A running retreat or running school

Imagine a week or a weekend during which you didn’t have to work. Days were spent running, meeting good people, eating, sleeping, and learning. In addition, you find yourself motivated for months afterward. This is the essence of what we do during our Galloway running retreats. Many of our participants tell me that the retreat was their reward for staying with their running program for three months, six months a year.

Others needed motivation improves after a layoff. More than a few times a year, Barbara and I conduct beach weekend retreats at Blue Mountain Beach, FL. Not only is there a beautiful white sand beach, but due to its location, there is a series of state parks and a forest preserve, which means hundreds of miles of beautiful trails that wind through pine forests. More often than not during the middle of July, we conduct a weeklong program in the Lake Tahoe area of California.

During each retreat, there are clinics on building endurance, nutrition, fat-burning, getting faster, motivation, shoes, strength, and more. Individual questions are asked constantly, and problem-solving situations are welcomed. Interacting with others results in new friendships and a lot of fun.

Joy Johnson is one of our long-term friends who inspire us every year. She has won her age group many times in the Boston and New York marathons. But that’s not the main source of inspiration. Last year, while on a hike, Joy slipped and hurt her leg so badly that she didn’t know that she would be able to run again.

When one is over eighty, the healing is much slower, but Joy was determined. One year later, Joy was back at Tahoe, training for the next marathon. She is also a beautiful person with a lot of determination. Each participant can receive an individualized running form evaluation. Suggestions are given for those who have challenges. Several form drills are taught to help improve running mechanics. Running schools are three-hour to five-hour focused sessions that cover the content areas taught at running retreats.

These are held in about twenty locations around the United States each year. During each session, I can cut through the conflicting advice, help design a focused training program, and deal with individual problems. I personally conduct each of these sessions. Sign up now and you’ll be motivated leading up to the retreat/school, with a boost for months afterward.

Age-related dehydration etiology

Age-related dehydration etiology - Reduced fluid intake and increased fluid loss in older adults put them at risk of dehydration. Water deprivation reduces thirst in even healthy older adults. Dehydration is reflected both in low thirst scores during dehydration and in reduced water intake after dehydration. 

It has been shown in several studies that older subjects are unable to return to their baseline plasma osmolality or sodium concentration even when water is freely available. Naloxone, an opiate antagonist, modifies fluid intake in young subjects, but not in older subjects, suggesting that the opioid receptor system in older individuals may be deficient, contributing to hypodypsia. Furthermore, presbynephrosis occurs as the elderly age, which contributes to their weakened ability to defend against dehydration as a result of renal concentrating capacity reduction. 

Aging seems to cause a multifactorial but specific problem with water homeostasis. Aldosterone and plasma renin levels diminish with age, as does the ability to respond appropriately to sodium deprivation by increasing aldosterone and plasma renin levels. However, plasma antidiuretic hormone (ADH) and arginine vasopressin (AVP) levels are higher in older dehydrated individuals compared to young people, indicating that this volume and tonicity defense mechanism does not diminish as we age. 

However, healthy older adults are not different from younger adults when it comes to responding to hypertonicity (induced by intravenous infusion of hypertonic saline). The aging process seems to have more to do with how the body senses volume than how it senses tonicity. The osmolality of plasma and the extracellular fluid volume was altered simultaneously by both dehydration and hypertonic saline infusion until recently, however. 

To address this question, a recent study used head-out water immersion, which increases hydrostatic pressure outside the body and drives blood into the thoracic cavity, thus expanding central blood volume by about 700 ml and leading to increased cardiac filling pressure and heart volume without altering plasma osmolality. The increased central volume seems to activate cardiac stretch receptors, attenuating thirst and drinking; this effect is markedly diminished in healthy older subjects, despite a comparable, or greater, increase in central blood volume and atrial natriuretic peptide. 

This experiment suggests that a centrally mediated response to volume, but not to osmolality, is reduced with aging. The changes listed above seem to be physiologic since they occur in healthy older subjects in the absence of chronic diseases. However, many degenerative age-related diseases worsen the tendency towards dehydration in older persons. 

These include delirium, dementia, diuretic use, swallowing problems, laxative abuse, and problems with hand dexterity or ambulation. In addition, dehydration is a common complication of acute illness in older persons. For example, among Medicare beneficiaries in the USA hospitalized with dehydration, 28% had pneumonia or influenza, 25% had a urinary tract infection and 10% had gastroenteritis.

Nursing Care

If someone in your family needs regular nursing care, their doctor may be able to arrange for a community or district nurse to visit them at home. This will not, of course, be a sleeping-in arrangement but simply involves a qualified nurse calling round when necessary. If you want more concentrated home nursing you will have to go through a private agency. 

Consultus can sometimes supply trained nurses. Additionally, there are many specialist agencies that can arrange hourly, daily or living-in nurses on a temporary or longer-term basis. Terms of employment vary considerably. Some nurses will literally undertake nursing duties only – and nothing else; and may even expect to have their meals provided. Others will do light housework and act as nurse companions. 

Fees vary throughout the country, with London inevitably being most expensive. Private health insurance can sometimes be claimed against part of the cost, but this is generally only in respect of qualified nurses. Your local health centre or social services department should be able to give you names and addresses of local agencies. 

There may come a time when you feel that it is no longer safe to live entirely on your own. One possibility is to engage a companion or housekeeper on a permanent basis but such arrangements are normally very expensive. Permanent help can also sometimes be provided by agencies (such as those listed under ‘Temporary living-in help’), who will supply continuous four-weekly placements. 

