5°C) to the prostate. Although the authors report encouraging results in the decrease of pain, these subjective patient assessments were not quantified by the NIH-CPSI or other index for CP/CPPS.
A second abstract discussed a randomized, sham-controlled comparative study utilizing transrectal microwave hyperthermia in 80 men with CP/CPPS. While this abstract noted a 75% symptomatic improvement in the treatment group, the study was available as an abstract only with no statistical significance or descriptive methodology reported. A third study also tested transrectal microwave hyperthermia for both chronic non-infectious and infectious prostatitis. While the study design incorporated obtaining measurement of prostatic secretions, uroflowmetry and transrectal color Dopplerographic mapping, the results from the study were not abstracted as the article was in Russian.
Herbal and nutritional supplement therapies have been most widely investigated for their utility in CP/CPPS and other prostate conditions such as BPH. While many formulations have been cited for their use in a wide variety of urological conditions, saw palmetto, pollen extract and quercetin were the supplements found with specific application to CP/CPPS. While most herbal and nutritional supplements contain a wide variety of synergistic ingredients upon compositional analysis, some of the active components such as phytosterols or antioxidants are listed in.
Saw palmetto (Serenoa repens) garnered much attention in urology based on a great deal of anecdotal evidence regarding its prostate specific properties. It is widely used in many Asian, African and European countries and compositional analysis of the berry of S. repens exhibits sterols and free fatty acids as its major constituents . Initial studies suggested that the efficacy of saw palmetto may be similar to that of the pharmaceutical enzyme inhibitors such as finasteride. This preliminary data prompted the exploration of mechanism, utility and efficacy of saw palmetto in in vitro analysis and in clinical trial settings. While a number of trials have examined saw palmetto use for symptoms related to BPH, only a few have focused on it specifically for CP/CPPS.
The first study compared the safety and efficacy of saw palmetto berry supplement versus finasteride in men with Category 3, CP/CPPS. This prospective, open label 1 year study randomized 64 men to the saw palmetto or finasteride group, respectively. After 1 year of treatment, the NIH-CPSI score decreased from 23.9 to 18.1 in the finasteride group (P < 0.003) and from 24.7 to 24.6 in the saw palmetto group (P = 0.41). While significance was only achieved in the finasteride treatment arm, it was notable that at the end of the trial 41 and 66% of participants opted to continue the therapies of saw palmetto and finasteride, respectively, regardless of achieved statistical significance.
The second clinical trial from China examined the effects of prostadyn sabale capsules containing saw palmetto berry in patients with CP/CPPS. While 125 men reported positive outcome and the NIH-CPSI was used as a primary end point, the article is only available in Chinese and the manufacturer, active constituents of the capsules and statistical significance was not reported.
A third multicenter study testing a saw palmetto abstract called Permixon analyzed the response of Permixon therapy in 61 patients with Category 3B prostatitis. While 65% of the Permixon group reported improvement based on the Patients Subjective Global Assessment (SGA), the total NIH-CPSI and the pain, voiding and QOL/impact domains of the NIH-CPSI, statistical significance was not reported. Additionally, prostate volume was unchanged in both the treatment and control groups. While this multicenter study suggests that Permixon may provide clinical benefit for CP/CPPS 3B, the dosages and components of the Permixon product were not listed in the abstract.
The assessments of saw palmetto studies for CP/CPPS are far fewer than those for BPH. However, marked and continued progress in molecular studies, increased mechanistic data and more clinical trials in CP/CPPS are warranted to ascertain the utility and reproducibility of saw palmetto use in men with chronic prostatitis.
Pollen extract is traditionally collected from the flowers of various plant types and it contains carbohydrates, fat, protein, vitamins and minerals. The particular pollen extract named cernilton has been suggested to benefit a variety of urological conditions. Anecdotal evidence and references from traditional herbal texts have implicated cernilton's potent anti-inflammatory properties and potential in treating symptomatic relief of urinary pain and dysfunction often present in both CP/CPPS and BPH. In vitro studies demonstrate a variety of experimentation on this particular extract including histopathological analysis of its effect on cell proliferation, apoptosis, serum cytokines and testosterone. The literature also lists quite a few clinical trials on pollen extract; however, five are in the Japanese language and one in the German language. While many of these studies report the positive activity of pollen extract and suggest its usefulness for CP/CPPS, data from these studies were not abstracted due to unavailability and translation of the articles.
One available study testing pollen extract reported a 78% favorable response of men with chronic prostatitis taking Cernilton® pollen extract at a dosage of 1 tablet TID for 6 months . While this study reported favorable results, the study was published in 1993 and similar subsequent larger phase clinical trials are not evident to further elucidate the possible utility of pollen extract in men with CP/CPPS.
Quercetin is known chemically as a mixture of 2-(3,4-dihydroxyphenyl)-3,5,7-trihydroxy-4H-1-benzopyran-4-one and 3,3′,4′,5,7-pentahydroxy flavone. It belongs to a group of polyphenolic substances known as flavonoids and is a member of the class of flavonoids called flavonols. It is commonly found in the plant kingdom in the rinds and barks of certain foods such as onions, grapes and green tea. Since quercetin is thought to have antioxidant, anti-inflammatory, antiviral, immunomodulatory, anticancer, gastroprotective and antiallergy activities it has been studied for a variety of conditions.
One prospective, randomized, double-blind, placebo-controlled trial was performed to test the action of this bioflavonoid in men with CP/CPPS. This placebo-based study assessed 30 men with CP/CPPS to receive the bioflavonoid quercetin, 500 mg twice daily or the placebo pill for 1 month. Significant change in the NIH-CPSI score was observed in the quercetin (P = 0.003) versus the placebo group, who had an insignificant mean improvement in the NIH-CPSI score. While this was the only clinical trial found testing quercetin for CP/CPPS, the positive outcome supports the need for further study including cost analysis of quercitin therapy in this patient population.
Finally, a wide variety of herbal compounds not previously discussed were found during this review, many of which are commonly used in the TCM herbal material medica. Some of the compounds are Nan mi qing capsules containing Rheum palmatum and Rx. astragalus memberanaceus, Ye Ju Hua Shuan, an herbal suppository of Flos Chrysanthemi Indici and a variety of other formulae or capsules of which the ingredients were not listed.
Initial in vitro studies examining some of the herbal compounds effects on markers of inflammation such as thromboxanes (TBX2) and 6-keto-PGF1-α are promising as the link between chronic inflammation in CP/CPPS is still under investigation. While the preliminary reports of additional herbal compounds are encouraging, a number of difficulties exist in the extraction of this data. Namely, the articles are in the Chinese or other language and data including the ingredients, constituents and other practices including good manufacturing are unable to be assessed. While this conundrum exists for many herbal agents despite their historical use in a variety of traditional herbal medicine systems, testing of safety and utility are still necessary. However, the variety of herbal agents available offers a large source to draw from and the possibility that other herbal products might be beneficial in the treatment of CP/CPPS.
A summary of the reviewed literature is outlined in Table 2 and a variety of CAM modalities tested in patients with CP/CPPS include practitioner-based therapies such as biofeedback, hyperthermia, acupuncture and electrostimulation, and biological-based therapies including herbal and nutritional supplements. As the challenges in treating this complex and chronic disorder remain, further evidence of efficacious CAM treatment options for men with CP/CPPS is needed. Thus far, promising data on the function and efficacy of certain CAM therapies suggest their potential as treatment options for this patient population. Further exploratory studies including more in vitro studies of herbal products, mechanistic data, cost analysis and randomized, controlled trials will assist in validation of certain CAM therapies as permanent treatment options for men with CP/CPPS.
|Posted by Maddalena Frau on December 26, 2013 at 11:50 PM||comments (0)|
With a new smartphone device, you can now take an accurate iPhone camera selfie that could save your life -- it reads your cholesterol level in about a minute.
Forget those clumsy, complicated, home cholesterol-testing devices. Cornell engineers have created the Smartphone Cholesterol Application for Rapid Diagnostics, or "smartCARD," which employs your smartphone's camera to read your cholesterol level.
"Smartphones have the potential to address health issues by eliminating the need for specialized equipment," said David Erickson, Cornell associate professor of mechanical engineering and senior author on a new peer-reviewed study. Thanks to advanced, sophisticated camera technology, Erickson and his colleagues have created a smartphone accessory that optically detects biomarkers in a drop of blood, sweat or saliva. The new application then discerns the results using color analysis.
When a user puts a drop of blood on the cholesterol test strip, it processes the blood through separation steps and chemical reactions. The strip is then ready for colorimetric analysis by the smartphone application.
The smartCARD accessory -- which looks somewhat like a smartphone credit card reader -- clamps over the phone's camera. Its built-in flash provides uniform, diffused light to illuminate the test strip that fits into the smartCARD reader. The application in the phone calibrates the hue saturation to the image's color values on the cholesterol test strip, and the results appear on your phone.
Currently, the test measures total cholesterol. The Erickson lab is working to break out those numbers in LDL ("bad" cholesterol), HDL ("good" cholesterol) and triglyceride measurements. The lab is also working on detecting vitamin D levels, and has previously demonstrated smartphone tests for periodontitis and sweat electrolyte levels.
"By 2016, there will be an estimated 260 million smartphones in use in the United States. Smartphones are ubiquitous," said Erickson, adding that although smartCARD is ready to be brought to market immediately, he is optimistic that it will have even more its advanced capabilities in less than a year. "Mobil health is increasing at an incredible rate," he concluded. "It's the next big thing."
|Posted by Maddalena Frau on December 9, 2013 at 12:40 AM||comments (0)|
The most common side effects of acupuncture are things everyone wants: better sleep, more energy, mental clarity, better digestion and less stress. One or several of these side effects occur routinely for many, many acupuncture goers.
Following the publication of an article on the most common side effects of acupuncture, AcuTake received multiple inquires from readers about certain unpleasant side effects of acupuncture and whether they too were common.
And indeed, there are other, less-pleasant side effects of acupuncture. These additional side effects are much rarer than the most common side effects of acupuncture, but they can and do occasionally happen.
None are life-threatening, and all typically are fleeting. Still, they are good to be aware of so that if you do experience them, you know they're normal and nothing to be too concerned about.
Infrequent But Possible Side Effects of Acupuncture
In my experience, the following seven side effects can occur after acupuncture.
While most people notice a marked improvement in their symptoms following acupuncture, some feel worse before they start feeling better. In natural medicine circles, this is sometimes referred to as a healing crisis. The idea is that as your body starts undergoing the changes involved in moving toward health, things get stirred up. This can cause not only an exacerbation of current symptoms but also the recurrence of previous ailments that had been dormant.
Acupuncture awakens your self-healing capabilities. With that can come an onslaught of bodily awareness. This usually is a positive experience but it also can mean heightened sensitivity or intolerance for things that previously felt normal. An example of this is someone who unconsciously adapts to stress by tightening and hunching up his shoulders. After an acupuncture treatment, once this person's bodily felt sense has been woken up, his mild upper back and neck tension might start screaming.
The good news about this side effect is that it's a sign that things are moving. In the case of acupuncture, this means that the primary objective is being met. That is, you are starting to transition on multiple levels from stuck to unstuck.
People can feel wiped out after acupuncture. A more common result is increased energy, but sometimes the "acu land" effect hangs on a little longer. This is your body telling you that it's depleted. Feeling fatigued after acupuncture is not cause for concern, but it is a warning sign that you need to rest.
If you have this experience, take it easy for the remainder of the day. Take a bath that night. Go to bed early. Come morning, the combination of acupuncture and rest will leave you feeling born again.
Body parts where acupuncture needles get inserted can feel sore after needles are removed. I've found that this most commonly occurs with points in the hands and feet, especially Large Intestine 4, an acupuncture point located between the thumb and index finger. You also may experience muscle soreness away from the needling site if a trigger or ashi point was released during your treatment.
Soreness from acupuncture typically dissipates within 24 hours. However, big trigger point releases can cause residual soreness that lasts a few days. Most acupuncturists will warn you about this before you leave your appointment.
