Chronic Back Pain: When There�s No Cure
Chronic Back Pain: Living with chronic pain can be exhausting and frustrating. But you can limit the severity of your pain�and the effect it has on you�with the following 3 strategies:
1. Become An Expert At Chronic Back Pain Management
No one pain management technique works for everyone; it helps to be open to trying all sorts of methods and techniques to diminish and manage your pain.
Keeping your pain at the lowest level possible will help keep you active, which in turn will minimize your chronic pain and keep it from getting worse. It will also help decrease the stress that is often associated with chronic pain. Common pain management techniques include:
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- Cold / heat therapy
- Over-the-counter or prescription pain medications
- A healthy exercise regimenAside from those above, which can be done on your own, some people find alternative treatments quite helpful, such as chiropractic care, acupuncture, or massage therapy.With patience, find what combination of treatments works best for you.
2. Find A Support Network
Chronic back pain can be an isolating experience. You may not be able to be as active as you once were, saying �No� to social gatherings, and limiting participation in some of your favorite activities.
As you become more isolated, your experience of chronic pain may increase because of less stimuli to distract you. You also increase the risk for developing mental health issues, such as depression.
It is encouraged you find a network of social support to limit the isolation effects of chronic pain. The key to a support network is not only finding people who are empathetic and supportive, but also finding a health distraction from the pain.
3. Practice Imagery Control Techniques
When treating your chronic back pain, it is important to remember the role your mind can play in reducing your perception of chronic pain.
In particular, imagery control techniques can bring you meaningful relief in a matter of minutes. You can start by trying �the altered focus technique.� Here is how to do it:
- Focus your attention on a part of your body other than your lower back.
- Next, alter the sensation in that part of your body. For example, you can imagine your hands becoming cold or warm (whichever feels better).
- Hold this sensation in your hands for several minutes, and your experience of pain will likely diminish.You can practice these techniques wherever, and however often, you want.If the above three strategies don�t help reduce your chronic pain, don�t despair. Instead, ask your doctor for a referral to a pain specialist to discuss other possible options for chronic back pain relief. There are a great many approaches to pain management.
Talk to Dr. Jimenez about specific questions related to your unique health situation.
915-412-6677
Learn More:http://www.spine-health.com/doctor/chiropractor/alex-jimenez-el-paso-tx
Chronic undernutrition is characterized by a progressive reduction of the�fat-free mass (FFM) and fat mass (FM)�and �which has deleterious consequences on health. Undernutrition is insufficiently screened and treated in hospitalized or at-risk patients despite its high prevalence and negative impact on mortality, morbidity, length of stay (LOS), quality of life, and costs [1�4]. The risk of underestimating hospital undernutrition is likely to worsen in the next decades because of the increasing prevalence of overweight, obesity, and chronic diseases and the increased number of elderly subjects. These clinical conditions are associated with FFM loss (sarcopenia). Therefore, an increased number of patients with FFM loss and sarcopenic obesity will be seen in the future.
Academic societies encourage systematic screening of undernutrition at hospital admission and during the hospital stay [14]. The detection of undernutrition is generally based on measurements of weight and height, calculations of BMI, and the percentage of weight loss. Nevertheless, screening of undernutrition is infrequent in hospitalized or nutritionally at-risk ambulatory patients. For example, in France, surveys performed by the French Health Authority [15] indicate that: (i) weight alone, (ii) weight with BMI or percentage of weight loss, and (iii) weight, BMI,�and percentage of weight loss are reported in only 55, 30, and 8% of the hospitalized patients� records, respectively. Several issues, which could be improved by specific educational programs, explain the lack of implementation of nutritional screening in hospitals (table 1). In addition, the accuracy of the clinical screening of undernutrition could be limited at hospital admission. Indeed, patients with undernutrition may have the same BMI as sex- and age- matched healthy controls but a significantly decreased FFM hidden by an expansion of the FM and the total body water which can be measured by bioelectrical impedance analysis (BIA) [13]. This example illustrates that body composition evaluation allows a more accurate identification of FFM loss than body weight loss or BMI decrease. The lack of sensitivity and specificity of weight, BMI, and percentage of weight loss argue for the need for other methods to evaluate the nutritional status.