This is an expensive option and the lack of continuity can at times be distressing for elderly people, particularly at the change-over point. But it can also lead to a happier atmosphere as the housekeeper comes fresh to the job and neither party has time to start getting on each other’s nerves.

Diagnosis of malignant mesothelioma

A definitive pathological diagnosis of malignant pleural mesothelioma usually requires a tissue (biopsy) specimen to demonstrate that the lesion has a mesothelial phenotype and that it shows neoplastic invasion, as opposed to benign entrapment of mesothelium as part of a fibro-inflammatory process. 

• Evidence of malignant mesothelioma on cytological examination of pleural effusion fluid should be confirmed by tissue biopsy or, if a biopsy is considered inadvisable, impractical, or unnecessary, the cyst diagnosis should be supported by clinical and radiological data as a surrogate for the histological demonstration of invasion. 

• The anatomical location and extent of the pleural tumor should be ascertained by imaging studies. 

• The histological appearances of malignant pleural mesothelioma can vary widely, from epithelioid, to sarcomatoid and biphasic mesotheliomas – together with distinctive subtypes – and such variation occurs not only from one mesothelioma to another but sometimes within single mesothelioma. 

• Recognition of the histological subtype can facilitate diagnosis and provides important prognostic information. 

• Immunohistochemistry is essential for the diagnosis and differential diagnosis of malignant pleural mesothelioma and should include positive and negative (carcinoma-related) markers.

The diagnosis of malignant mesothelioma can be difficult, with symptoms and clinical findings that can mimic and be mimicked by other diseases. Pleural mesothelioma patients may present with dyspnoea, chest pain (pleuritic or non-pleuritic), cough, weight loss, or any combinations of these symptoms. Initial clinical and radiological examination usually reveals a pleural effusion, often massive. 

Rarely, patients are asymptomatic at the time when a radiological abnormality is demonstrated, and patients seldom present with metastatic disease. Some patients with malignant mesothelioma experience a long interval between the first onset of symptoms and subsequent diagnosis, but whether a long interval signifies enhanced or diminished survival following diagnosis is unclear. 

Most patients with malignant pleural mesothelioma have a background of asbestos exposure, and some may have had antecedent symptoms associated with the benign asbestos-related disease – for example, symptoms related to asbestosis or benign asbestos pleuritis with effusion. Others may have radiological evidence of past asbestos exposure, such as pleural plaques. 

In general, biopsy, immunohistochemical analysis, and correlation with radiological and clinical features are needed for the diagnosis of mesothelioma. When immunohistochemical findings are non-diagnostic or discordant, electron microscopy – including electron microscopic examination of tissue retrieved from blocks of paraffin embedded biopsy tissue or cytology cell blocks – can be used, but electron microscopy is not recommended for ‘routine’ diagnosis of mesothelioma. 

Although several cytological and histological findings may raise varying levels of suspicion of malignant pleural mesothelioma a current requirement for the definitive clinicopathological diagnosis of malignant pleural mesothelioma is the demonstration of neoplastic invasion – for example, infiltration into subpleural fat, chest wall skeletal muscle, rib or lung – by histological examination or by imaging studies, and by the clinical exclusion of alternative causes for an atypical mesothelial proliferation. 

A component of malignant mesothelioma in situ can be diagnosed when invasion has been demonstrated in the same or different biopsy or by imaging studies. This applies specifically to epithelioid malignant mesotheliomas. Sarcomatoid malignant mesotheliomas are rarely diagnosable from effusion fluid cytology and are usually identified histologically, by the demonstration of invasion or overtly sarcomatoid areas.

What are Cyanogenic Glycosides?

Cyanogenic glycosides are chemical compounds that occur naturally in many plants, including species of Prunus (wild cherry), Sambucus (elderberry), Manihot (cassava), and Linum (flax), Bambusa (bamboo), and Sorghum (sorghum). Chemically, they are defined as glycosides of the a-hydroxynitriles. 

These compounds are potentially toxic as they are readily broken down by enzymic hydrolysis to liberate hydrogen cyanide when the plant suffers physical damage. Occurrence in Foods There are approximately 25 known cyanogenic glycosides, and a number of these can be found in the edible parts of some important food plants. 

These include amygdalin (almonds), dhurrin (sorghum), lotaustralin (cassava), linamarin (cassava, lima beans), prunasin (stone fruit), and taxiphyllin (bamboo shoots). Some of the main food sources of cyanogenic glycosides and their estimated potential yield of hydrogen cyanide are released on hydrolysis. Bitter apricot kernels have been marketed as a health food in the UK and elsewhere. They can contain high levels of the cyanogenic glycoside amygdalin.

Effects on Health

The toxicity of a cyanogenic plant depends largely on the amount of hydrogen cyanide that could be released on consumption of the plant. Adequate processing or preparation is required to ensure that detoxification of the food is complete before consumption. However, if the processing or preparation is insufficient to ensure detoxification, the potential hydrogen cyanide concentration released during consumption can be high. 

Upon consumption of the food, the enzyme b-glycosidase will be released and hydrolysis of the cyanogenic glycoside will commence, resulting in hydrogen cyanide formation. Certain gut microflora also produces b-glycosidases, which can contribute to the breakdown of cyanogenic glycosides into hydrogen cyanide. Hydrogen cyanide is cytotoxic and blocks the activity of cytochrome oxidase – an enzyme critical for cellular respiration. 