Although less common than soreness, bruising can occur at the needling site. Sometimes bruising is the result of a hematoma, a localized collection of blood that gets initiated when the needle punctures the skin. Bruises, unfortunately, usually last longer than soreness from an acupuncture needle. Still, they generally are not anything to worry about beyond the aesthetic inconvenience.
It is unknown why some people bruise from acupuncture. I have a few patients who, no matter what I try in terms of needle brand, size or technique, they bruise every time. (Again, I often see it happen at Large Intestine 4.) Others -- the majority -- never experience bruising anywhere.
Every time I get acupuncture, no matter where the needles are placed, my right quadricep muscle twitches like crazy. Don't ask me why. People may experience involuntary muscle twitching during or after acupuncture. I've seen this occur in muscles that receive acupuncture needles and, as in my case, on seemingly random parts of the body that are far away from any needles.
Muscle twitching is different from full-on muscle spasm. If during or after an acupuncture treatment you feel that one of your muscles is acutely spasming, especially if it's a muscle that was just needled, tell your acupuncturist. He or she might be able to release it before you go on your merry way.
This is pretty rare, but it can happen -- and on very rare occasions, post-acupuncture lightheadedness can result in fainting. Getting up quickly from the acupuncture table can cause lightheadedness, as can coming for acupuncture on an empty stomach. Remember that eating is one of the key things to remember before an acupuncture appointment.
When your acupuncture session is over, take your time getting up and move gently as you gather your things to leave. If you find yourself feeling lightheaded after the treatment, sit in your acupuncturist's waiting room for a few minutes and take some deep breaths. Acupuncture can be a physically and emotionally intense experience, and sometimes our bodies are not fully recovered at exactly the moment our hour is up. It is okay if you need a little extra time.
Sometimes people cry in acupuncture. Not because they're in pain, but because their emotions, which can get stifled while powering through life, become free-flowing. The emotional release that can happen in acupuncture usually is a positive experience, but it can be surprising, especially for people who tend to be more emotionally stoical.
Feeling extra sensitive or tear-prone in an acupuncture session, or in the days that follow, is completely normal. It's also a sign that the acupuncture is working. Even if you're seeking acupuncture for a physical ailment, increased emotional expression is an indication that healing is happening. From an acupuncture perspective, physical and emotional health are interconnected, so emotional shifts suggest forthcoming physical changes as well.
While these side effects are rarely cause for concern, you know your body best. If any of the above side effects feel like they're too severe or lasting too long -- or if you notice any additional negative reactions to an acupuncture treatment -- you should contact your acupuncturist.
|Posted by Maddalena Frau on November 14, 2013 at 3:25 AM||comments (0)|
There is good evidence to show that stress
can increase a person's heart rate, lower the immune system's ability
to fight colds and increase certain inflammatory markers but can stress
also raise a person's cholesterol?
It appears so for some people, according to a new study that examines
how reactions to stress over a period of time can raise a person's lipid
This finding is reported in the November issue of Health Psychology, published by the American Psychological Association (APA). In a sample of 199 healthy middle-aged men and women, researchers Andrew Steptoe, D.Sc., and Lena Brydon, Ph.D., of University College London examined how individuals react to stress and whether this reaction can increase cholesterol and heighten cardiovascular risk in the future. Changes in total cholesterol, including low-density lipoprotein (LDL) and high-density lipoprotein (HDL), were assessed in the participants before and three years after completing two stress tasks
This finding is reported in the November issue of Health Psychology,
published by the American Psychological Association (APA). In a sample
of 199 healthy middle-aged men and women, researchers Andrew Steptoe,
D.Sc., and Lena Brydon, Ph.D., of University College London examined how
individuals react to stress and whether this reaction can increase
cholesterol and heighten cardiovascular risk in the future. Changes in
total cholesterol, including low-density lipoprotein (LDL) and
high-density lipoprotein (HDL), were assessed in the participants before
and three years after completing two stress tasks.
The study found that individuals vary in their cholesterol responses to stress, said Dr. Steptoe. "Some of the participants show large increases even in the short term, while others show very little response. The cholesterol responses that we measured in the lab probably reflect the way people react to challenges in everyday life as well. So the larger cholesterol responders to stress tasks will be large responders to emotional situations in their lives. It is these responses in everyday life that accumulate to lead to an increase in fasting cholesterol or lipid levels three years later. It appears that a person's reaction to stress is one mechanism through which higher lipid levels may develop."
The stress testing session involved examining the participants' cardiovascular, inflammatory and hemostatic functions before and after their responses to performance on moderately stressful behavioral tasks. The stress tasks used were computerized color-word interference and mirror tracing. The color-word task involved flashing a series of target color words in incongruous colors on a computer screen (ex. Yellow letters spelling the color blue). At the bottom of the computer screen, four names of colors were displayed in incorrect colors. The object of the task was to match the name of the color to the target word. The other task used was mirror tracing, which required the participant to trace a star seen in a mirror image. The participants were told to focus more on accuracy than on speed in both tasks.
At the follow up three years later, cholesterol levels in all the participants in the study had gone up, as might be expected through passage of time. However, individuals with larger initial stress responses had substantially greater rises in cholesterol than those with small stress responses. The people in the top third of stress responders were three times more likely to have a level of 'bad' (low-density lipoprotein) cholesterol above clinical thresholds than were people in the bottom third of stress responders. These differences were independent of their baseline levels of cholesterol levels, gender, age, hormone replacement, body mass index, smoking or alcohol consumption.
The authors found no sex differences among the participants in their cholesterol levels and response to stress. Steptoe and Brydon speculate on the reasons why acute stress responses may raise fasting serum lipids. One possibility may be that stress encourages the body to produce more energy in the form of metabolic fuels - fatty acids and glucose. These substances require the liver to produce and secrete more LDL, which is the principal carrier of cholesterol in the blood. Another reason may be that stress interferes with lipid clearance and a third possibility could be that stress increases production of a number of inflammatory processes like, interleukin 6, tumor necrosis factor and C-Reactive protein that also increase lipid production.
Even though these lipid responses to stress were not large, said Dr. Steptoe, "the levels are something to be concerned about. It does give us an opportunity to know whose cholesterol may rise in response to stress and give us warning for those who may be more at risk for coronary heart disease."
Article: "Associations Between Acute Lipid Stress Responses and Fasting Lipid Levels 3 Years Later," Andrew Steptoe, D.Sc., and Lena Brydon, Ph.D., University College London; Health Psychology, Vol. 24, No. 6.
|Posted by Maddalena Frau on October 25, 2013 at 1:20 AM||comments (0)|
Most hormones are produced by a group of glands known collectively as the endocrine system. Even though these glands are located in various parts of the body, they are considered one system because of their similar functions and relationship to each other.
Hormones are extremely potent substances. It takes only a minute amount to initiate an action. Hormones are secreted into the bloodstream by the glands. From there, they travel to all parts of the body. But only the cells sensitive to that hormone—called the target tissue--will respond to the chemical signal the hormone carries. Traveling through the blood, hormones enter cells through “receptor” sites, much as a key unlocks a door. Once inside, they get to work, flipping the switches that govern growth, development, and mental and physical functions throughout life. All that changes when your hormones become unbalanced due to physical and emotional stress or the effects of aging. Signals do not reach the right place at the right time. Sometimes cell functions shut down completely. In other cases, cells are over stimulated. All this chaos causes unpleasant symptoms, at the very least. In severe situations, these imbalances can lead to chronic disorders or disease.
Most hormones cannot be stored in the cells of the body. Therefore, they must be made and released into the blood at the precise time they are needed. To maintain the intricate systems in which hormones operate, the body must constantly fine-tune hormone release to keep levels within proper limits. This balance is accomplished through an intricate series of positive and negative feedback mechanisms. For example, an overproduction of one hormone usually prompts the release of one or more complementary hormones in an effort to restore balance. Because of the complexity of these interactions, a hormonal issue rarely stems from only one type of hormone. More often, the problem involves a series of hormones. In addition, a disruption in the balance of hormones produced by one gland or set of glands can cause other gland systems to malfunction.
You've probably heard more about hormones and hormonal imbalances recently - as researchers have become more aware of evidence showing this may be the root cause of many chronic health issues you could be experiencing.
Your hormones should exist in harmony with each other. When levels of each hormone are in the right proportions, body systems are stable. When balance is lost, hormone deficiencies and excesses can cause chronic symptoms and disorders, and raise risks for disease.
A whole host of symptoms may signify an imbalance:
The symptoms of hormonal shifts occuring in our bodies can be very strong and can even make you feel out of control at times.
If you have tried to figure out what is happening or perhaps treated your symptoms in ways that don't seem to work, testing your hormones may be the first step to feeling better.
Saliva and blood spot testing reliably identify hormone imbalances. Hormones exist in harmony with each other – partners in a delicate balancing act. When levels of each hormone are in the right proportions, body systems are stable. When balance is lost, hormone deficiencies and excesses can become toxic to the body causing unwanted symptoms, disorders and disease.
The ovaries produce many hormones. Chief among them are estrogen, progesterone, and testosterone. The ovarian hormones estrogen and progesterone interact to coordinate a woman’s menstrual cycle during her reproductive years. The brain produces the hormones follicle stimulating hormones (FSH) and luteinizing hormone (LH) which trigger hormone production from the ovaries. When any of the hormones coming from the brain or the ovaries are imbalanced, symptoms may occur. Imbalances are most common in puberty and menopause, but imbalances can happen at any age. Several conditions are well known to be associated with hormonal imbalance including: polycystic ovarian syndrome (PCOS), endometriosis, breast disease, and menstrual irregularities.
Symptoms of female hormone imbalance
ZRT offers simple tests for hormone imbalances using saliva, dried blood spots, and dried urine strips, which can be performed easily at a health care practitioner's office or at home. The sample is then sent to ZRT for analysis. With ZRT's innovative testing, there is no more wasted time and resources going to a lab for a painful blood draw.
The testes produce nearly 95% of all male testosterone. The balance is supplied by the adrenal glands. They also produce small amounts of estrogen. The brain produces the pituitary hormones follicle stimulating hormone (FSH) and luteinizing hormone (LH) which trigger hormone production from the testes. As a man gets older, testosterone levels fall and estrogen levels tend to rise. Lower testosterone levels may affect bone density, muscle strength, body composition and sex drive. The imbalance that occurs when testosterone is low in relation to estrogen may also contribute to prostate problems.
Symptoms of male hormone imbalance
When hormones are out of balance, these imbalanced interactions may provoke a wide range of symptoms.
|Posted by Maddalena Frau on October 14, 2013 at 1:50 AM||comments (0)|
Native to southeastern parts of the Americas, passionflower is now grown throughout Europe. It is a perennial climbing vine with herbaceous shoots and a sturdy woody stem that grows to a length of nearly 10 meters (about 32 feet).
Each flower has 5 white petals and 5 sepals that vary in color from magenta to blue. According to folklore, passionflower got its name because its corona resembles the crown of thorns worn by Jesus during the crucifixion. The passionflower's ripe fruit is an egg-shaped berry that may be yellow or purple. Some kinds of passionfruit are edible.
Many species have been found to contain beta-carboline harmala alkaloids, which are MAO inhibitors with anti-depressant properties. The flower and fruit have only traces of these chemicals, but the leaves and the roots are often more potent and have been used to potentiate the effects of mind-altering drugs.
The most common of these alkaloids is harman (1-methyl-9H-β-carboline), but harmaline (4,9-dihydro-7-methoxy-1-methyl-3H-pyrido[3,4-b]indole), harmalol (1-methyl-2,3,4,9-tetrahydropyrido[3,4-b]indol-7-one), harmine (7-methoxy-1-methyl-9H-pyrido[3,4-b]indole) and harmol were found.
