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  1. That is why the veteran will require their doctor to write a NEXUS letter. Most doctors will not do it. You can also get a Nurse Practioner or Physical Assistant to write it as well. Better yet, you write it and bring in the supporting documentation. Have the doc's admin assistant put it on his/her letter head and ask them to sign it. If your going to have more than one provider sign the statement, have more than one NEXUS letter written up. If the VA believes it's a form letter, they will put little value on it.
  2. Here are more studies you can cite. All from docguide: t least one in three people with Type 2 diabetes mellitus referred to a diabetes centre has symptomatic obstructive sleep apnoea; Storgaard H, Mortensen B, Almdal T, Laub M, Tarnow L; Diabetic Medicine (Apr 2014) Tags: Diabetes Sleep Apnoea Read/Add Comments | Email This | Print This | PubMed | Get Full Text AIMS To investigate the prevalence of symptomatic obstructive sleep apnoea in unselected patients with Type 2 diabetes referred to a tertiary diabetes clinic. METHODS In a cross-sectional design, all newly referred patients were offered a stepwise screening for obstructive sleep apnoea with: (1) The Berlin questionnaire; then, if indicative: (2) overnight home monitoring with the ApneaLink(®) device. Patients with an apnoea-hypopnoea index ≥ 5/h were offered referral for diagnostic polygraphy and treatment initiation. RESULTS A total of 200 patients participated (61% men; age 59.6 ± 10.5 years, diabetes duration 8.3 ± 6.3 years and BMI 31.7 ± 6.7 kg/m(2) ). According to the questionnaire, 106 patients showed 'high risk' of obstructive sleep apnoea, and 72 of these were referred to polygraphy based on ApneaLink screening corresponding to a prevalence of symptomatic obstructive sleep apnoea of 39%. Patients with symptomatic obstructive sleep apnoea had significantly higher BMI, poorer glycaemic control and lower plasma HDL cholesterol levels as compared with patients unlikely to have obstructive sleep apnoea. The groups were not different with respect to sex, age, diabetes duration, blood pressure, diabetic complications or medication use. In multiple regression analyses, age, BMI and HDL cholesterol levels were all significant, independent predictors of obstructive sleep apnoea. CONCLUSIONS At least one third of people with Type 2 diabetes referred to a diabetes clinic in Denmark has symptomatic obstructive sleep apnoea. Our data suggest higher age, a compromised plasma lipid profile and a more obese phenotype in patients with Type 2 diabetes who have obstructive sleep apnoea, highlighting the need to focus on screening and treatment of obstructive sleep apnoea in these patients. This article is protected by copyright. All rights reserved. Nonalcoholic fatty pancreatic disease and cardio-metabolic risk: is there is a place for obstructive sleep apnea?; Mirrakhimov A; Cardiovascular Diabetology 13 (1), 29 (2014) Tags: Diabetes Sleep Apnoea Read/Add Comments | Email This | Print This | PubMed | Free Full Text BACKGROUND Obstructive sleep apnea is a common disorder acting as a risk factor for the development and progression of cardiometabolic derangements including non-alcoholic fatty liver disease. Recent research data suggest that non-alcoholic fatty pancreatic disease may be a more sensitive marker than non-alcoholic fatty liver disease for early subclinical metabolic risk and may contribute to the progression of subclinical disease to overt type 2 diabetes mellitus. PRESENTATION OF THE HYPOTHESIS We postulate that obstructive sleep apnea may be a risk factor for non-alcoholic fatty pancreatic disease. It is well known that intermittent hypoxia related to obstructive sleep apnea leads to hormonal derangements. Excessive lipolysis, enhanced lipid synthesis and systemic and local inflammation may favor ectopic fat deposition similarly to non-alcoholic fatty liver disease. Furthermore, it is possible that obstructive sleep apnea can lead to pancreatic beta cell damage via intermittent hypoxia. TESTING OF THE HYPOTHESIS Future research should focus on the following: first, whether non-alcoholic fatty pancreatic disease is an independent risk factor for the development of metabolic disease including diabetes mellitus or is a simple consequence of obesity; second, the prevalence of non-alcoholic fatty pancreatic disease among people with obstructive sleep apnea and vice versa, which should be compared to the prevalence of these diseases in general population; third, whether coexistence