When cytochrome oxidase is blocked, ATP production stops, and cellular organelles cease to function. However, cyanide is readily detoxified in animals as all animal tissues contain the enzyme rhodanese – a thiosulfate sulfurtransferase enzyme that converts cyanide to thiocyanate, which is then excreted in the urine. Acute poisoning only occurs when this detoxification mechanism is overwhelmed. 

The symptoms of acute cyanide poisoning include rapid breathing, drop in blood pressure, raised pulse rate, dizziness, headache, stomach pains, vomiting, diarrhea, confusion, twitching, and convulsions. In extreme cases, death may occur. The minimum lethal dose of hydrogen cyanide taken orally is approximately 0.5–3.5 mg/kg body weight or 35–245mg for a person weighing 75 kg. The chronic effects of cyanide consumption are associated with regular long-term consumption of foods containing cyanogenic glycosides in individuals with poor nutrition. 

These effects are most notable in the tropics, where cassava, and to a lesser extent, sorghum, bamboo shoots, and lima beans are staple components of human diets. 

Malnutrition, growth retardation, diabetes, congenital malformations, neurological disorders, and myelopathy are all associated with cassava-eating populations subject to chronic cyanide intake. There are a number of documented cases of poisoning caused by the consumption of apricot kernels. One report concerned a 41-year-old female found comatose after eating approximately 30 bitter apricot kernels, who eventually recovered after treatment. 

There are also case reports of children being poisoned after consumption of wild apricot kernels and where the kernels were made into sweets without proper processing. The UK Committee on Toxicity recommended in March 2006 that a tolerable daily intake (TDI) of 20 mg cyanide/kg BW/day be applied, which is the equivalent of 1–2 bitter apricot kernels per day. There are over 2500 known species of plants that produce cyanogenic glycosides, usually in combination with a corresponding hydrolytic enzyme – a beta-glycosidase. 

When the cell structure of the plant is disrupted in some way, for example by predation, the beta-glycosidase is brought into contact with its substrate – the cyanogenic glycoside. This leads to the breakdown of the glycoside into sugar and a cyanohydrin, which rapidly decomposes to release hydrogen cyanide. The purpose of the reaction is to protect the plant from predation. Stability in Foods Cyanogenic glycosides break down when the cells of the plant are damaged, for example during preparation and processing, and release hydrogen cyanide. Hydrogen cyanide itself is not heated and stable and does not survive boiling and cooking processes. 

It can also be eliminated by fermentation. Processing Adequate processing of cyanogenic glycoside-containing plants should be sufficient to significantly reduce or remove the toxic agents prior to consumption. Processing procedures, such as peeling and slicing disrupt the cell structure of the plant so that b-glycosidases are released and the cyanogenic glycosides are hydrolyzed. 

Hydrogen cyanide is thus released and can be removed by cooking processes such as baking, boiling, or roasting. Fermentation is also used to remove hydrogen cyanide. These methods are particularly suitable for products such as cassava and bamboo shoots. There are two main types of cassava – bitter cassava and sweet cassava. The sweet variety contains a significantly lower concentration of cyanogenic glycosides than the bitter variety, and it is the sweet variety that is used commercially. 

Cassava is consumed largely as cassava flour, cassava chips, and tapioca pearls, all of which are processed products with a long history of safe consumption. Treatments for removing cyanogenic compounds from flaxseed include boiling in water, dry and wet autoclaving, and acid treatment followed by autoclaving. Solvent extraction has also been used to remove cyanogenic glycosides from flaxseed and oil. 

Legislation 

A safe level of cyanide in cassava flour for human consumption has been set by the WHO at 10 ppm. Low levels of cyanide are also present in almonds, sweet apricot kernels and in the stones of other fruit such as cherries, as well as in bitter apricot kernels. In the UK, the maximum level of cyanide that can be present as a result of using such materials as flavourings is regulated under the terms of the Flavourings in Food Regulations 1992 (as amended).

Mesothelial progenitor and side population cells

Proliferative tissues such as skin and bone marrow are maintained by a stable population of progenitor cells with self-renewing properties. Tumors are also proliferative tissues, possibly maintained by a self-renewing cancer stem cell population. Therefore leukemia can be viewed as a tumor maintained by a subset of bone marrow progenitor cells that have tumor-initiating properties. Analogously, mesothelioma may be a tumor maintained by a mesothelial progenitor cell population. Normal mesothelium consists of a single layer of simple squamous mesothelial cells of mesodermal origin that function to maintain serosal fluid production in order to provide a frictionless and protective surface for organ movement. 

Mesothelial cells also participate in material transport across the serosal membrane; and mediate regulatory inflammatory, immune, and tissue repair responses (Mutsaers, 2007). There is evidence for a mesothelial progenitor cell population (Herrick, 2004). First, mesothelial cells express characteristics of mesodermal, epithelial and mesenchymal phenotypes- supportive evidence for multipotential differentiation of a progenitor cell population. In addition, mesothelial cells exhibit plasticity by transforming into tissues such as myofibroblasts and vascular grafts under specific growth conditions (Lv, 2011 & Sparks, 2002). 