The species known to bear such alkaloids include: P. actinea, P. alata (winged-stem passion flower), P. alba, P. bryonioides (cupped passion flower), P. caerulea (blue passion flower), P. capsularis, P. decaisneana, P. edulis (passion fruit), P. eichleriana, P. foetida (stinking passion flower), P. incarnata (maypop), P. quadrangularis (giant granadilla), P. ruberosa, P. subpeltata and P. warmingii.
Other compounds found in passion flowers are coumarins (e.g. scopoletin and umbelliferone), maltol, phytosterols (e.g. lutenin) and cyanogenic glycosides (e.g. gynocardin) which render some species, i.e. P. adenopoda, somewhat poisonous. Many flavonoids and their glycosides have been found in Passiflora, including apigenin, benzoflavone, homoorientin, 7-isoorientin, isoshaftoside, isovitexin (or saponaretin), kaempferol, lucenin, luteolin, n-orientin, passiflorine (named after the genus), quercetin, rutin, saponarin, shaftoside, vicenin and vitexin. Maypop, Blue Passion Flower (P. caerulea), and perhaps others contain chrysin, a flavone with confirmed anxiolytic and anti-inflammatory, and supposed aromatase inhibitor properties.
Also documented to occur at least in some Passiflora in quantity are the hydrocarbon nonacosane and the anthocyanidin pelargonidin-3-diglycoside.
As regards organic acids, the genus is rich in formic, butyric, linoleic, linolenic, malic, myristic, oleic and palmitic acids as well as phenolic compounds, and the amino acid α-alanine. Esters like ethyl butyrate, ethyl caproate, n-hexyl butyrate and n-hexyl caproate give the fruits their flavor and appetizing smell.
Sugars, contained mainly in the fruit, are most significantly d-fructose, d-glucose and raffinose. Among enzymes, Passiflora was found to be rich in catalase, pectin methylesterase and phenolase
The medical utility of very few species of Passiflora has been scientifically studied. In initial trials for treatment of generalized anxiety disorder, maypop extract performed as well as oxazepam but with fewer short-term side effects. It was recommended to follow up with long-term studies.
In another study performed on mice, it was shown that Passiflora alata has a genotoxic effect on cells, and further research was recommended before this one species is considered safe for human consumption.
Passionflower herb (Passiflorae herba) from P. incarnata is official in the European Pharmacopoeia. The herbal drug should contain not less than 1.5% total flavonoids expressed as vitexin. It is used in sedative tea mixtures with other calming herbs.
No studies have examined the effects of passionflower in children, so do not give passionflower to a child without a doctor's supervision. Adjust the recommended adult dose to account for the child's weight.
The following are examples of forms and doses used for adults. Speak to your doctor for specific recommendations for your condition:
The use of herbs is a time honored approach to strengthening the body and treating disease. Herbs, however, can trigger side effects and can interact with other herbs, supplements, or medications. For these reasons, you should take herbs with care, under the supervision of a health care provider.
Do not take passionflower if you are pregnant or breastfeeding.
For others, passionflower is generally considered to be safe and nontoxic in recommended doses.
Passionflower may interact with the following medications:
Sedatives (drugs that cause sleepiness) -- Because of its calming effect, passionflower may make the effects of sedative medications stronger. These medications include:
Antiplatelets and anticoagulants (blood thinners) -- Passionflower may increase the amount of time blood needs to clot, so it could make the effects of blood thinning medications stronger and increase your risk of bleeding. Blood thinning drugs include:
Monoamine oxidase inhibitors (MAO inhibitors or MAOIs) -- MAO inhibitors are an older class of antidepressants that are not often prescribed now. Theoretically, passionflower might increase the effects of MAO inhibitors, as well as their side effects, which can be dangerous. These drugs include:
Passionflower | University of Maryland Medical Center http://umm.edu/health/medical/altmed/herb/passionflower#ixzz2hfsMoeKh
University of Maryland Medical Center
|Posted by Maddalena Frau on May 14, 2013 at 11:40 PM||comments (0)|
In a small, preliminary study of regular migraine sufferers, scientists have found that measuring a fat-derived protein called adiponectin (ADP) before and after migraine treatment can accurately reveal which headache victims felt pain relief.
A report on the study of people experiencing two to 12 migraine headaches per month, led by researchers at Johns Hopkins, is published in the March issue of the journal Headache.
"This study takes the first steps in identifying a potential biomarker for migraine that predicts treatment response and, we hope, can one day be used as a target for developing new and better migraine therapies," says study leader B. Lee Peterlin, D.O., an associate professor of neurology and director of headache research at the Johns Hopkins University School of Medicine. She cautioned that larger, confirmatory studies are needed for that to happen.
Experts estimate that roughly 36 million Americans, or 12 percent of the population, suffer from debilitating migraine headaches that last four hours or longer. Migraines are defined as headaches with at least two of four special characteristics: unilateral or one-side-of-the-head occurrence; moderately to severely painful; aggravated by routine activity and of a pounding or throbbing nature. Sufferers generally also feel nauseated or are sensitive to light and sound. Women are three times as likely to get migraines as men.
Such complicated diagnostic criteria mean that diagnosis is tricky, a fact driving efforts, Peterlin says, to find better diagnostic tools.
For the study, Peterlin and her colleagues collected blood from 20 women who visited three headache clinics between December 2009 and January 2012 during an acute migraine attack. Blood was taken before treatment with either sumatriptan/naproxen sodium (a drug routinely given to people with migraines) or a placebo. The investigators re-drew blood at 30, 60 and 120 minutes after the study drug was given. Eleven women received the drug and nine got the placebo.
The researchers measured blood levels of ADP, a protein hormone secreted from fat tissue and known to modulate several of the pain pathways implicated in migraine. The hormone is also implicated in sugar metabolism, insulin regulation, immunity and inflammation, as well as obesity, which is a risk factor for migraines.
Peterlin and her colleagues looked at total adiponectin levels and two subtypes or fragments of total ADP in circulation in the blood: low molecular weight (LMW)-adiponectin and high molecular weight (HMW)-adiponectin. LMW is composed of small fragments of ADP and it is known to have anti-inflammatory properties, while HMW is made up of larger fragments of ADP and is known to have pro-inflammatory properties. Inflammatory pathways in blood vessels in the head are at work in migraine headache.
The researchers found that in all 20 participants when levels of LMW increased, the severity of pain decreased. When the ratio of HMW to LMW molecules increased, the pain severity increased.
"The blood tests could predict response to treatment," Peterlin says.
At onset of pain -- even before study drug was given -- the researchers could identify who would be a responder to treatment and who would not, as there was a greater ratio of HMW to LMW in those who would be responders as compared to those who were not.
After study treatment changes in adiponectin were also seen. Interestingly, in those patients who reported less pain after receiving study drug to treat the migraine -- whether they got the active migraine medication or a placebo -- researchers were able to see a decrease in total levels of ADP in the blood.
Peterlin says the findings indicate it may be possible to develop a treatment that would reduce levels of ADP or parts of adiponectin such as HMW or LMW adiponectin. She says should ADP prove to be a biomarker for migraine, it could help physicians identify who has migraine and know who is likely to respond to which type of medication. It also may help doctors make better medication choices and try alternate drugs sooner.
The study was supported by a grant from GlaxoSmithKline and from the National Institutes of Health's National Institute of Neurological Disorders and Stroke (K23 10896737).
Other Johns Hopkins researchers who contributed to the study include Linda W. White, C.R.N.P.; Paul D. Dash, M.D.; Edward R. Hammond, M.D., M.P.H.; and Jennifer A. Haythornwaite, Ph.D.
|Posted by Maddalena Frau on May 11, 2013 at 5:10 AM||comments (0)|
The psychophysiological procedure utilized to study the emotional reactivity of the body is called stress profiling.
Looking for correlates to emotions extends throughout the history of psychophysiology (Lacey & Lacey, 1958; Lader & Mathews, 1968 ; Malmo & Shagass, 1949), with the hope that we would be able to objectively determine the individual's emotional state without having to rely upon self report.
And as investigations moved into applied clinical research, the questions were directed more at can we identify those individuals who are at risk for a particular disorder.
For excellent reviews on these topics, see Haynes (1980) and Schwartz (1987). In this article, I will briefly review and explore some of the traditional conceptualizations for stress profiling, while introducing and demonstrating a unique perspective which reaches back to ancient Vedic writings.
On a purely mind-body level, a key attribute of muscles is that of emotional display. In addition we can conceptualize emotions as muscle activation patterns which lie at the foundation of intentional movement (e-motion).
When the muscle activation associated with emotions occurs, more energy is sent out into the neuromuscular system, taking up the "slack" in the system and increasing the tonic or resting level.
This emotional bracing (Jacobson, 1932; Whatmore, 1974) or increased tonus also effects the quality of movement. Professional athletes certainly know how emotional arousal can "unintentionally" alter their levels of exertion and change the timing associated with coordinated movement.
In addition, it is not uncommon for patients to react to stressful events in a "stereotypic" fashion. Individual Response Stereotypy (Engel, 1960) is the tendency for an individual to respond to a variety of stressors with a similar physiologic response.
This tendency was first noted in the early 60's, where some individuals were observed to always respond to a stressful event by, say, speeding up their heart rate or by tensing their shoulder muscles.
Within the neuromuscular system, emotional arousal and associated stereotypy have been studied for the facial muscles (Ekman & Frissen, 1972), the postural muscles (Goldstien, 1972) and the muscle spindle (McNutty, et al, 1974).
So, where do we search for these stereotypic patterns? We can look for signs of autonomic arousal through recordings from hand temperature and electrodermal activity (EDA). Recordings from the wide frontalis placement is very popular since is provides an excellent barometer of the negative emotional displays found on the upper face.
Or a simple visual observations of depressed patients usually indicates stooped shoulders and fallen chest, while the anxious patient may have their shoulders markedly elevated as if to protect their neck. Whatmore (Whatmore & Ellis, 1959; Whatmore and Kohli, 1962) has validated these phenomena using sEMG recordings.
Reactivity in the trunk muscles may show a high level of specificity. Cram (1997) has presented a case example of sEMG recordings from the right and left trapezius muscle groups using the cervical trapezius placement on a patient who had injured their right upper quarter during a fall down some stairs resulting in headache and right upper quarter pain.
For this patient, it was only the right cervical trapezius lead which responded to the stressor, followed by a very poor recovery pattern (return to baseline).
The uninjured left aspect show only a small, insignificant response. Flor et al (Flor, et al, 1985) have also demonstrated the specific effects of emotions on the muscles of the low back. In their study of the right and left aspect of the erector spinae muscles were studied in a group of low back patients, a group of general pain patients (i.e., pain other than low back) and a group of healthy controls.
Each group was presented with various types of stressors.
The findings of their study clearly demonstrated that only the low back pain patients experienced an emotional response (activation pattern), primarily in the left erector spinae muscle set and only during stressors relevant to the patient's condition.
Thus, the literature on stress profiling demonstrates that predictable patterns of reactivity may be seen at traditional sites for emotional display, sites of injury or sites of reported of pain. While these perspectives have provided us with a wealth of information, they are limited by their pure psychophysiologic basis.
Stress Profiling, Flower Essences
and A Matter Of Heart
In a recent study on stress profiling, I was asked to investigate whether or not a Flower Essence could attenuate the stress response.
The particular essence which was to be studied, The Five Flower Formula (Flower Essence Services) was first developed by Dr. Edward Bach in the 1930's and later refined by Julian and Martine Barnard for the treatment of physical trauma, emergencies and crisis situations.
According to a long history of anecdotal case reports on its effectiveness, it seemed a likely candidate to influence the stress response system in some way. Yet no studies on the mechanisms of action of the flower essence had been performed to date.
If one is to study the effects of a subtle energy such as a flower essence, it might be necessary to embrace traditional recording sites, yet broaden the conceptual framework of stress profiling to include the possible metaphysical influences of flower essences.
Thus, rather than routinely sticking to sEMG recording sites of the frontal, neck, shoulder or forearm, it was decided to study the biological energy at multiple sites along the human spine. These sites reflected the location of the chakras, while simultaneously recording from some of the more traditional sEMG placement sites.