of these conditions is related to greater cardiometabolic risk than either disease alone; and fourth, whether the treatment of obstructive sleep apnea will translate into the resolution of non-alcoholic fatty pancreatic disease. IMPLICATIONS OF THE HYPOTHESIS If proven, this hypothesis will provide new knowledge on the complex interplay between various metabolic insults. Second, screening for NAFPD may identify individuals at risk for developing type 2 diabetes mellitus for targeted prevention. Third, screening for the presence of non-alcoholic fatty pancreatic disease in patients with obstructive sleep apnea may help to decrease the incidence of diabetes mellitus through a targeted prevention. Gestational Diabetes Mellitus and Sleep-Disordered Breathing; Bisson M, Sériès F, Giguère Y, Pamidi S, Kimoff J, Weisnagel S, Marc I; Obstetrics & Gynecology (Feb 2014) Tags: Depression Diabetes Pregnancy Sleep Apnoea Sleep Disorders - Apnoea Read/Add Comments | Email This | Print This | PubMed | Get Full Text OBJECTIVE: To examine the link between gestational diabetes mellitus (GDM) and sleep-disordered breathing using complete polysomnography and questionnaires in a case-control study of pregnant women. METHODS: Pregnant women (body mass index [bMI] less than 35, no prior diabetes or hypertension) were eligible as cases (n=26) if diagnosed with GDM by routine 75-g oral glucose tolerance test. Women in the control group without GDM (n=26) were matched for gestational age at polysomnography, BMI, and age. Polysomnography were conducted at home at 24-32 weeks of gestation. Sleepiness score (Epworth Sleepiness Scale), subjective sleep quality (Pittsburgh Sleep Quality Index), risk for depression (Edinburgh Postnatal Depression Scale), and restless legs syndrome were assessed by questionnaire. RESULTS: Primary outcome apnea-hypopnea index (4.2±3.9 events per hour in women in the case group compared with 3.8±2.3 events per hour in women in the control group) as well as other objective and subjective sleep measures, including oxygen desaturation index, snoring, and flow limitation, were not significantly different between groups. Sleepiness was greater in women in the case group than in women in the control group (9.8±3.6 compared with 7.2±3.6, P=.05). Additionally, 23% of women in the case group compared with 0% of women in the control group (P<.01) reported an Edinburgh Scale score of at least 10 (suggesting significant depression) and 46% of women with GDM reported restless legs syndrome compared to 19% of women in the control group (P=.07). CONCLUSION: There was no association between GDM and sleep-disordered breathing in pregnant women with prepregnancy BMIs under 35 and no medical comorbidities. LEVEL OF EVIDENCE:: II. Obstructive sleep apnea syndrome causes a pseudo-Cushing's state in Japanese obese patients with type 2 diabetes mellitus; Tamada D, Otsuki M, Kashine S, Hirata A, Onodera T, Kitamura T, Shimomura I; Endocrine Journal (Sep 2013) Tags: dexamethasone Diabetes Obesity Sleep Apnoea Read/Add Comments | Email This | Print This | PubMed Activation of the hypothalamic-pituitary-adrenal axis has been reported in some patients with the obstructive sleep apnea syndrome (OSAS). In current study, we investigated whether OSAS affect the screening test for subclinical Cushing's disease using 0.5 mg overnight dexamethasone suppression test (DST) in Japanese obese diabetic patients with OSAS. Among Japanese obese patients with type 2 diabetes mellitus who had been hospitalized in our department, we selected 20 patients with moderate to severe untreated OSAS (apnea-hypoxia index, AHI, of ≥15 events/hour). All patients underwent 0.5 mg DST. The same test was repeated in patients with positive response of it within a few days after continuous positive airway pressure (CPAP) therapy. We found that five patients showed positive response of DST (25%). Three of these patients continued to use CPAP, and they showed normal response of DST after CPAP therapy. Serum cortisol after 0.5 mg DST measured before CPAP therapy correlated significantly with fasting serum cortisol level (r=0.764, p<0.0001), but not with various clinical parameters, including AHI (P=0.784), body mass index (P=0.984), waist circumference (p=0.957), HbA1c (p=0.261), fasting plasma glucose (p=0.420) and HOMA-IR (p=0.500). Our study show that OSAS causes a pseudo-Cushing's syndrome in obese patients with type 2 diabetes mellitus, which phenomena can be reversed by CPAP therapy. Obstructive Sleep Apnea and Diabetic Nephropathy: A cohort study; Tahrani