After mesothelial tissue injury, new mesothelium regenerates from both cells at the wound edge and from the surrounding serosal fluid, which may be mesothelial progenitor cells capable of tissue regeneration. Mesothelial progenitor cells with such stem cell-like properties are potentially a source of a cancer stem cell population in mesothelioma. Another potential cancer stem cell population in mesothelioma is side population (SP) cells. Defined as cells that efflux the DNA-binding dye Hoechst 33342, SP cells can be enriched for using flow cytometry. Side population cells express ATP-binding cassette (ABC) membrane transporters that efflux the Hoechst 33342 dye, and these transporters are also involved in efflux of drugs such as chemotherapeutic. 

Side population cells are found in both normal and malignant tissues. In cancer, SP cells have been considered a potential cancer stem cell population as well as a cell population responsible for resistance to therapy. SP cells have been identified as a potential cancer stem cell population in various tumors, including ovarian carcinoma and osteosarcoma (Fong, 2010 & Murase, 2009). A group that isolated SP cells from human malignant mesothelioma cell lines illustrated that SP cells had enhanced proliferation and higher expression of stem-cell genes (Kiyonori, 2010). However, the SP cells did not have increased tumorigenic potential in immunodeficiant mice. 

A more recent study reported that SP cells isolated from malignant pleural mesothelioma not only expressed stem cell markers, but also showed self-renewal, chemoresistance, and tumorigenicity (Frei, 2011). Further the subset of SP cells characterized as WT1 negative/D2- 40 positive/CD105 (low) were found to be even more tumorigenic. The increased stem cellness of the SP cells isolated from this study by Frei et al. compared to the study by Kiyonori et al. could be due to their isolation from malignant tissue rather than from mesothelioma cell lines. 

Since cancer stem cells remain to be fully characterized and defined, a diversity of cell types- including progenitor cells and side population cells- may qualify as cancer stem cells in tumors (Bjerkvig, 2005). How a normal mesothelial progenitor cell or side population cell transforms into a cancer stem cell remains to be elucidated. 

Traditional thinking of transformation of a normal differentiated cell into a tumor cell requires multiple hits to the genome resulting in genetic instability and a selective survival advantage. Cancer stem cells may be products of a similar transformative process. Human mesothelial cells exposed to asbestos and SV40 virus were reported to transform via an Akt-mediated cell survival mechanism (Cacciotti, 2005). These authors concluded that mesothelioma originates from a subpopulation of transformed stem cells. 

More work illustrating this important concept is necessary and offers potential targets for therapy to abrogate this transformation process. Hypothetically, the advantage for a tumor to arise from a transformed stem cell rather than from a transformed differentiated cell includes the ability for the tumor to have multiple phenotypes for growth in different microenvironments; an additional mechanism for a metastatic phenotype; and resistance to current therapies. Interestingly, mesothelioma exhibits aspects of all three of these tumor characteristics. Diffuse malignant mesothelioma can be classified histologically into three major classes: epithelioid, sarcomatoid, and mixed-type. Epithelioid is the most common phenotype and the mixed-type can be found in 30% of tumors. 

Sarcomatoid tumors are rare but carry the worst prognosis. There are also rare variants including desmoplastic, undifferentiated and deciduoid types. This wide variety of phenotypes could be explained by a cancer stem cell origin for mesothelioma, such as a transformed mesothelial progenitor cell population that has been shown to differentiate into multiple cell types. Currently, determining the histological subtype is important for diagnosis, prognosis and treatment (Tischoff, 2011). 

If, however, all the histological subtypes are derived from a single stem cell population, earlier diagnosis could be determined before histological differentiation occurs; prognosis could be improved overall; and treatment could be focused on targeting these stem cells. Mesothelioma is an aggressive tumor that often metastasizes. In tumor biology epithelialmesenchymal transition (EMT) is associated with increased tumor invasiveness and metastasis. This transition is reminiscent of the epithelioid versus sarcomatoid type of mesothelioma, and therefore has important implications in the metastastic feature of this tumor. 

EMT is a transdifferentiation program used in normal embryonic development. Activation of this program in carcinogenesis would confer a metastatic phenotype to the tumor cells. Not only can EMT increase cell invasiveness and migration, but it also contributes to additional properties that promote tumor cell survival; such as resistance to apoptosis and senescence, and increased immunosuppression (Thiery, 2009). 

In addition, EMT has been shown to induce stem cell-like properties. Many cancer stem cell traits are consistent with a metastatic phenotype- self-renewal, ability to initiate tumors in a new environment, motility, invasiveness, and resistance to apoptosis (Chaffer, 2011). Evidence of EMT occurring in mesothelioma includes expression of proteins involved in the EMT axis in malignant pleural mesothelioma tissue samples from untreated patients, and expression of the periostin protein in particular by sarcomatoid tumors, which in turn correlated with shorter survival in these patients (Schramm, 2010). 

Successful colonization of metastatic cells to the distant tissues requires activation of genetic and epigenetic programming for survival in the new tissue environment. This area of research is relatively new, but it is believed that the self-renewal property of stem cells offers one explanation for homing success. Once in the new microenvironment, metastatic cells need to successfully utilize the local growth factors and cytokines to gain mitogenic potential and the ability to self-renew. Subsequently the metastatic cells would need to recruit the stroma to aid in cell survival, such as inducing a blood supply (Chambers, 2002). 