Two previous studies have demonstrated the sensitivity of sEMG recordings at these chakra sites while studying the subtle influences of procedures such as Therapeutic Touch (Wirth and Cram, 1994) and Distant Prayer (Wirth and Cram, 1993).
The chakras sites have specific locations in the human body, and are where the flow of pranic energy is purported to be the greatest. In addition, each of the chakras has its own psychophysical and metaphysical attributes. The sites which were studied may be described below in both traditional and metaphysical ways:
Metaphysical (chakra) meaning
|Wide Frontal||Seat Of Negative Emotions.||3rd Eye: Divine Joy. Also Seat Of Knowledge / Enlightenment.|
|Mastoid to Mastoid Process||
Muscle Tension Of Axis.
Postural: Head Position.
|Medulla Oblongata: The Ego. Also The Entry Point of Prana Which Regulates Breath.|
|Bilateral C4 Paraspinals||
Muscle Tension Of Neck.
Postural: Anti-Gravity Muscles
|Throat Chakra: Center of Will. Also Associated With Calmness.|
|Bilateral T6 Paraspinals||
Intrascapular Muscle Tension
Postural: Anti-Gravity Muscles
Heart Chakra: Divine Love.
Also Desires and Attachments.
|Bilateral T12 Paraspinals||
Muscle Tension at the Thoracic Lumbar Junction.
Postural: Anti-Gravity Muscles
|Lumbar Chakra: Firely Self Control, Self Image.|
|Bilateral L4 Paraspinals||
Muscle Tension of the Lumbar Sacral Area.
Postural: Anti-Gravity Muscles
|Sacral Chakra: Creativity, Power, Sexuality.|
The procedure of the study followed the "standard of care" for stress profiling. Electrodes were connected to the above sites, along with hand temperature probe and EDA recording electrodes.
A five minute baseline was recorded, followed by a pre-recorded three minute serial arithmetic task (Hartje's Flow Chart), followed by a five minute recovery period.
The only nuance for the study was the administration of either a placebo or the five flower essence approximately five minutes prior to the initiation of the first baseline period.
The analysis of the data was conducted using a standard analysis of variance with repeated measures. Two post hoc analyses were conducted for each site. The first looked at the interaction of period (Baseline - Stress - Recovery) with Time (3 minutes of each period) to determine whether or not there had been a psychophysiological response.
The response patterns and their significance is presented for Figures 1 - 8. As can be seen, a significant response pattern is noted for all sites with the exception of the T6 / Heart and L4 paraspinal / Sacral site.
The lack of responsivity for the T6 / Heart chakra site may be attributed to the effects of the flower essence (see below). Figure 9 shows the magnitude of the sEMG response from baseline to the stress period. As can be seen, the mastoid to mastoid / Medulla recording site shows the largest response pattern, nearly three times greater than any other site. Lastly, the influence of the Five Flower Formula Essence is shown for each site in Figures 10 -17. As can be seen, significant effects were noted only for the T6 / Heart and C4 / Throat chakra sites.
So, what can we learn from the observations of this study?
First of all, it appears that the stress response occurs all along the spine, not only at our favorite electrode placement sites, such as the wide frontal placement all together. In fact, had we stuck to the traditional sites, we would have missed the clinical effects of the flower essence. I was very surprised and impressed by the magnitude of the stress response at the mastoid to mastoid / Medulla chakra site.
This site has been pretty well ignored in the stress profiling literature, and currently is not commonly used in clinical practice.
The only other notation for recordings from this site are found in the work by Mark Schwartz at the Mayo Clinic (Schwartz, 1985). He has utilized this site to study headaches for years, and a study by Hudzynski and Lawrence (1988) has validated its clinical utility for assessment purposes.
One could interpret the increased of sEMG activity at this site to represent a locking of the head to the spine at a time of threat so as to minimize damage to this important junction if a struggle were to pursue. From a metaphysical point of view, it might suggest that the Ego was engaged or disengaged as the case might be.
Or from a mechanical point of view, Body Work professionals have known about the importance of the axis / atlas relationships for years.
Chiropractors and physical therapists frequently manipulate this site to alleviate headaches, the Alexander Technique has based the foundation of its work at this site and John Upledger uses it as the basis of cranial sacral therapy.
Perhaps, we in the biofeedback arena should more completely explore the potential of this site for assessment and treatment purposes. Are we missing the possible etiology of headaches because we monitor only from frontalis and trapezius?
Secondly, I was duly impressed by the psychophysiological effects of the flower essence studied.
The flower essence therapy administered just prior to the stress profiling procedure significantly reduced the level of reactivity at the C4 / Throat and T6 / Heart chakras sites. Why did it effect these two sites and not the frontal site or other sites? From a strictly emotional model, the reduction in cervical sEMG might have been predicted, but certainly not the T6 paraspinals. Next, it doesn't make sense to place the effects of a flower essence into a strict mechanical model.
That is unless we begin to think of gravity as the basis of the unified field theory. Perhaps the clinical effects came about because of the homeopathic similarities between the attributes of flower essences and those of the chakras.
According to Kaminski (1995), the five flower essence was specifically designed to "bring about stabilization and calmness (Rock Rose), to "draw one back into present time" (Clematis), to "balance and soothe away impulsiveness and irritability" (Impatiens), to "bring about inner peace and stillness which allows us to ease the contraction felt in the body" (Cherry Plum), and to "help us regain our composure" and "for learning and mastery of our lives" (Star of Bethlehem).
The empirical data clearly suggests that the flower essence works primarily on the centers for calmness (C4/Throat) and love (T6/Heart). It appears to assist us in letting go of our attachments and desires, while promoting a sense of calmness.
Biofeedback practitioners may want to learn more about how to use these adjunctive tools may assist their patients in mastering the stress in their lives.
To conclude, psychophysiology provides a viable tool by which to investigate subtle energies, especially when guided by the metaphysical wisdom of the ages. This represents a blending of the old and new, East and West. For what is the basis of science but to describe what is all ready known with the latest tools of our culture.
Jeffrey R. Cram, Ph.D. (1949-2005)
|Posted by Maddalena Frau on April 27, 2013 at 3:00 AM||comments (0)|
The "Bottom Line" -- The Main Point of
If your depressions are complicated; if you have mood swings, but not "mania", you can still be "bipolar enough" to need a treatment that's more like the treatments we use in more easily recognized Bipolar Disorder. You'll read here about those forms which do not have "mania" to make them stand out or easily recognizable, including Bipolar II. Depression is the main symptom, including especially sleeping too much, extreme fatigue, and lack of motivation. What makes bipolar depression different is the presence of something else as well.
But that "something else" often does not look anything like mania. "Hypomania", which you'll learn about here, can show up as huge sleep changes, irritability, agitation/anxiety, and difficulty concentrating.
And finally, some people can have some bipolarity without any hypomania at all.
What happened to "manic-depressive" (now bipolar I)?
Somewhere along the way you probably learned about manic-depressive illness:
episodes of mania, and episodes of severe depression. Here are the symptoms of "mania"
What happened to "manic-depressive"?
As our understanding of bipolar disorder has grown, the naming system has changed as well. Recently the concept of a "mixed state" of bipolar disorder, in which manic symptoms and depressive symptoms are found at the same time, was added. Obviously this changes the understanding of manic-depressive illness from one in which the two mood states alternate, to one in which they can co-occur! Things are getting more complicated.
Psychiatry has a diagnostic "rule book" that lists the symptoms people must have in order to meet the definition of a particular "disorder", called the Diagnostic and Statistical Manual. The most recent edition came out in 1994, the "DSM-IV". "Bipolar II" was added in this edition, although it was first described as a pattern of mood change long before that. Technically Bipolar II describes a pattern in which patients experience "hypomania" (to be discussed in detail below), alternating with episodes of severe depression.
However, one of the most experienced professionals in this field, who has bipolar disorder herself, has criticized even this advance as too limited:
"The clinical reality of manic-depressive illness is far more lethal and infinitely more complex than the current psychiatric nomenclature, bipolar disorder, would suggest. Cycles of fluctuating moods and energy levels serve as a background to constantly changing thoughts, behaviors, and feelings. The illness encompasses the extremes of human experience. Thinking can range from florid psychosis, or "madness," to patterns of unusually clear, fast and creative associations, to retardation so profound that no meaningful mental activity can occur. Behavior can be frenzied, expansive, bizarre, and seductive, or it can be seclusive, sluggish, and dangerously suicidal. Moods may swing erratically between euphoria and despair or irritability and desperation. The rapid oscillations and combinations of such extremes result in an intricately textured clinical picture." (Kay Jamison, Ph.D.)
Everything you will read below can be found in a recent review by two mood experts, except that their version is written in full medical jargon.
Even the International Society for Bipolar Disorders has advocated a change in diagnostic procedure, moving beyond the DSM-IV, using what we've learned since 1994 in the diagnostic process (Ghaemi and colleagues; if you look closely you'll see that my name is on the list of co-authors: I was honored to be invited to participate and write for this 2008 update on bipolar diagnosis guidelines). Their recommendations are very consistent with what you'll read below.
What is the official definition of Bipolar II?
Technically, this is literally a "little" mania — the familiar symptoms but less so:
You may have noticed that "delusions" have disappeared from the list: these are by definition not found in Bipolar II. A patient who has had the above symptoms repeatedly, without having delusions, is much less likely to ever lose contact with reality (including weird experiences like auditory hallucinations, which are common in bipolar mania) than a patient who has experienced delusions.
"Bipolar II" is technically the combination of hypomanic phases with separate phases of severe depression If the depressive phases are only mild, the term "cyclothymia" is used. Getting confused? I certainly was, until I began to think of these variations as points on a continuous spectrum. I hope the following discussion will impress you as simpler.
What is the "mood spectrum?" (references updated 4/2008)
Until very recently, depression and "manic-depressive illness" were understood as completely independent: a patient either had one or the other. Now the two are seen by many mood specialists as two extremes on a continuum, with variations found at all points in between, as in the graph below (e.g. Ghaemi; Pies; Moller; Birmaher; Skeppar; Mackinnon; Angst and Cassano; Akiskal to name just a few important articles since 2001; and finally, my ISBD review in 2008):
On the left, the "unipolar" extreme represents straightforward depression with no complications. There are many forms of depression, of course. For an overview, see the appendix: "What kinds of depression are there?". The depressions discussed further below are of a more genetic, or "chemical" nature; versus those of a more situational type, like losing a loved one. Situational depressions may respond well to time or therapy and not require "bipolar" thinking.
On the right, the "manic-depressive" extreme is defined by the presence of manic episodes, just the kind that most people have seen or heard of: full delusional mania. But in between these extremes is a large area which some mood experts think includes more people than either extreme. In other words, it might be the most common form of bipolar disorder, this middle group.
Consider the following points A and B on this spectrum:
Point A on the continuum describes people who have a complex depression but who still respond well to antidepressant medication or psychotherapy.
Around point B, however, there is some sort of threshold where these approaches are no longer completely or continuously effective: either they don’t work at all, offer only partial relief, or help for a while then "stop working" (which may account for some or much of "Prozac poop-out", now regarded as a "soft sign" of bipolar disorder, described below).
Until 1994 and the publication of the DSM-IV, there was no official name for all the variations between B and the "manic-depressive" extreme.
It was as though these variations did not exist. In the minds of a few, they still don’t, including some psychiatrists who have not adopted this new "spectrum" way of thinking about diagnosis.
The DSM-IV itself does not describe this "spectrum" concept. In it, the entire span between blue and green is still "Major Depression", the same as the violet end to your left. Only the orange and red zones are clearly "bipolar".
Light green and yellow is BP NOS, Bipolar Not Otherwise Specified. That diagnosis means you have something that looks like bipolar disorder but does not meet the criteria for BP II or BP I. Isn't it simpler just to think of it as a continuum? That is much closer to reality. We see all sorts of variations in between these named points on the graph above.
What do "bipolar variations" look like?