In 2008, twelve and thirty percent of the worldwide adult population was obese or overweight; this is two times higher than in 1980 [16]. The prevalence of overweight and obesity is also increasing in hospitalized patients. A 10-year comparative survey performed in a European hospital showed an increase in patients� BMI, together with a shorter LOS [17]. The BMI increase masks undernutrition and FFM loss at hospital admission. The increased prevalence of obesity in an aging population has led to the recognition of a new nutritional entity: �sarcopenic obesity� [18]. Sarcopenic obesity is characterized by increased FM and reduced FFM with a normal or high body weight. The emergence of the concept of sarcopenic obesity will increase the number of situations associated with a lack of sensitivity of the calculations of BMI and�body weight change for the early detection of FFM loss. This supports a larger use of body composition evaluation for the assessment and follow-up of nutritional status in clinical practice (fig. 1).
Fig. 2. Current and potential applications of body composition evaluation in clinical practice. The applications are indicated in the boxes, and the body composition methods that could be used for each application are indicated inside the circles. The most used application of body composition evaluation is the measurement of bone mineral density by DEXA for the diagnosis and management of osteoporosis. Although a low FFM is associated with worse clinical outcomes, FFM evaluation is not yet implemented enough in clinical practice. However, by allowing early detection of undernutrition, body composition evaluation could improve the clinical outcome. Body composition evaluation could also be used to follow up nutritional status, calculate energy needs, tailor nutritional support, and assess fluid changes during perioperative period and renal insufficiency. Recent evidence indicates that�a low FFM is associated with a higher toxicity of some chemo- therapy drugs in cancer patients. Thus, by allowing tailoring of the chemotherapy doses to the FFM in cancer patients, body com- position evaluation should improve the tolerance and the efficacy of chemotherapy. BIA, L3-targeted CT, and DEXA could be used for the assessment of nutritional status, the calculation of energy needs, and the tailoring of nutritional support and therapy. Further studies are warranted to validate BIA as an accurate method for fluid balance measurement. By integrating body composition evaluation into the management of different clinical conditions, all of these potential applications would lead to a better recognition of nutritional care by the medical community, the health care facilities, and the health authorities, as well as to an increase in the medico-economic benefits of the nutritional evaluation.
Body Composition Techniques For FFM Measurement
Body composition evaluation allows measurement of the major body compartments: FFM (including bone mineral tissue), FM, and total body water. Table 2 shows indicative values of the body composition of a healthy subject weighing 70 kg. In several clinical situations, i.e. hospital admission, chronic obstructive pulmonary dis- ease (COPD) [21�23], dialysis [24�26], chronic heart failure [27], amyotrophic lateral sclerosis [28], cancer [5, 29], liver transplantation [30], nursing home residence [31], and Alzheimer�s disease [32], changes in body compartments are detected with the techniques of body composition evaluation. At hospital admission, body composition evaluation could be used for the detection of FFM loss and undernutrition. Indeed, FFM and the FFM index (FFMI) [FFM (kg)/height (m2)] measured by BIA are significantly lower in hospitalized patients (n = 995) than in age-, height-, and sex-matched controls (n = 995) [3]. Conversely, clinical tools of nutritional status assessment, such as BMI, subjective global assessment, or mini-nutritional assessment, are not accurate enough to estimate FFM loss and nutritional status [30, 32�34]. In 441 patients with non-small cell lung cancer, FFM loss deter- mined by computerized tomography (CT) was observed in each BMI category [7], and in young adults with all�types of cancer, an increase in FM together with a de- crease in FFM were reported [29]. These findings reveal the lack of sensitivity of BMI to detect FFM loss. More- over, the FFMI is a more sensitive determinant of LOS than a weight loss over 10% or a BMI below 20 [3]. In COPD, the assessment of FFM by BIA is a more sensitive method to detect undernutrition than anthropometry [33, 35]. BIA is also more accurate at assessing nutrition- al status in children with severe neurologic impairment than the measurement of skin fold thickness [36].