Distant metastatic lesions of mesothelioma, amongst other tumors both epithelial and nonepithelial, have been reported to highly express the self-renewal gene Bmi-1, suggesting that a state of self-renewal is linked to metastatic potential (Glinsky, 2005). Whether the metastatic cells in mesothelioma represent a cancer stem cell population derived from the primary tumor, or mesothelioma cells that acquired stem cell-like properties such as selfrenewal en route to and after homing to the distant metastatic site, remains to be studied. However these finding support a role for stem cells in the pathogenesis of mesothelioma. 

Epigenetic mechanisms that do not change the DNA sequence but that do alter gene expression at the mRNA and protein levels are exciting new potential targets for therapy. A number of epigenetic mechanisms have been described in tumors, including microRNA (miRNA) regulation of mRNA expression, histone acetylation/deacetylation, and gene promoter methylation/demethylation. By suppressing expression of tumor suppressor genes or increasing expression of oncogenes, these epigenetic proteins regulate tumorigenesis at an additional level of complexity. 

A study identifying a panel of miRNAs downregulated in malignant pleural mesothelioma tissue samples found redundant miRNA regulators of Wnt signaling, an important pathway in stem cell self renewal (Gee, 2010). Wnt signaling in mesothelioma suggests a cell population with stemness properties, and whose expression appears to be regulated at an epigenetic level. The existence of a cancer stem cell population in mesothelioma is supported by evidence of cells with stem cell-like properties in normal mesothelium, primary mesothelial tumors, and metastatic lesions. 

A definitive cancer stem cell population capable of re-initiating mesotheliomal tumors remains to be identified. If such a cancer stem cell population is discovered, the prospects of earlier diagnosis and novel therapy for malignant mesothelioma would be of utmost importance for further research. 

RT, PDT, and Surgical Cytoreduction

Definitive approaches to managing patients with MPM typically involve combinations of multiple standard treatment modalities and must address both widespread local disease and the high risk of systemic disease. This is made more challenging because the potential morbidity of highly aggressive local treatment strategies can limit the implementation of aggressive systemic treatment strategies and vice versa. Nevertheless, in patients with good performance status and few comorbidities, therapy with definitive intention (and higher RT doses) can lead to significantly higher median survivals than have been reported with palliative therapies. 

In this context, it is important to note that no single modality, including surgery, is highly effective in the treatment of MPM and that the strategy in any surgery-based multimodal treatment plan is to use surgery to achieve a macroscopic complete resection and to then employ other modalities in an attempt to control the inevitably present residual microscopic disease. RT has been used definitively in the absence of surgical resection in selected patients to treat bulky areas of disease or even all glycolytically active (FDG-avid) disease (Feigen et al. 2011), but current RT techniques are not sufficient to allow high dose RT to all pleural surfaces without unacceptable toxicity. Accordingly, definitive radiotherapy is frequently associated with surgical therapy, and this section will discuss the role of PDT and RT in the surgically based multimodality therapy of patients with MPM.

In the overwhelming majority of MPM patients, even the most aggressive surgical resection results in high rates of local relapse. For this reason, both RT and PDT have been used to treat microscopic residual disease following surgery that was performed with the goal of achieving a macroscopically complete resection (MCR). One strategy for MCR involves an extrapleural pneumonectomy (EPP), in which the parietal pleura, diaphragm, pericardium, and lung are resected en bloc. The other commonly used strategy is the lung-sparing pleurectomy/decortication (P/D), which when performed with the intent of achieving an MCR is often referred to as an extended P/D (eP/D) or radical pleurectomy. As there is no surgical procedure accepted as the standard of care for pleural malignancies, there is certainly no procedure acknowledged as the standard cytoreductive operation, and both EPP and eP/D are performed at high-volume MPM surgical centers (see chapter Surgery Approaches in Mesothelioma of this volume by Wolf and Flores).

Types of Chiropractors:

 There are many types of chiropractors:

• Chiropractors who focus on primary care and wellness

• Chiropractic neurologists who work with the nervous system

• Chiropractic orthopedic physicians who work with the bones and joints

• Chiropractics who practice physical therapy and rehabilitation

• Chiropractices who specialize in sports medicine

• Chiropractists who focus on pediatric care

• Chiropractic nurses

• Chiropracticians who work in hospitals

• Chiropractorst who work in schools

• Chiropracting doctors who work with seniors

• Chiropractologists who work in geriatric clinics

• Chiropractic surgeons who perform spinal surgeries

• Chiropracters who work with cancer patients

• Chiropractical physiotherapists who work with people recovering from injuries

• Chiropractically trained massage therapists

• Chiropractic dentists

• Chiropractical psychologists

• Chiropracticular nutritionists

• Chiropractorst who work with pregnant women

• Chiropracterst who work with infants

• Chiropracteres who work with children

• Chiropractisrts who work with adolescents

• Chiropractistst who work with adults

• Chiropractoars who work with senior citizens

• Chiropractorsts who work with athletes

• Chiropractors who work with animals

• Chiropractorst who work with babies

• Chiropractortst who work with cancer patients and survivors

• Chiropractosts who work with children with special needs

• Chiropractors who treat back pain

• Chiropractorst who treat headaches

• Chiropractoryst who treat neck pain

• Chiropractorst who treat shoulder pain

• Chiroproctologistst who treat digestive disorders

• Chiropractorst who treat ear infections

• Chiropractorgastroenterologistst who treat gastrointestinal problems

• Chiropractormedical technitians who work with x-rays

• Chiropractornursing technitians who work in hospital settings

• Chiropractorst who work with pregnant women and newborns

• Chiropractoresearch scientists who work to find new ways to help people

• Chiropractorcure practitioners who use hands-on techniques

• Chiropractorcure teachers who teach others how to do it

• Chiropractorst who work with the elderly

• Chiropractotrist who works with people with developmental disabilities

• Chiropractors who practice acupuncture

• Chiropractorst who work with autism

• Chiropractorkinesiology (chiropractic)