Warning: The following represents my clinical experience taking referrals from primary care physicians. Most patients I see have been on 3 or more antidepressants before I see them. This selects very directly for "bipolar spectrum" patients. However, note that none of these descriptions are found in the DSM, nor are they widely spoken of by mood experts. This is my personal formulation based on almost 15 years of full-time selection for such patients.
Roller coaster depression
Many people have forms of depression in which their symptoms vary a lot with time: "crash" into depression, then up into doing fine for a while, then "crash" again — sometimes for a reason, but often for no clear reason at all.
They feel like they are on some sort of mood "roller coaster". They wonder if they have "manic-depression".
But, most people know someone or have heard of someone who had a "manic" episode: decreased need for sleep, high energy, risky behaviors, or even grandiose delusions (‘I can make millions with my ideas"; "I have a mission in space"; "I’m a special representative for God"). So they think "well, I can’t have that — I’ve never had a manic episode".
However, the new view of bipolar disorder means it’s time to reconsider that conclusion.
Hypomania doesn’t look or feel at all like full delusional mania in some patients.
Sometimes there is just a clear sense of something cyclic going on. Some mood disorder experts consider depression that occurs repeatedly to have a high likelihood of having a manic phase at some pointFawcett, especially if the first depression occurred before age twenty.Geller, Rao These two features--repeated recurrence, and early onset--are also included among the bipolar "soft signs" below: not enough to make a diagnosis, but suggestive, especially if they occur with several other such signs, even if "hypomania" is not detectable at all.Ghaemi
Depression with profound anxiety
Many people live with anxiety so severe, their depression is not the main problem. They seem to handle the periods of low energy, as miserable as they are.
Often they sleep for 10, 12, even 14 hours a day during those times. But the part they can’t handle is the anxiety: it isn’t "good energy".
Many say they feel as though they just have too much energy pent up inside their bodies.
They can’t sit still. They pace. And worst of all, their minds "race" with thoughts that go over and over the same thing to no purpose.
Or they fly from one idea to the next so fast their thoughts become "unglued", and they can’t think their way from A to C let alone A to Z.
When this is severe, people who enjoy books can find themselves completely unable to read: they just go over and over the same paragraph and it doesn’t "sink in". They will get some negative idea in their head and go around and around with it until it completely dominates their experience of the world. Usually these "high negative energy" phases come along with severely disturbed sleep (see Depression with Severe Insomnia, below). Thoughts about suicide are extremely common and the risk may be high.Fawcett(b)
Depressive episodes with irritable episodes
Many people with depression go through phases in which even they can recognize that their anger is completely out of proportion to the circumstance that started it. They "blow up" over something trivial. Those close to them are very well aware of the problem, of course. Many women can experience this as part of "PMS". As their mood problems become more severe, they find themselves having this kind of irritability during more and more of their cycle. Similarly, when they get better with treatment, often the premenstrual symptoms are the "last to go". Others can have this kind of cyclic irritability without any relationship to hormonal cycles. Many men with bipolar variations say they have problems with anger or rage.
Depression that doesn’t respond to antidepressants (or gets worse, or "poops out")
Many people have repeated episodes of depression. Sometimes the first several episodes respond fairly well to antidepressant medication, but after a while the medications seem to "stop working". For others, no antidepressant ever seems to work. And others find that some antidepressants seem to make them feel terrible: not just mild side effects, but severe reactions, especially severe agitation. These people feel like they’re "going crazy". Usually at this time they also have very poor sleep. Many people have the odd experience of feeling the depression actually improve with antidepressants, yet overall —perhaps even months later —they somehow feel worse overall. In most cases this "worse" is due to agitation, irritability, and insomnia.
In some cases, an antidepressant works extremely well at first, then "poops out".Byrne The benefits usually last several weeks, often months, and occasionally even years before this occurs. When this occurs repeatedly with different antidepressants, that may mark a "bipolar" disorder even when little else suggests the diagnosis.Sharma
Depression with periods of severe insomnia
Finally, there are people with depression whose most noticeable symptom is severe insomnia. These people can go for days with 2-3 hours of sleep per night. Usually they fall asleep without much delay, but wake up 2-4 hours later and the rest of the night, if they get any more sleep at all, is broken into 15-60 minute segments of very restless, almost "waking" sleep. Dreams can be vivid, almost real. They finally get up feeling completely unrested. Note that this is not "decreased need for sleep" (the Bipolar I pattern). These people want desperately to sleep better and are very frustrated.
Unofficial but evidence-based markers of Bipolar Disorder
You have probably figured it out by now: making a diagnosis of bipolar disorder can be pretty tricky sometimes! You're about to read a list of eleven more factors that have been associated with bipolar disorder. None of these factors "clinches" the diagnosis. They are suggestive of bipolarity, but not sufficient to establish it. They are best regarded as markers which suggest considering bipolar disorder as a possible explanation for symptoms. They are not a scoring system, where you might think "the more I have of these, the more likely it is that I have bipolar disorder." That way of thinking about these factors has not been tested.
Here's the list of items which are found with bipolar disorder more often than you would expect by chance alone. This list is adapted from a landmark article by Drs. Ghaemi and Goodwin and Ko. (Drs. Goodwin and Ghaemi are among the most respected authorities on bipolar diagnosis in the world. This important article is online https://ww1.cpa-apc.org/Publications/Archives/CJP/2002/march/inReviewCadesDisease.asp).
There is a very radical idea buried in these 11 items, which we should look at before going on, but you should be aware that this idea is likely be dismissed with a "hmmmph" by many practicing psychiatrists. The idea is this: Dr. Ghaemi and colleagues propose that there might be a version of "bipolar disorder" that does not have any mania at all, not even hypomania. They call it "bipolar spectrum disorder".
This is strange, you are saying to yourself. "I thought bipolar disorder was distinguished from 'unipolar' depression by the presence of some degree of hypomania. Don't you have to have some hypomania in order to be bipolar? How could it be 'bi' - polar if there is no other pole!?"
But Dr. Ghaemi and colleagues assert that there are versions of depression that end up acting more like bipolar disorder, even though there is no hypomania at all that we can detect (or, as in item #9, only when an antidepressant has been used). These conditions often do not respond well, in the long run, to antidepressant medications (which "poop out" or actually start making things worse). They respond better to the medications we routinely rely on in bipolar disorder, the "mood stabilizers" you'll be introduced to in the Treatment section of this website (including several non-medication approaches). And these patients have other folks in their family with bipolar disorder or something that looks rather more like that (e.g. dramatic "mood swings", even if the person never really gets ill enough to need treatment).
In Dr. Ghaemi's description, then, there are people whose depression looks so "unipolar" that even a "fine-toothed comb" approach to looking for hypomania will not identify it as part of the "bipolar spectrum". According to Ghaemi and colleagues, these people should be regarded as "bipolar", in a sense, because of the way they will end up responding to treatment. In other words, there is something in these people which doesn't look like our old idea of bipolar disorder, or even our newer idea of bipolar disorder (bipolar II, etc.), but will still better describe their future (their prognosis) and the medications that are most likely to help them. Remember that this is the very purpose of "diagnosis", to describe the likely outcomes with and without treatment, and to identify effective treatments. So, on that basis, it seems reasonable to include these patients on the "bipolar spectrum", like this:
The idea that someone can "have" bipolar disorder and yet not have any hypomania at all is not widely understood. You probably would get blank looks from most psychiatrists if you mention it, and frank disbelief from nearly all primary care doctors, who don't have time to read the literature on the diagnosis of bipolar disorder. So, if you mention this idea to anyone, be prepared for some serious resistance. As of 2005 the Harvard-associated Mood Disorder program started using this approach to diagnosis. They call it the Bipolarity Index.
Other researchers are also beginning to use the same framework of thought. For example, one research group just reported that patients with migraine headaches are much more likely to have these bipolar spectrum traits.Oedgaard (Migraines are much more common in patients with unipolar and Bipolar II than in Bipolar I, interestingly.Fasmer) One recent summary article for primary care doctors, about bipolar disorder, discusses these "soft signs" in considerable detail.Swann The concept of a bipolar "spectrum" is supported by work from a research group calling themselves the Spectrum Project.e.g. Cassano
Probably better not to raise this issue unless you have to, but if you must, cite the source. Here's that article link again.Ghaemi Dr. Ghaemi is the chairman of the committee on diagnosis for the International Society for Bipolar Disorder. One of his two co-authors is Dr. Frederick Goodwin, who wrote the "bible" of bipolar disorder for our lifetime (Manic-Depressive Illness, with Dr. Kay Jamison). These are highly respected researchers amongst mood experts. Dr. Ghaemi emphasizes the need to rely on evidence in all his papers on diagnosis and treatment and is very frequently cited by other authors on this topic . But he is certainly not the only such voice. If you haven't seen enough references yet, here's another similar recent one, by other international mood experts.Mitchell
Anxious depression could be "bipolar"?!
Warning: leaving DSM-IV territory
The remainder of this "diagnosis" discussion cannot be found in the DSM. I will repeatedly reference mood disorder experts, but many of these views are controversial. You must evaluate for yourself the validity of what follows.
Unfortunately, "hypomania" is quite a mis-naming. There are many patients whose "hypomanic" phases are an extreme and very negative experience. As noted above by Dr. Jamison, mania can be negative as often as it is positive. The "racing thoughts" can have a very negative focus, especially self-criticism. The high energy can be experienced as a severe agitation, to the point where people feel they must pace the floor for hours at a time. Sleep problems can show up as insomnia: an inability to sleep, rather than decreased need. (If you or a friend or doctor is skeptical about anxiety as a "bipolar" symptom, try that link for more details and references.)
Most of these people come to treatment with a combination of agitation, anxiety and self-criticism — and they can’t sleep well. Is this "anxiety?" Is this some mood variation? How could you tell the difference? Is there a difference? What is really going on chemically? Unfortunately, this is still almost completely unknown. See the appendix "What’s the latest on why?", which I will try to keep updated frequently, for the latest research about the cause of this illness.
Again, my opinion: you can’t easily distinguish "anxious depression" from bipolar II in a mixed state. I doubt that there is a distinction to be made, ultimately (when we know, hopefully someday relatively soon, what the chemical basis for anxiety with depression really is). For example there is nearly complete overlap between Generalized Anxiety Disorder and Bipolar II.
For now, the only way to tell is by how treatment turns out. Depression that is not bipolar can get better and stay better: with time, or counseling, or formal psychotherapy, or antidepressants. If you get better — great! If you don’t, you may need this new understanding of mood disorders in order to consider mood stabilizers medications, discussed in detail below, as an option.
Meanwhile, at least one experienced mood researcher warns that anxiety in someone who is depressed is associated with a high suicide risk.Fawcett(b) So although there is diagnostic confusion, there are tremendous stakes involved. Approaching this situation with an open mind seems wise, given this risk.
What does Hypomania actually feel
It's true that hypomania is a milder version of mania -- just how mild, you'll see in a moment. Mind you, Bipolar II is not a milder version of Bipolar I, though it is very often described that way, to my utter dismay.
The suicide rate in Bipolar II is the same or higher than the rate for Bipolar I, for example.Dunner So the BP II version is definitely not a "mild" illness. The depression phases are as bad as in BP I, and often more common (that is, they occur more frequently and represent a more dominant part of the person's life).
Nevertheless, hypomania can indeed by subtle, certainly by comparison with full mania, as shown in this graph (from Smith and Ghaemi). Here are the symptoms which people with clear-cut hypomania actually experience -- and how often. For example, at the bottom of the graph you see that nearly 100% of people with hypomania will have an increase in their activity. By comparison, optimism is prominent only about 70% of the time in hypomania.
As you can see, these "symptoms" are not clearly abnormal. Everyone experiences these feelings from time to time. When they are extreme; and when they show up over and over again in cycles of mood/energy change; when they are accompanied by other signs of bipolarity, such as phases of depression; that's when we should think of this as "abnormal", or at least as warranting caution if someone wants to treat those depressed phases with an antidepressant.