FFM loss is correlated with survival in different clinical settings [5, 21�28, 37]. In patients with amyotrophic lateral sclerosis, an FM increase, but not an FFM in- crease, measured by BIA, was correlated with survival during the course of the disease [28]. The relation between body composition and mortality has not yet been demonstrated in the intensive care unit. The relation between body composition and mortality has been demonstrated with anthropometric methods, BIA, and CT. Measurement of the mid-arm muscle circumference is an easy tool to diagnose sarcopenia [38]. The mid-arm muscle circumference has been shown to be correlated with survival in patients with cirrhosis [39, 40], HIV infection [41], and COPD in a stronger way than BMI [42]. The relation between FFM loss and mortality has been extensively shown with BIA [21�28, 31, 37], which is the most used method. Recently, very interesting data suggest that CT could evaluate the disease prognosis in relation to muscle wasting. In obese cancer patients, sarcopenia as assessed by CT measurement of the total skeletal muscle cross-sectional area is an independent predictor of the survival of patients with bronchopulmonary [5, 7], gastrointestinal [5], and pancreatic cancers [6]. FFM assessed by measurement of the mid-thigh muscle cross- sectional area by CT is also predictive of mortality in COPD patients with severe chronic respiratory insufficiency [43]. In addition to mortality, a low FFMI at hospital admission is significantly associated with an in- creased LOS [3, 44]. A bicentric controlled population study performed in 1,717 hospitalized patients indicates that both loss of FFM and excess of FM negatively affect the LOS [44]. Patients with sarcopenic obesity are most at risk of increased LOS. This study also found that ex- cess FM reduces the sensitivity of BMI to detect nutritional depletion [44]. Together with the observation that the BMI of hospitalized patients has increased during the last decade [17], these findings suggest that FFM and�FFMI measurement should be used to evaluate nutritional status in hospitalized patients.
Numerous methods of body composition evaluation have been developed: anthropometry, including the 4-skinfold method [58], hydrodensitometry [58], in vivo neutron activation analysis [59], anthropogammametry from total body potassium-40 [60], nuclear magnetic resonance [61], dual-energy X-ray absorptiometry (DEXA) [62, 63], BIA [45, 64�66], and more recently CT [7, 43, 67]. DEXA, BIA, and CT appear to be the most convenient methods for clinical practice (fig. 2), while the other methods are reserved for scientific use.
The evaluation of FFM could be used for the calculation of energy needs, thus allowing the optimization of nutritional intakes according to nutritional needs. This could be of great interest in specific situations, such as severe neurologic disability, overweight, and obesity. In 61 children with severe neurologic impairment and intellectual disability, an equation integrating body composition had good agreement with the doubly labeled water method. It gave a better estimation of energy expenditure than did the Schofield predictive equation [36]. However, in 9 anorexia nervosa patients with a mean BMI of 13.7, pre- diction formulas of resting energy expenditure including FFM did not allow accurate prediction of the resting energy expenditure measured by indirect calorimetry [76]. In overweight or obese patients, the muscle catabolism in response to inflammation was the same as that observed�in patients with normal BMI. Indeed, despite a higher BMI, the FFM of overweight or obese individuals is similar (or slightly increased) to that of patients with normal BMI. Thus, the use of actual weight for the assessment of the energy needs of obese patients would result in over- feeding and its related complications. Therefore, the ex- perts recommend the use of indirect calorimetry or calculation of the energy needs of overweight or obese patients as follows: 15 kcal/kg actual weight/day or 20�25 kcal/kg ideal weight/day [77, 78], although these predictive formulas could be inaccurate in some clinical conditions [79]. In a US prospective study conducted in 33 ICU medical and surgical ventilated ICU patients, daily measurement of the active cell mass (table 2) by BIA was used to assess the adequacy between energy/protein intakes and needs. In that study, nutritional support with 30 kcal/ kg actual body weight/day energy and 1.5 g/kg/day protein allowed stabilization of the active cell mass [75]. Thus, follow-up of FFM by BIA could help optimize nutritional intakes when indirect calorimetry cannot be performed.
Body composition evaluation allows a qualitative assessment of body weight variations. The evaluation of body composition may help to document the efficiency of nutritional support during a patient�s follow-up of numerous clinical conditions, such as surgery [59], anorexia nervosa [76, 80], hematopoietic stem cell transplantation [81], COPD [82], ICU [83], lung transplantation [84], ulcerative colitis [59], Crohn�s disease [85], cancer [86, 87], HIV/AIDS [88], and acute stroke in elderly patients [89]. Body composition evaluation could be used for the follow-up of healthy elderly subjects [90]. Body composition evaluation allows characterization of the increase in body mass in terms of FFM and FM [81, 91]. After hematopoietic stem cell transplantation, the increase in BMI is the result of the increase in FM, but not of the increase in FFM [81]. Also, during recovery after an acute illness, weight gain 6 months after ICU discharge could be mostly related to an increase in FM (+7 kg) while FFM only increased by 2 kg; DEXA and air displacement plethysmography were used to measure the FM and FFM [91]. These two examples suggest that body composition evaluation could be helpful to decide the modification and/or the renewal of nutritional support. By identifying the patients gaining weight but reporting no or insufficient FFM, body composition evaluation could contribute to influencing the medical decision of continuing nutrition- al support that would have been stopped in the absence of body composition evaluation.