• Chiropractordentistry

• Chiropractosurgery

• Chiropractors who have a background in osteopathy

• Chiropractorst who work with cancer

• Chiropractorest who work with diabetes

• Chiropractores who work with eating disorders

• Chiropractorst who work with fibromyalgia

• Chiropractorst who work with heart disease

• Chiropractorset who work with HIV/AIDS

• Chiropractoret who work with kidney stones

• Chiropractories who work with migraines

• Chiropractorst who work with multiple sclerosis

• Chiropractiorst who work with Parkinson’s Disease

• Chiropractioarst who work with rheumatoid arthritis

• Chiropractiors who work with stroke victims

• Chiropractorst who work with thyroid conditions

• Chiropractics who work with urinary tract infections

• Chiropractorst who work with weight loss

• Chiropracts who work with women's health issues

• Chiropractorst who work with whiplash injuries

• Chiropractorst who work with workers' compensation claims

• Chiropractorse who work with yoga

• Chiropractorshipst who work with sports medicine

• Chiropractorst who work with spinal cord injury

• Chiropractorth who work with sleep apnea

• Chiropractords who work with temporomandibular joint disorder

• Chiropracters who work with TMJ

• Chiropractorst who work with total body wellness

• Chiropractorts who work with vaccines

• Chiropractists who work with vitamin supplements

• Chiropracticst who work with vision care

Benefits of Heat therapy

Heat therapy has become very popular over the years. Many people claim that heat therapy helps them relax and relieve stress. Is it really true?

Heat therapy is a form of treatment where hot water or steam is applied to the body. The idea behind heat therapy is to increase blood flow to the skin and stimulate the release of endorphins. This leads to relaxation and pain relief.

There are several benefits of heat therapy. It can be used to treat muscle soreness, arthritis, and other conditions. In addition, heat therapy can also be used to reduce inflammation and promote healing.

What Are the Different Types of Heat Therapy?. There are different types of heat therapy. They include:

1) Steam Baths

A steam bath is a great way to relax after a long day or week. It's also a good way to get rid of some stress and tension. In addition, steam baths help improve circulation and increase blood flow. They're also a great way to detoxify your body.

2) Hot Water Massage

Hot water massage is another type of heat therapy. It involves applying warm water directly on the muscles. You can use a shower head for this purpose. However, you can also use a tub filled with hot water.

3) Warm Saunas

Warm saunas are one of the most relaxing forms of heat therapy. They involve sitting in a heated room filled with smoke. The smoke contains aromatic oils which make you feel relaxed.

4) Deep Tissue Massages

Deep tissue massages are done by trained therapists who knead your muscles using their hands. These massages are meant to loosen up tight muscles and knots. They're also effective at relieving chronic pain.

5) Infrared Sauna

Infrared sauna uses infrared rays instead of heat. It delivers an even heating effect throughout the entire body. This makes it more effective than regular saunas.

6) Dry Needling

Please write an article about dry needling. This is a treatment for muscle pain or injury. It involves inserting fine needles into the skin to stimulate the release of endorphins and other chemicals that reduce pain.

7) Electrotherapy

Electrotherapy is the use of electricity to treat medical conditions. It includes a wide range of treatments such as electro-acupuncture, transcutaneous electrical nerve stimulation (TENS), and low-frequency ultrasound.

Here are a number of benefits of heat therapy. 

- It Can Improve Your Immune System

- It Can Reduce Stress Levels

- It Can Make You Feel Happier

- It Can Help With Depression

- It Can Help with Anxiety

- It Can Help Prevent Cancer

- It Can Help Treat Diabetes

- It Can Help to Heal Wounds

- It Can Help To Boost Energy Levels

- It Can Help Get Rid Of Acne

- It Can Help Fight Off Infections

- It Can Help Keep You Healthy

- It Can Help Increase Blood Circulation

- It Can Help Lower Cholesterol

- It Can Help Reduce The Risk Of Heart Disease

- It Can Help Slow Down Aging Process

- It Can Help Strengthen Bones

- It Can Help To Maintain A Healthy Body

- It Can Help In Regulating Body Temperature

- It Can Help in Healing Burns, Scars, And Skin Ulcers

- It Can Help Stop Hair Loss

- It Can Help Repair Damaged

 

 

 

 

 

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Enlarge Hair Pores on Breast

 Enlarged hair follicles on breasts are a common condition that affects many. In this blog post, we will discuss what causes enlarged hair follicles on breasts and how to treat them. We will also provide some tips for preventing them from occurring in the first place.

There are many reasons why someone can develop enlarged hair follicles. Some people have them naturally, while others may experience them due to aging or hormonal changes. It could also be caused by an underlying medical problem such as diabetes mellitus type II (DMII) if left untreated over time without treatment these problems will lead to complications such as gangrene and amputation of limbs that require immediate attention from a doctor. 