However, hypomania is not always positive. Just as manic phases can be very negative (so-called "dysphoric mania"), hypomania also can be very unpleasant. Here is an example of how hypomania can change from a positive experience to a very negative one/
First, the positive phase:
Increased energy. A extraordinary feeling of happiness with myself and the world. A very loving feeling towards the people I care about. An uncommon ability to get things done. A huge burst of energy from the moment I awaken until I go to bed. An expanded ability to multi-task. An organizational acuity that is second to none. A willingness to engage with people. A desire to spend more time with people I care about--and even those I don't.
Then, the negative phase of hypomania (still pretty subtle):
I start feeling burned out. While I still have a lot of energy, I don't have that "I love the world" feeling. If I've been playing my Autoharp at my mother's assisted living facility, and jumping up and down to help all the participants turn the pages and stay with me, I suddenly feel that the staff should be more helpful in doing this.
... things don't just slide off my back. While I try not to "snap" back at people, I am not always successful. I am certainly less willing to ignore things that days or weeks earlier wouldn't have bothered me at all.
I become far less happy, joyful, and kind. I dislike being criticized in any which way.
How short can an episode of hypomania be?
Officially, the answer is "four days", according to the DSM. But in real life, it's very clear that episodes can be shorter, and that's agreed upon by nearly all mood experts I've ever heard. They might disagree whether we should shorten the required duration in the DSM, as that would "admit" a lot more people into the bipolar camp which is already a controversial issue. But no one really seems to think that a hypomanic episode lasting only 3 days instead of four is anything other than hypomania; it just doesn't "meet criteria", that's all.
Indeed, a recent studyBauer showed that episodes lasting as little as one day are common. So don't get hung up on length of episodes as an issue if you're trying to figure out if you "have bipolar disorder" or not. Remember, that's the wrong question anyway... Instead, it's "how bipolar are you?" as affirmed in a recent editorial Smith in the British Journal of Psychiatry (one of the biggies...).
What does bipolar depression actually feel
Theoretically, bipolar depression is exactly the same as "unipolar" or straight Major Depression. Theoretically, you can't distinguish between the two, so you can't tell if someone has bipolar disorder just by looking at their depressions.
But I think there is a different quality to the depressions that people with bipolar disorder experience, because before they start feeling sad and having difficulty experiencing pleasure from their usual activities, they very often have problems with energy. To emphasize this I'd just like you to look at this list of symptoms which people with bipolar disorder said they have when they're just starting to get depressed.
If you think "that's me!", careful: this does not mean you have bipolar depressions. But it might help to see what people with bipolar disorder have said about their experience. I don't hear about these symptoms so much when people have a more purely "unipolar" -- not bipolar -- depression.
Granted, people in this study also endorsed "loss of interest in activities" and "feeling sad, wanting to cry" but these are her typical symptoms in official "Major Depression". And low energy can also be seen in Major Depression. But look at how prominent it is in this study. I think that might be telling us something about the nature of bipolar depression. Certainly matches what I hear from patients.
Finally, the original intent of this list was to help people identify symptoms that mark the beginning of another episode of depression. He might find it useful in that respect also.
I hope it may now make sense to you to think of mood symptoms as falling on a continuum between plain depression and "depression plus", the far end of which is Bipolar I, with many variations falling in between.
If you are wondering whether what you've just read is "mainstream" or "fringe" (that's a good thing to wonder), you'll find the same "spectrum" concept coming from the head of the Harvard Bipolar Clinic, in this 2005 interview: Sachs.
By contrast, another mood disorder expert has shown that bipolar disorder is overdiagnosed (Zimmerman, 2008; here is a close examination of his findings). He's certainly right, if one sticks to the DSM rules (although his paper also shows a notable underdiagnosis rate as well). And there are quite a few people getting this diagnosis who might be better understood with a different diagnostic framework, like Post-Traumatic Stress Disorder (PTSD). But in my view, one of the things that can help you figure out what's going on is to learn more about "bipolarity", as you have done here. You are an important part of the diagnostic process.
Is there a test for bipolar disorder? Can you be sure if you have it or not?
This used to be simple. When "manic" only meant one thing (classic mania) one could ask "have you ever had a manic episode?" and many people knew what was being asked:
As you now know afresh if you came from elsewhere), this list looks for obvious mania. It misses all the complexity we have just discussed. What you might be wanting is a "no way!" bipolar test. Something to provide a clear statement, like: "no, you don’t have it, or anything like it". Or you might be looking for the opposite: "you definitely have bipolar II". Sorry, that is not possible, but please read on.
On other websites you'll find a test called the Mood Disorders Questionnaire (MDQ) which is supposed to give you a "yes or no" answer. But another test came along after the MDQ which is better suited to looking for subtle versions of bipolar II.
Think about it: if by this point on this website you're saying to yourself "that's me!", which some people do, then you really don't need some test to tell you that you should go ahead and consider treatment. Or that the diagnostic basis for that treatment should include a consideration of bipolar II. On the other hand, if someone else thinks you might have it, but you don't think you do, is a test result going to make a difference to you? If so, go ahead and take one of these tests.
Family or friends could "take the test", answering as if they were you, on the basis of what they've seen you do or heard you say. And then they could gently wonder out loud if perhaps the test might mean something, who knows, no one can tell for sure, but darn it sure seems like your life is a struggle sometimes, wow, what if there was a tool out there that would make life a bit smoother sometimes, not even necessarily a medication treatment, oh well, just thinking about this, of course you'd want to decide for yourself, not for me to say of course, etc. etc.
The people who are in a position to benefit from taking one of these diagnostic tests are those who are wondering if a "bipolar" variation might be worth considering to explain their symptoms. Here's the test I'd recommend for you, called the Bipolar Spectrum Diagnostic Scale. It won't give you a yes-or-no answer. I hope by this point you understand why that's a good thing. If after all that you still want to use a "fine-toothed comb" to look for hypomanic/manic symptoms, as I sometimes do when people are still wondering about the diagnosis after learning all this, here is a 32-item checklist of such symptoms.
Thank you for patiently reading all the way to this point. It's a lot to swallow at once, isn't it? read more about diagnosis issues in the Diagnosis Details section, or go on to Treatment.
|Posted by Maddalena Frau on April 2, 2013 at 12:45 AM||comments (0)|
The deadliest form of malaria is caused the protozoan Plasmodium falciparum. During its life-cycle in human blood, the parasite P. falciparum expresses unique proteins on the surface on infected blood cells.
Antibodies to these proteins are associated with protection from malaria, however, the identity of surface protein(s) that elicit the strongest immune response is unknown.Dr. James Beeson and colleagues at the Walter and Eliza Hall Institute of Medical Research in Victoria, Australia have developed novel assays with transgenic P. falciparum expressing modified surface proteins, allowing the researchers to quantify serum antibodies to surface proteins among malaria-exposed children and adults.
They found that most of the human antibody response to the surface proteins targets a parasite protein known as PfEMP1.Moreover, the showed that people with PfEMP1-specific antibodies had a reduced risk of malaria symptoms, whereas antibodies to other surface antigens were not associated with protective immunity.
These findings suggest antibodies against PfEMP mediate human immunity to malaria and have implications for future malaria vaccine development.More information: Targets of antibodies against Plasmodium falciparum-infected erythrocytes in malaria immunity,
Provided by Journal of Clinical Investigation
|Posted by Maddalena Frau on February 27, 2013 at 12:50 AM||comments (0)|
A novel tool exploits baker's yeast to expedite the development of new drugs to fight multiple tropical diseases, including malaria, schistosomiasis, and African sleeping sickness.
The unique screening method uses yeasts which have been genetically engineered to express parasite and human proteins to identify chemical compounds that target disease-causing parasites but do not affect their human hosts.
Parasitic diseases affect millions of people annually, often in the most deprived parts of the world. Every year, malaria alone infects over 200 million people, killing an estimated 655,000 individuals, mostly under the age of five.
Unfortunately, our ability to treat malaria, which is caused by Plasmodium parasites, has been compromised by the emergence of parasites that are resistant to the most commonly used drugs.
There is also a pressing need for new treatments targeting other parasitic diseases, which have historically been neglected.Currently, drug-screening methods for these diseases use live, whole parasites.
However, this method has several limitations. First, it may be extremely difficult or impossible to grow the parasite, or at least one of its life cycle stages, outside of an animal host.
(For example, the parasite Plasmodium vivax, responsible for the majority of cases of malaria in South America and South-East Asia, cannot be continuously cultivated in laboratory conditions.)
Second, the current methods give no insight into how the compound interacts with the parasite or the toxicity of the compound to humans.
In an effort to develop new drugs to fight parasitic diseases, scientists from the University of Cambridge have collaborated with computer scientists at Manchester University to create a cheaper and more efficient anti-parasitic drug-screening method.
The clever screening method identifies chemical compounds which target the enzymes from parasites but not those from their human hosts, thus enabling the early elimination of compounds with potential side effects.
Professor Steve Oliver, from the Cambridge Systems Biology Centre and Department of Biochemistry at the University of Cambridge, said: "Our screening method provides a faster and cheaper approach that complements the use of whole parasites for screening.
This means that fewer experiments involving the parasites themselves, often in infected animals, need to be carried out.
The new method uses genetically engineered baker's yeast, which either expresses important parasite proteins or their human counterparts.
The different yeast cells are labelled with fluorescent proteins to monitor the growth of the individual yeast strains while they grow in competition with one another.
High-throughput is provided by growing three to four different yeast strains together in the presence of each candidate compound.
This approach also provides high sensitivity (since drug-sensitive yeasts will lose out to drug-resistant strains in the competition for nutrients), reduces costs, and is highly reproducible.
The scientists can then identify the chemical compounds that inhibit the growth of the yeast strains carrying parasite-drug targets, but fail to inhibit the corresponding human protein (thus excluding compounds that would cause side-effects for humans taking the drugs).
The compounds can then be explored for further development into anti-parasitic drugs.In order to demonstrate the effectiveness of their screening tool, the scientists tested it on Trypanosoma brucei, the parasite that causes African sleeping sickness.
By using the engineered yeasts to screen for chemicals that would be effective against this parasite, they identified potential compounds and tested them on live parasites cultivated in the lab. Of the 36 compounds tested, 60 per cent were able to kill or severely inhibit the growth of the parasites (under standard lab conditions).
Dr Elizabeth Bilsland, the lead author of the paper from the University of Cambridge, said: "This study is only a beginning.
It demonstrates that we can engineer a model organism, yeast, to mimic a disease organism and exploit this technology to perform low-cost, fully-automated drug screens to select and optimise drug candidates as well as identify and validate novel drug targets.""In the future, we hope to engineer entire pathways from pathogens into yeast and also to construct yeast strains that mimic diseased states of human cells.
The research is published today, 27 February, in the journal Open Biology.
|Posted by Maddalena Frau on February 26, 2013 at 11:40 PM||comments (0)|
Eating a Mediterranean diet appears to be associated with less risk of mild cognitive impairment—a stage between normal aging and dementia—or of transitioning from mild cognitive impairment into Alzheimer's disease, according to a report in the February issue of Archives of Neurology.
"Among behavioral traits, diet may play an important role in the cause and prevention of Alzheimer's disease," the authors write as background information in the article.
Previous studies have shown a lower risk for Alzheimer's disease among those who eat a Mediterranean diet, characterized by high intakes of fish, vegetables, legumes, fruits, cereals and unsaturated fatty acids, low intakes of dairy products, meat and saturated fats and moderate alcohol consumption.
Nikolaos Scarmeas, M.D., and colleagues at Columbia University Medical Center, New York, calculated a score for adherence to the Mediterranean diet among 1,393 individuals with no cognitive problems and 482 patients with mild cognitive impairment.
Participants were originally examined, interviewed, screened for cognitive impairments and asked to complete a food frequency questionnaire between 1992 and 1999.
Over an average of 4.5 years of follow-up, 275 of the 1,393 who did not have mild cognitive impairment developed the condition.