In clinical situations when weight and BMI do not reflect the FFM, the evaluation of body composition should be used to adapt drug doses to the FFM and/or FM absolute values in every patient. This point has been recently illustrated in oncology patients with sarcopenic obesity. FFM loss was determined by CT as described above. In cancer patients, some therapies could affect body com- position by inducing muscle wasting [92]. In patients with advanced renal cell carcinoma [92], sorafenib induces a significant 8% loss of skeletal muscular mass at 12 months. In turn, muscle wasting in patients with BMI less than 25 was significantly associated with sorafenib toxicity in patients with metastatic renal cancer [8]. In metastatic breast cancer patients receiving capecitabine treatment, and in patients with colorectal cancer receiving 5-fluorouracile, using the convention of dosing per unit of body surface area, FFM loss was the determinant of chemotherapy toxicity [9, 10] and time to tumor progression [10]. In colorectal cancer patients administered 5-fluoruracil, low FFM is a significant predictor of toxicity only in female patients [9]. The variation in toxicity between women and men may be partially explained by the fact that FFM was lower in females. Indeed, FFM rep- resents the distribution volume of most cytotoxic chemo- therapy drugs. In 2,115 cancer patients, the individual variations in FFM could change by up to three times the distribution volume of the chemotherapy drug per body area unit [5]. Thus, administering the same doses of chemotherapy drugs to a patient with a low FFM compared to a patient with a normal FFM would increase the risk of chemotherapy toxicity [5]. These data suggest that FFM loss could have a direct impact on the clinical outcome of cancer patients. Decreasing chemotherapy doses in case of FFM loss could contribute to improving cancer patients� prognosis through the improvement of the tolerance of chemotherapy. These findings justify the systematic evaluation of body composition in all cancer patients in order to detect FFM loss, tailor chemotherapy doses according to FFM values, and then improve the efficacy- tolerance and cost-efficiency ratios of the therapeutic strategies [93]. Body composition evaluation should also be used to tailor the doses of drugs which are calculated based on patients� weight, e.g. corticosteroids, immuno-suppressors (infliximab, azathioprine or methotrexate), or sedatives (propofol).
The implementation of body composition evaluation in routine care presents a challenge for the next decades. Indeed the concomitant increases in elderly subjects and patients with chronic diseases and cancer, and in the prevalence of overweight and obesity in the population, will increase the number of patients nutritionally at risk or undernourished, particularly those with sarcopenic obesity. Body composition evaluation should be used to improve the screening of undernutrition in hospitalized patients. The results of body composition should be based on the same principle as BMI calculation, towards the systematic normalization for body height of FFM (FFMI) and FM [FM (kg)/height (m)2 = FM index] [94]. The results could be expressed according to previously de- scribed percentiles of healthy subjects [95, 96]. Body com- position evaluation should be performed at the different stages of the disease, during the course of treatments and the rehabilitation phase. Such repeated evaluations of body composition could allow assessment of the nutritional status, adjusting the calculation of energy needs as kilocalories/kilogram FFM, following the efficacy of 
Anabolic-Androgenic Steroids
Anabolic-androgenic steroids (AAS) are testosterone derivatives that exert anabolic (tissue building) and androgenic (masculinizing) influences on the body.3 Since the discovery of the chemical structure of testosterone in 1935, attempts to separate the anabolic and androgenic effects of AAS�have been unsuccessful.3 
Dehydroepiandrosterone (DHEA) is a precursor to testos- terone produced primarily in the adrenal glands.4,14 Natural sources of DHEA include wild yams. The FDA banned sale of DHEA in 1996 due to insuf cient evidence of safety and value; however, DHEA remains a legal and popular item sold as a nutritional supplement.14,15
Androstenedione is a testosterone pre-cursor produced in the adrenal glands and gonads. Several professional athletes have used this substance, bringing it to national attention.2 Androstenedione is found naturally in the pollen of Scottish pine trees.19
The increased visibility of ergogenic aids in the last de- cade has occurred primarily because of the passage of the United States Dietary Supplement Health and Education Act (DSHEA) of 1994.22 Certain vitamins, minerals, amino acids, herbs, and other botanical preparations can be classified as a �dietary supplement� under the DSHEA guidelines. Dietary supplements, as a result of DSHEA, are no longer under the direct regulatory control of the FDA. In fact, substances sold as a dietary supplement do not require FDA evaluation for safety or efficacy, and do not have to meet quality control standards expected of approved drugs.5 The content and purity of dietary supplements are not regulated and can vary widely.5,23 Since androstenedione and DHEA have been found to occur naturally in plant sources, these testosterone precursors can be labeled as �dietary supplements� and sold legally over-the-counter.