The most common cause is genetics; this issue runs in families so it’s important for parents who have the condition themselves not to pass along those genes onto their children through a marriage where there might already exist another family member with this condition at some point during their lives. Another common cause is hormonal changes; this happens during puberty when estrogen levels rise and testosterone decreases in both sexes which leads to increased production of sebum from the skin’s oil glands leading to large amounts of hair growing around our bodies.

There are many ways that people can treat their enlarged hair follicles on breasts, and it all depends on what caused them in the first place. For example, if genetics were responsible then there isn’t much to be done except accept yourself or perhaps consider plastic surgery later down life if things get too uncomfortable; however, if hormones were involved due hormone therapy may lessen these effects over time as estrogen levels decline. 

If it’s an underlying medical problem such as DMII, then the treatment for that will need to be addressed in order to stop the hair follicles from enlarging. In general, some ways to treat enlarged hair follicles include: using topical treatments like creams or ointments; using prescription medications such as minoxidil (Rogaine) or finasteride (Propecia); undergoing laser therapy; and/or having surgery.

TORTICOLLIS - WHO WILL BENEFIT FROM SURGERY

Congenital muscular torticollis (CMT) is an idiopathic postural deformity evident shortly after birth, typically characterized by lateral flexion of the head to one side and cervical rotation to the opposite side due to unilateral shortening of the sternocleidomastoid muscle. CMT may be accompanied by other neurological or musculoskeletal conditions. Key Points: Infants with CMT are frequently referred to physical therapists (PTs) to treat their asymmetries. 

This evidence-based clinical practice guideline (CPG) provides guidance on which infants should be monitored, treated, and/or referred, and when and what PTs should treat. Based upon critical appraisal of literature and expert opinion, 16 action statements for screening, examination, intervention, and follow-up are linked with explicit levels of evidence. 

The CPG addresses referral, screening, examination and evaluation, prognosis, first-choice, and supplemental interventions, consultation, discharge, follow-up, suggestions for implementation and compliance audits, flow sheets for referral paths and classification of CMT severity, and research recommendations. All surgical procedures carry the risk of producing excessive weakness or paralysis, causing infection or internal bleeding, complications of anesthesia, or simply not being effective. 

In light of these considerations, how are candidates for surgery selected from among ST patients? Simply put, all nonsurgical treatments are attempted first. Surgery is never considered as a first-line or early treatment, even in fairly severe cases of dystonia, because some cases may resolve spontaneously, given time. Additionally, the specific muscles involved at the beginning may change over time. Some muscles may stop contracting and new ones may become involved. 

The proper muscles to target may not become obvious until the disorder stabilizes. Chemodenervation with botulinum toxin remains the mainstay of treatment for ST, supplemented by oral medications and pain management. As discussed previously, some patients may develop resistance to botulinum toxin after years of repeated injections. Those patients for whom chemodenervation is no longer effective may be considered for surgery. 

Among those patients, surgery works best for those with rotational torticollis, and less well for those who predominantly have retrocollis or anterocollis. Other factors may influence a patient’s suitability for surgery. The coexistence of medical conditions such as heart disease, diabetes, lung or breathing problems, or blood clotting abnormalities will add to the risk of adverse outcomes from surgery. 

Selective peripheral denervation is becoming the procedure of choice for those patients who are appropriate candidates for surgery. Note that, as opposed to surgical denervation, the injection of phenol or botulinum toxin achieves chemical denervation. Chemodenervation is not permanent, but destructive surgery is. Also, surgery of any kind rarely completely cures ST. 

Peripheral surgeries on the nerves and muscles do not alter the abnormality in the extrapyramidal system of the brain. The brain may recruit adjacent muscles, usually smaller and often not previously involved in the ST, into activity in order to bring the head back to its abnormal set point. Patients who undergo surgery do not usually become free from the need for continued treatment. Many of them must continue receiving botulinum toxin injections and/or medications. All of the factors discussed above must be considered together in selecting any one patient for surgery.

If available, physical therapy by an experienced therapist may improve pain symptoms. The goals of physical therapy include bringing the head position back toward normal, increasing the range of motion, and decreasing pain, thereby increasing functional ability. The physical therapist may employ a variety of techniques to achieve these goals. 

Primarily, he will gently move the neck through its range of motion, stretching the spasming agonist muscles. He may take advantage of the effect of geste antagoniste, stimulating the skin by gentle stroking or by applying ice to decrease the contraction of agonists during neck maneuvers. For some patients, gentle neck traction using a mechanical device may alleviate pain. Physical therapy techniques such as ultrasound or diathermy also may help with the pain.

While it is used extensively by some of our patients and is a fairly effective treatment for tension cervicalgia, local massage tends to have mixed results in ST. While it almost always feels good while being performed, pain control is very short-lived. In some patients, massage, especially deep massage, aggravates the spasms and contractions of agonist muscles. As a result, pain may actually increase the following a massage. 

However, we have found that an acupressure type treatment, in which the point of an elbow is applied to a spasming trapezius muscle, or to muscles in the back of the neck, is often beneficial. Pressure should not be applied to the sternocleidomastoid muscle, which runs along the front and side of the neck, since doing so is ineffective and may even cause injury. Overall, we have found that properly applied acupressure is a most economical and effective pain relief measure with very low risk or side effects, and it may be performed at home by a spouse or family member.