Compared with the one-third who had the lowest scores for Mediterranean diet adherence, the one-third with the highest scores for Mediterranean diet adherence had a 28 percent lower risk of developing mild cognitive impairment and the one-third in the middle group for Mediterranean diet adherence had a 17 percent lower risk.Among the 482 with mild cognitive impairment at the beginning of the study, 106 developed Alzheimer's disease over an average 4.3 years of follow-up. Adhering to the Mediterranean diet also was associated with a lower risk for this transition.
The one-third of participants with the highest scores for Mediterranean diet adherence had 48 percent less risk and those in the middle one-third of Mediterranean diet adherence had 45 percent less risk than the one-third with the lowest scores.
The Mediterranean diet may improve cholesterol levels, blood sugar levels and blood vessel health overall, or reduce inflammation, all of which have been associated with mild cognitive impairment.
Individual food components of the diet also may have an influence on cognitive risk. "For example, potentially beneficial effects for mild cognitive impairment or mild cognitive impairment conversion to Alzheimer's disease have been reported for alcohol, fish, polyunsaturated fatty acids (also for age-related cognitive decline) and lower levels of saturated fatty acids," they write.
Read more at: http://phys.org/news153419152.html#jCp
|Posted by Maddalena Frau on February 9, 2013 at 2:05 PM||comments (0)|
The causes of ADHD.
According to the U.S. National Institute of Mental Health, attention deficit hyperactivity disorder (ADHD) is a legitimate psychologic condition.
ADHD is a syndrome generally characterized by the following symptoms:
Inattention Distractibility Impulsivity Hyperactivity
Some doctors categorize ADHD into three subtypes:
Behavior marked by hyperactivity and impulsivity, but not inattentiveness Behavior marked by inattentiveness, but not hyperactivity and impulsivity A combination of the above twoThere is some debate over these criteria.
Some argue the condition is overdiagnosed. Others say it's underdiagnosed.
One-third of cases are accompanied by learning disabilities and other neurologic or emotional problems, making an ADHD diagnosis particularly difficult.
It is likely that the term attention-deficit hyperactivity disorder will eventually give way to subgroups of problems that include some of these general symptoms.
ADHD is a genuine disorder, but it is telling that the U.S. accounts for 90% of worldwide prescriptions for stimulants for ADHD.
It is not known whether this reflects a real increase in ADHD, or a better ability to recognize it. Some say it may be an indication of a culture that places excessive value on normalcy and academic achievement at the expense of more frequent diagnoses.
Symptoms of ADHD usually occur around the age of 7. Studies indicate that ADHD symptoms in preschool children with ADHD do not differ significantly from older children.
The classic ADHD symptoms do not always adequately describe the child's behavior, nor do they describe what is actually happening in the child's mind.
Some researchers focused on deficits in "executive functions" of the brain to understand and describe all ADHD behaviors. Such impaired executive functions in ADHD children can cause the following problems:
Inability to hold information in short-term memoryImpaired organization and planning skills
Difficulty in establishing and using goals to guide behavior, such as selecting strategies and monitoring tasksInability to keep emotions from becoming overpoweringInability to shift efficiently from one mental activity to anotherHyperactivity.
The term hyperactive is often confusing since, for some, it suggests a child racing around non-stop.
A boy with ADHD playing a game, for instance, may have the same level of activity as another child without the syndrome. But when a high demand is placed on the child's attention, his brain motor activity intensifies beyond the levels of the other children. In a busy environment, such as a classroom or a crowded store, children with ADHD often become distracted and react by pulling items off the shelves, hitting people, or spinning out of control into erratic, silly, or strange behavior.
Impulsivity and Temper Explosions. Even before the "terrible twos," impulsive behavior is often apparent. The toddler may gleefully make erratic and aggressive gestures, such as hair pulling, pinching, and hitting.
Temper tantrums, normal in children after age 2, are usually exaggerated and not necessarily linked to a specific negative event in the life of a child with ADHD. One of the most painful events a parent may experience is an abrupt and aggressive attack that may occur after cuddling a young child with ADHD.
Often this reaction seems to be caused not by anger, but by the child's apparent inability to endure over stimulation or displays of physical affection.
Attention and Concentration. Children with ADHD are usually distracted and made inattentive by an overstimulating environment (such as a large classroom).
They are also inattentive when a situation is low-key or dull. Some researchers theorize that certain parts of the brain in ADHD children may be underactive, so the children fail to be aroused by nonstimulating activities.
In contrast, they may exhibit a kind of "super concentration" to a highly stimulating activity (such as a video game or a highly specific interest).
Such children may even become over-attentive -- so absorbed in a project that they cannot modify or change the direction of their attention.
Impaired Short-Term Memory. Many doctors now believe that an essential feature in ADHD, as well as in learning disabilities, is an impaired working (also called short-term) memory. People with ADHD can't hold groups of sentences and images in their mind long enough to extract organized thoughts.
They are not necessarily inattentive. Instead, a patient with ADHD may be unable to remember a full explanation (such as a homework assignment), or unable to complete processes that require remembering sequences, such as model building.
In general, children with ADHD are often attracted to activities (television, computer games, or active individual sports) that do not tax the working memory, or produce distractions.
Children with ADHD have no differences in long-term memory compared with other children.
Inability to Manage Time. Studies suggest that children with ADHD have difficulties being on time and planning the correct amount of time to complete tasks. (This may coincide with short-term memory problems.)
Lack of Adaptability. Children with ADHD have a very difficult time adapting to even minor changes in routines, such as getting up in the morning, putting on shoes, eating new foods, or going to bed. Any shift in a situation can precipitate a strong and noisy negative response.
Even when they are in a good mood, they may suddenly shift into a tantrum if met with an unexpected change or frustration. In one experiment, These children can closely focus their attention when directly cued to a specific location, but they have difficulty shifting their attention to an alternative location.
Hypersensitivity and Sleep Problems.. Children with ADHD are often hypersensitive to sights, sounds, and touch.
They may complain excessively about stimuli that seem low key or bland to others. Sleeping problems usually occur well after the point when most small children sleep through the night. In one study, 63% of children with ADHD had trouble sleeping.
Adult ADHDAlthough ADHD is primarily thought of as a childhood disorder, diagnoses of attention-deficit disorder in adults are on the rise.
Methylphenidate (Ritalin) was prescribed for nearly 800,000 adults in the U.S. in 1997, nearly three times the number in 1992. It is estimated that ADHD affects about 4.1% of adults ages 18 - 44 years in a given year. The disorder appears to be distributed equally between adult women and men.
Accompanying Mental Health Disorders. About 20 % of adults with ADHD also have major depression or bipolar disorder. Up to 50 % have an anxiety disorder. Bipolar disorder plus ADHD, in fact, may be very difficult to differentiate from ADHD alone in adults.
Accompanying Learning Disorders. About 20% of adults with ADHD have learning disorders, usually dyslexia and auditory processing problems. These problems should be considered in any treatment plan.
Effect on Work. Compared to adults without ADHD, those with the condition tend to reach lower educational levels, earn less money, and be fired more often. In fact, one study reported that by the time they are in their 30s, about 35% of ADHD adults are self-employed.
Substance Abuse. About 1 in 5 adults with ADHD also contend with substance abuse. Studies indicate that adolescents with ADHD are twice as likely to smoke cigarettes as their peers who do not have ADHD.
Cigarette smoking during adolescence is a risk factor for the development of substance abuse in adulthood.
Research using advanced imaging techniques shows there is a difference in the size of certain parts of the brain in children with ADHD compared to children who do not have ADHD. The areas showing change include the prefrontal cortex, the caudate nucleus and globus pallidus, and the cerebellum.
Abnormal activity of certain brain chemicals in the prefrontal cortex may contribute to ADHD. The chemicals dopamine and norepinephrine are of special interest. Dopamine and norepinephrine are neurotransmitters, or chemical messengers, that affect both mental and emotional functioning. They also play a role in the "reward response." This response occurs when a person experiences pleasure in response to certain stimuli (such as food or love). Studies suggest that increased levels of the brain chemicals glutamate, glutamine, and GABA -- collectively called Glx -- interact with the pathways that transport dopamine and norepinephrine.
Another area of interest is a network of nerves called the basal-ganglia thalamocortical pathways. Abnormalities along this neural route have been associated with ADHD, Tourette syndrome, and obsessive-compulsive disorders, all of which share certain symptoms.
Genetic factors may play the most important role in ADHD. The relatives of ADHD children (both boys and girls) have much higher rates of ADHD, antisocial, mood, anxiety, and substance abuse disorders than the families of non-ADHD children. Some twin studies report that up to 90% of children with a diagnosis of ADHD shared it with their twin.
Most of the research on the underlying genetic mechanisms targets the neurotransmitter dopamine. Variations in genes that regulate specific dopamine receptors have been identified in a high proportion of people with addictions and ADHD.
Gender and ADHD
ADHD is most often diagnosed in boys. However, there is some evidence that it is underdiagnosed in girls. Until recently, all major studies were conducted using boys as subjects. More studies on girls with ADHD are now underway. A major study reported that girls with the condition experience the same multiple impairments as boys do.
ADHD tends to run in families. A child who has a parent or sibling with ADHD has an increased risk of also developing ADHD.
Some research suggests that prenatal exposure to tobacco and alcohol may increase the risk for ADHD. Environmental lead exposure before age 6 may also raise the risk for ADHD.
Several dietary factors have been researched in association with ADHD, including sensitivities to certain food chemicals, deficiencies in fatty acids (compounds that make up fats and oils) and zinc, and sensitivity to sugar. No clear evidence has emerged, however, that implicates any of these nutritional factors as risk factors for developing ADHD.
Resourceswww.aap.org -- American Academy of Pediatricswww.nimh.nih.gov -- National Institute of Mental Healthwww.chadd.org -- Children and Adults with Attention-Deficit Disorderwww.add.org -- Attention Deficit Disorder Associationwww.aabt.org -- Association for Behavioral and Cognitive Therapieswww.psych.org -- American Psychiatric Associationwww.parentsmedguide.org -- Medication Guide for Treating ADHDwww.aacap.org -- American Academy of Child and Adolescent Psychiatrywww.nichcy.org -- National Dissemination Center for Children with Disabilitieswww.ncld.org -- National Center for Learning Disabilitieswww.ldaamerica.org -- Learning Disabilities Association of America
|Posted by Maddalena Frau on February 9, 2013 at 1:35 PM||comments (0)|
ARE YOU CHEMICALLY DEPENDENT?
Ask yourself the following questions and answer them as honestly as you can.
Do you lose time from work due to alcohol/drug usage?
Is alcohol/drug usage making your home life unhappy?
Do you drink/use drugs because you are shy with other people?
Is alcohol/drug usage affecting your reputation?
Have you ever felt remorse after alcohol/drug usage?
Have you ever gotten into financial difficulties as a result of alcohol/drug usage?
Do you turn to lower companions and an inferior environment when drinking/using drugs?
Does your drinking/drug usage make you careless of your family's welfare?
Has your ambition decreased since drinking/using drugs?
Do you crave a drink or other drugs at a definite time daily?
Do you want a drink or other drugs the next morning?
Does drinking/drug usage cause you to have difficulty in sleeping?
Has your efficiency decreased since drinking/using drugs?
Is drinking/drug usage jeopardizing your job or business?
Do you drink/use drugs to escape from worries or trouble?
Do you drink/use drugs alone?
Have you ever had a complete loss of memory as a result of drinking/using drugs?
Has your physician ever treated you for drinking/drug usage?
Do you drink/use drugs to build up your self-confidence?
Have you ever been to a hospital or institution on account of your drinking/drug usage?
If you have answered YES to any one of the questions, there is a definite warning that you may be chemically dependent.
If you answered YES to any two, the chances are that you are chemically dependent.
If you have answered YES to three or more, you are definitely chemically dependent.