Dietary supplements containing Chinese ephedra, also known as Mahaung, are marketed as performance enhancers and weight-loss aids.24 Ephedra species of herb have been used for over 5,000 years for respiratory ailments.25 Currently, ephedrine alkaloids are found in hundreds of prescriptions and over-the-counter products, such as antihistamines, decongestants, and appetite suppressants.24-26 Ephedra and related ephedrine alkaloids are sympathomimetic agents that�mimic epinephrine effects.
Creatine use in athletes has grown as a result of a 1992 study that showed that creatine supplementation produced a 20% increase in skeletal muscle creatine concentration.2,35 In the phosphorylated form, creatine serves as an energy substrate that contributes to adenosine triphosphate (ATP) re-synthesis during high-intensity exercise.36 Creatine re- mains popular with power and resistance athletes as it is thought to produce increases in strength, muscle mass, and to delay fatigue.2,14,36
Human growth hormone (hGH) is a polypeptide produced in the anterior pituitary gland. After its release from the pituitary, hGH can exert its effect in all cells of the body via tissue specific receptors. Human growth hormone is shown to promote protein anabolism, carbohydrate tolerance, lipolysis, natriuresis, and bone and connective tissue turnover.4,50
Recombinant EPO (r-EPO) was approved by the FDA for manufacture in 1989 after the EPO gene was cloned in 1985.14 Since its approval, r-EPO has been abused for athletic personal gain as an alternative to blood doping.3,14 Recombinant EPO has largely replaced the practice of blood doping, as r-EPO produces a dose-dependent increase in hematocrit.2 In theory, r-EPO should provide all of the benefits of blood doping without the risks involved in blood transfusion.3
The antioxidant capabilities of certain vitamins are believed by many to counter-act the production of free-radials that occurs during exercise.14 Most of the research to date involves vitamin E, vitamin C, and beta carotene.2 The existing literature does not support the notion that antioxidants have significant ergogenic capabilities.2,14,57 There are currently no recommendations for antioxidant use in athletes that exceeds the normal adult recommended daily allowance (RDA).
Beta-hydroxy-beta-methylbutyrate (HMB) is a metabolite of the branched-chain amino acid leucine. HMB is theorized to inhibit muscle breakdown during strenuous exercise but its exact mechanism of action remains unknown.14,58 Studies show that HMB supplementation may significantly lower serum lactate dehydrogenase (LDH), lower serum creatine phosphokinase (CPK) levels and delay blood lactate accumulation after endurance training compared to placebo.59,60 Furthermore, short-term HMB use has been shown to significantly increase strength gains with resistance-exercised training over placebo in one double-blinded study.61
Caffeine is a methylxanthine occurring naturally in many species of plants. Caffeine is thought to work through a variety of mechanisms. The central nervous system effect of caffeine is probably the result of adrenergic receptor antagonism.3 Its use by athletes stems from the theory that caffeine may delay fatigue by enhancing skeletal muscle contractility and spare muscle glycogen levels by enhancing fat metabolism.6 Multiple studies have reported an improved endurance time with caffeine use.6,62,63 There is evidence that caffeine use may enhance performance with more intense short-duration exercise as well.2 The caffeine dosages most associated with an ergogenic effect range in the literature from 3 to 9 mg per kilogram of body weight.2,6
DD Palmer wrote a chapter in 1914 entitled Inflammation, stating that, “inflammation is present in most, if not all diseases, in the acute if not chronic.” 100 years later, all chronic diseases are inflammatory conditions within local tissues . Chronic systemic inflammation and related pathophysiological changes involve structures and functions that are silent.
Loss of sleep, sedentary living, stress and diet all encourage inflammation.
Laboratory tests are the best approach to spot chronic inflammation. High levels of glucose, triglycerides, hemoglobin A1c protein along with reduced levels of vitamin D and HDL cholesterol are the most reliable in identifying chronic inflammation.
Diet is a problem for most people with over two-thirds of the population being overweight. Obesity is known to be a chronic inflammatory state associated with chronic pain and degenerative diseases.