Lack of Sleep

Getting Them to SLEEP! “LACK OF SLEEP” is probably every nonparent’s biggest fear. Certainly, your sleep schedule requires the biggest adjustment during the first few months of parenthood. Those first few weeks? It is what it is. Your baby needs to eat every few hours (maybe even every 90 minutes), and if you’re breastfeeding, that’s going to be your new around-the-clock alarm clock. 

With Honor, I was just about at my breaking point (especially because I couldn’t drink coffee while nursing), when my girlfriend Kelly Sawyer said the magic word: “Schedule!” She had successfully transitioned both of her kids to a consistent 7:00 p.m. to 7:00 a.m. sleep schedule. It totally changed her life and then mine. Caveat: This is a (kinder, gentler) form of sleep training, and that’s not for everyone. 

Definitely discuss this strategy with your partner and your pediatrician many experts have written about this subject and there is a wide variety of opinion. I’m simply sharing what worked for us in the hopes that it can help you and your little ones get a better night’s sleep. That being said, here’s what Kelly’s Genius Sleep Schedule looks like you can start it with a child as young as a few months old, then phase out the daytime naps when your baby stops needing to sleep as much. “It may take your baby a week or so to get used to the new routine, so be patient,” Kelly warns. “The key is to wake them up at the end of each naptime right on schedule as hard as that seems! 

If they sleep too much during the day, they won’t sleep at night. It’s that simple.” Kelly says she implemented the schedule at four months with her first daughter, and “as soon as humanly possible” with number two. With Honor, we were able to get her on this schedule by about three months. By four weeks old, she was big enough to sleep for 6 hours at a stretch, and at that point, we started letting her be awake and fussing a bit before we’d go in to get her gradually, we were able to stretch this from 6 to 8 to 10 to 12 hours. 

Amazing! With Haven, it took a little longer maybe four or five months before she had the full 12 hours down. But we got there, and I added my own twist to Kelly’s schedule: a midnight feeding (right before I went to bed) that would help her sleep through until 7:00 or 8:00 a.m. (The key was to make sure it was at least 4 hours since her last feeding of the day, so it didn’t make her sick and to keep it very low key; lights off, no talking, just feed, change, back to bed.) 

Gradually, since she was sleeping less during the day, Haven started eating more and wanted to go for longer and longer stretches of sleep at night. Of course, we aren’t militant about this. Some nights, it’s closer to 7:30, and when we travel, all bets are off. But we do our best to be as consistent as possible, and it really does work most of the time. You might feel selfish at first, trying to get your baby on a schedule that lets you have 12 uninterrupted hours to yourself every night don’t. 

That big chunk of “you time” is actually just a side benefit. Babies and little kids crave routine and stability plus all of the health benefits that come with eating at regular intervals and getting a good night’s sleep. Babies learn self-soothing more quickly this way, which I think translates to having more confidence and self-reliance as they grow. 

Both of my girls are pretty independent, and I think a lot of that has to do with our strategy of letting them figure themselves out as much as possible. Plus, a happier, less-sleep-deprived mommy means happier kids, too! I had almost no baby blues with either of my kids, and I think the schedule was a big part of it; it helped me wrap my head around a day and a night. This is not to knock co-sleeping or less scheduled parenting whatsoever again, this is all about figuring out the best approach for you and your baby.

Diabetes and Oxidative Stress

Most researchers are in basic agreement that the theory of oxidative stress is central to explaining the cause of diabetes. To understand the theory, one must first conceptualize that a "free radical" is any atom or molecule which has an "unpaired electron" in its outer ring. Because it is lacking an electron, it is unstable and very much wants to find one electron to fill its need. 

This "free radical" will steal an electron from any other molecule it encounters that is more willing to give one up and thus it becomes satisfied. but now the victim molecule has become a free radical itself and so it now will look for another victim molecule to steal its much-desired electron from thus propagating this cycle over and over again. 

This cycle is called "the chain reaction of free radicals". The chief danger of free radicals comes from the damage they can do when they react with important cellular components such as DNA, or the cell membrane. Cells may function To prevent free radical damage the body has a defense system of antioxidants. Antioxidants are molecules that can safely interact with free radicals and terminate the chain reaction before vital molecules are damaged. 

Although there are several enzyme systems within the body that scavenge free radicals, the principle antioxidants are glutathione, SOD (superoxide dismutase), beta carotene, vitamin E, vitamin C, CoQ10, melatonin, and alpha-lipoic acid. According to the theory of oxidative stress, free radicals run rampant through the body wreaking havoc. 

In the case of type 1 diabetes damaging beta cells in the pancreas, negatively impacting their ability to produce insulin in the case of type 2 diabetes damaging cell membranes, leading to a breakdown in intercellular signaling. And if that were not bad enough free radicals deplete our body's reserve of antioxidants further contributing to the problem. 

This is why it is so important to lower oxidative stress with a better diet, more exercise, an improved lifestyle; and to take all the antioxidant supplements known to neutralize the excess free radicals. There is still a lot to learn about the causes of diabetes, but what is known, is that our bodies may begin to malfunction five to seven years before we are ever diagnosed with diabetes. 

That is why researchers believe that nearly 30-50% of the people who have diabetes don't even know it. It is vital for the person with diabetes to measure his blood sugar and get to KNOW not to GUESS about his body. he needs to know how stress affects him, how carbs affect him, and how everything affects his blood sugar. Knowledge is power. Sometimes we find that just certain foods, just certain stresses just certain times of the month make the diabetes work.