Note: The above test questions are derived from a questionnaire used by Johns Hopkins University Hospital, Baltimore, Maryland in deciding whether or not a patient is alcoholic.
|Posted by Maddalena Frau on December 5, 2012 at 2:45 AM||comments (0)|
A new study from MIT neuroscientists sheds light on a neural circuit that makes us likelier to remember what we're seeing when our brains are in a more attentive state.
The team of neuroscientists found that this circuit depends on a type of brain cell long thought to play a supporting role, at most, in neural processing.
When the brain is attentive, those cells, called astrocytes, relay messages alerting neurons of the visual cortex that they should respond strongly to whatever visual information they are receiving.
The findings, published this week in the online edition of the Proceedings of the National Academy of Sciences, are the latest in a growing body of evidence suggesting that astrocytes are critically important for processing sensory information, says Mriganka Sur, the Paul E. and Lilah Newton Professor of Neuroscience at MIT and senior author of the paper.
Sur's lab has been studying astrocytes for about five years, as part of a longstanding interest in revealing the functions of different cell types in the cortex. The star-shaped cells were first discovered and named 150 years ago, but since then, "it's been a mystery what they do," says Sur, who is a member of MIT's Picower Institute for Learning and Memory and director of the Simons Center for the Social Brain at MIT.Lead authors of the paper are graduate student Naiyan Chen and research scientist Hiroki Sugihara.
Other authors are research scientist Jitendra Sharma, postdocs Gertrudis Perea and Jeremy Petravicz, and technical assistant Chuong Le.
Attention strengthens responseIn this study, the researchers focused on what astrocytes do when the brain is stimulated to pay attention to a specific visual stimulus.
When someone is paying close attention to something, the nucleus basalis—a structure located deep within the brain, behind the eyes—floods the brain with a neurotransmitter called acetylcholine. Some of this acetylcholine targets astrocytes in the visual cortex.
To explore how astrocytes react to this stimulation, the researchers measured what happened in the visual cortex as they showed mice several visual patterns composed of parallel lines oriented in different directions. For one of the visual patterns, the researchers also provoked the nucleus basalis to release acetylcholine at the same time.
This greatly boosted calcium levels in the astrocytes, indicating high activity.When the mice were shown the same stimuli a few minutes later, the pattern that had been presented along with acetylcholine stimulation provoked a much stronger response in neurons of the visual cortex than the other patterns.
The researchers then did the same test in genetically engineered mice whose astrocytes were disabled. In those mice, the acetylcholine released by the nucleus basalis did not strengthen neurons' response to visual stimuli."If you are paying attention to something, which causes this release of acetylcholine, that leads to a long-lasting memory of that stimulus.
If you remove the astrocytes, that doesn't happen," Sur says.
The strengthening effect lasts for tens of minutes, after which the neurons return to their original activity level in response to the selected stimulus."More directly than any other study to date, it illustrates the critical role of astrocytes in plasticity," says Michael Merzenich, a professor emeritus of neuroscience at the University of California at San Francisco, who was not part of the research team.
"It's a crystal-clear demonstration."'Major players in brain disorders'It is already known that acetylcholine levels drop in the brains of patients with Alzheimer's disease. In fact, a commonly used treatment that can boost memory in Alzheimer's patients is a drug that blocks the degradation of acetylcholine.
In a follow-up study, the researchers are planning to study how astrocytes are affected in mouse models of Alzheimer's.Sur's lab is also studying the effects of nucleus basalis stimulation on inhibitory neurons.
Those effects are thought to be shorter term, lasting seconds or fractions of seconds."You cannot understand brain disorders without understanding the basic mechanisms of cortical brain function," Sur says.
"These cell types—astrocytes, inhibitory neurons—are emerging as major players in brain disorders, in unexpected ways.
"Journal reference: Proceedings of the National Academy of Sciences search
more info websiteProvided by Massachusetts Institute of Technology search and more info website
This story is republished courtesy of MIT News (web.mit.edu/newsoffice/), a popular site that covers news about MIT research, innovation and teaching.
|Posted by Maddalena Frau on November 19, 2012 at 11:45 PM||comments (0)|
Deciphering what causes the brain cell degeneration of Parkinson's disease has remained a perplexing challenge for scientists. But a team led by scientists from The Scripps Research Institute (TSRI) has pinpointed a key factor controlling damage to brain cells in a mouse model of Parkinson's disease. The discovery could lead to new targets for Parkinson's that may be useful in preventing the actual condition.
The team, led by TSRI neuroscientist Bruno Conti, describes the work in a paper published online ahead of print on November 19, 2012 by the Journal of Immunology.Parkinson's disease plagues about one percent of people over 60 years old, as well as some younger patients.
The disease is characterized by the loss of dopamine-producing neurons primarily in the substantia nigra pars compacta, a region of the brain regulating movements and coordination.Among the known causes of Parkinson's disease are several genes and some toxins. However, the majority of Parkinson's disease cases remain of unknown origin, leading researchers to believe the disease may result from a combination of genetics and environmental factors.
Neuroinflammation and its mediators have recently been proposed to contribute to neuronal loss in Parkinson's, but how these factors could preferentially damage dopaminergic neurons has remained unclear until now.Making ConnectionsConti and his team were looking for biological pathways that could connect the immune system's inflammatory response to the damage seen in dopaminergic neurons.
After searching human genomics databases, the team's attention was caught by a gene encoding a protein known as interleukin-13 receptor alpha 1 chain (IL-13Ra1), as it is located in the PARK12 locus, which has been linked to Parkinson's.IL-13rα1 is a receptor chain mediating the action of interleukin 13 (IL-13) and interleukin 4 (IL-4), two cytokines investigated for their role as mediators of allergic reactions and for their anti-inflammatory action.With further study, the researchers made the startling discovery that in the mouse brain, IL-13Ra1 is found only on the surface of dopaminergic neurons.
"This was a 'Wow!' moment," said Brad Morrison, then a TSRI postdoctoral fellow and now at University of California, San Diego, who was first author of the paper with Cecilia Marcondes, a neuroimmunologist at TSRI.
Conti agrees: "I thought that these were very interesting coincidences. So we set out to see if we could find any biological significance.
"The scientists did—but not in the way they were expecting.'Something New Going On'The scientists set up long-term experiments using a mouse model in which chronic peripheral inflammation causes both neuroinflammation and loss of dopaminergic neurons similar to that seen in Parkinson's disease.
The team looked at mice having or lacking IL-13Ra1 and then compared the number of dopaminergic neurons in the brain region of interest.The researchers expected that knocking out the IL-13 receptor would increase inflammation and cause neuronal loss to get even worse. Instead, neurons got better."We were very surprised at first," said Conti. "When we stopped to think, we got very excited because we understood that there was something new going on.
"Given that cells fared better without the receptor, the team next explored whether damage occurred when dopaminergic neurons that express IL-13Rα1 were exposed to IL-13 or IL-4. But exposure to IL-13 or IL-4 alone did not induce damage.However, when the scientists exposed the neurons to oxidative compounds, they found that both IL-13 and IL-4 greatly enhanced the cytotoxic effects of oxidative stress.
"This finally helps us understand a basic mechanism of the increased susceptibility and preferential loss of dopaminergic neurons to oxidative stress associated with neuroinflammation," said Marcondes.
The finding also demonstrated that anti-inflammatory cytokines could contribute to neuronal loss. In their article, the authors note they are not suggesting that inflammation is benign but that IL-13 and IL-4 may be harmful to neurons expressing the IL-13Rα1, despite their ability to ultimately reduce inflammation. "One could say that it is not the fall that hurts you, but how you stop," said Conti.More CluesAlong with these results, additional clues suggest that the IL-13 receptor system could be a major player in Parkinson's.
For instance, some studies show Parkinson's as more prevalent in males, and the gene for IL-13Rα1 is located on the X chromosome, where genetic variants are more likely to affect males.And, though not definitive, other studies have suggested that Parkinson's disease might be more common among allergy sufferers.
Since IL-13 plays a role in controlling allergic inflammation, Conti wonders if the IL-13 receptor system might explain this correlation.If further research confirms the IL-13 receptor acts in a similar way in human dopaminergic neurons as in mice, the discovery could pave the way to addressing the underlying cause of Parkinson's disease.
Researchers might, for instance, find that drugs that block IL-13 receptors are useful in preventing loss of dopaminergic cells during neuroinflammation. And, since the IL-13 receptor forms a complex with the IL-4 receptor alpha, this might also be a target of interest. With much exciting research ahead, Conti said, "This is just the beginning."More information: "IL-13Rα1 expression in dopaminergic neurons contributes to their oxidative stress-mediated loss following chronic systemic treatment with LPS," Journal of Immunology.
Journal reference: Journal of Immunology
Provided by Scripps Research Institute
|Posted by Maddalena Frau on October 9, 2012 at 12:45 AM||comments (0)|
Long-term, heavy cannabis use may be associated with structural abnormalities in areas of the brain known as the hippocampus and amygdala, according to a report in the June issue of Archives of General Psychiatry, one of the JAMA/Archives journals.
Conflicting evidence exists regarding the long-term effects of cannabis use, according to background information in the article.
"Although growing literature suggests that long-term cannabis use is associated with a wide range of adverse health consequences, many people in the community, as well as cannabis users themselves, believe that cannabis is relatively harmless and should be legally available," the authors write. "With nearly 15 million Americans using cannabis in a given month, 3.4 million using cannabis daily for 12 months or more and 2.1 million commencing use every year, there is a clear need to conduct robust investigations that elucidate the long-term sequelae of long-term cannabis use."Murat Yücel, Ph.D., M.A.P.S., of ORYGEN
Research Centre and the Melbourne Neuropsychiatry Centre at the University of Melbourne, Australia, and colleagues from the University of Wollongong performed high-resolution structural magnetic resonance imaging on 15 men (average age 39.8 years) who smoked more than five joints daily for more than 10 years.
Their results were then compared with images from 16 individuals (average age 36.4) who were not cannabis users. All participants also took a verbal memory test and were assessed for subthreshold (below the standard of disease diagnosis) symptoms of psychotic disorders, which include schizophrenia and mania.
The hippocampus, thought to regulate emotion and memory, and the amygdala, involved with fear and aggression, tended to be smaller in cannabis users than in controls (volume was reduced by an average of 12 percent in the hippocampus and 7.1 percent in the amygdala).
Cannabis use also was associated with sub-threshold symptoms of psychotic disorders. "Although cannabis users performed significantly worse than controls on verbal learning, this did not correlate with regional brain volumes in either group," the authors write.Source: JAMA and Archives Journals
|Posted by Maddalena Frau on October 9, 2012 at 12:45 AM||comments (0)|
Cannabis users have a greater chance of relapse to cannabis use when they experience certain withdrawal symptoms, according to research published Sep. 26 in the open access journal PLOS ONE led by David Allsop of the National Cannabis Prevention and Information Centre (NCPIC) at the University of New South Wales.
The authors tested a group of dependent cannabis users over a two week period of abstinence for impairment related to their withdrawal symptoms.
Findings were correlated with the probability of relapse to cannabis use during the abstinence period, and the level of use one month later.
They found that in more dependent users, certain withdrawal symptoms, such as physical tension, sleep problems, anxiety, depression, mood swings and loss of appetite, were more strongly associated with relapse than other symptoms, such as hot flashes, fatigue, or night sweats.
Participants with greater dependence before the abstinence attempt reported more severe impairment from the withdrawal. Participants with greater impairment from cannabis withdrawal consumed more cannabis during the month following the abstinence attempt.If these results extend to treatment seeking cannabis users seeking treatment for withdrawal, the research may help improve counseling and treatment strategies for those looking for support.
"Tailoring treatments to target withdrawal symptoms contributing to functional impairment during a quit attempt may improve treatment outcomes" says Allsop.
More information: Allsop DJ, Copeland J, Norberg MM, Fu S, Molnar A, et al. (2012) Quantifying the Clinical Significance of Cannabis Withdrawal. PLOS ONE 7(9): e44864. doi:10.1371/journal.pone.0044864