A, Ali A, Raymond N, Begum S, Dubb K, Altaf Q, Piya M, Barnett A, Stevens M; Diabetes Care 36 (11), 3718-25 (Nov 2013) Tags: Diabetes Sleep Apnoea Read/Add Comments | Email This | Print This | PubMed | Get Full Text OBJECTIVE Diabetic nephropathy (DN) is a leading cause of end-stage renal disease (ESRD). Obstructive sleep apnea (OSA) is common in type 2 diabetes and increases oxidative stress. Hence, OSA could promote the development and progression of DN. RESEARCH DESIGN AND METHODS This was a cohort study in adults with type 2 diabetes. Patients with known OSA or ESRD were excluded. DN was defined as the presence of albuminuria or an estimated glomerular filtration rate (eGFR)<60 mL/min/1.73 m(2). DN progression was based on eGFR measurements. OSA was defined as apnea hypopnea index (AHI) ≥5 events/h. Serum nitrotyrosine abundance (a marker of nitrosative stress) was measured by ELISA. RESULTS A total of 224 patients were included. OSA and DN prevalence was 64.3 and 40.2, respectively. DN prevalence was higher in patients with OSA (OSA(+)) compared with those without OSA (OSA(-)) (49.3% vs. 23.8%, P<0.001). After adjustment, OSA (odds ratio 2.64 [95% CI 1.13-6.16], P = 0.02) remained independently associated with DN. After an average follow-up of 2.5 (0.7) years, eGFR decline was greater in OSA(+) compared with OSA(-) patients (median -6.8% [interquartile range -16.1 to 2.2]vs. -1.6% [-7.7 to 5.3%], P = 0.002). After adjusting, both baseline OSA (B = -3.8, P = 0.044) and AHI (B = -4.6, P = 0.02) remained independent predictors of study-end eGFR. Baseline serum nitrotyrosine abundance (B = -0.24, P = 0.015) was an independent predictor of study-end eGFR after adjustment. CONCLUSIONS OSA is independently associated with DN in type 2 diabetes. eGFR declined faster in patients with OSA. Nitrosative stress may provide a pathogenetic link between OSA and DN. Interventional studies assessing the impact of OSA treatment on DN are needed. Association of obstructive sleep apnea in REM sleep with reduced glycemic control in type 2 diabetes: Therapeutic implications; Grimaldi D, Beccuti G, Touma C, Van Cauter E, Mokhlesi B; Diabetes Care (Oct 2013) Tags: Diabetes Sleep Apnoea Read/Add Comments | Email This | Print This | PubMed | Get Full Text ObjectiveSeverity of obstructive sleep apnea (OSA) has been associated with poorer glycemic control in type 2 diabetes. It is not known whether obstructive events during rapid eye movement (REM) sleep have a different metabolic impact compared to those during non-REM (NREM) sleep. Treatment of OSA is often limited to the first half of the night, when NREM rather than REM sleep predominates. We aimed to quantify the impact of OSA in REM versus NREM sleep on hemoglobin A1c (HbA1c) in subjects with type 2 diabetes.Research Design and MethodsAll participants underwent polysomnography and glycemic control was assessed by HbA1c.ResultsOur analytic cohort included 115 subjects (65 women, age 55.2 ± 9.8 years; BMI 34.5 ± 7.5 kg/m(2)). In a multivariate linear regression model, REM AHI was independently associated with increasing levels of HbA1c (p=0.008). In contrast, NREM AHI was not associated with HbA1c (p=0.762). The mean adjusted HbA1c increased from 6.3% in subjects in the lowest quartile of REM AHI to 7.3% in subjects in the highest quartile of REM AHI (p=0.044 for linear trend). Our model predicts that 4 hours of CPAP use would leave 60% of REM sleep untreated and would be associated with a decrease in HbA1c by about 0.25%. In contrast, 7 hours of CPAP use would cover more than 85% of REM sleep and would be associated with a decrease in HbA1c by as much as 1%.ConclusionsIn type 2 diabetes, OSA during REM sleep may influence long-term glycemic control. The metabolic benefits of CPAP therapy may not be achieved with the typical adherence of 4 hours per night.
  3. I disagree with Veldrina. You can go to the web site and set yourself up as an administrator and do a search between Sleep Apnea and Diabetes Below is one such study. You can then use this study to have a NEXUS letter written to show the link between the two. there are several studies out there that support the link. Impact of Untreated Obstructive Sleep Apnea on Glucose Control in Type 2 Diabetes Renee S. Aronsohn 1, Harry Whitmore1, Eve Van Cauter1, and Esra Tasali1 1 Department of Medicine, University of Chicago, Chicago, Illinois Rationale : Obstructive sleep apnea (OSA), a treatable sleep disorder that is associated with alterations in glucose metabolism in individuals without diabetes, is a highly prevalent comorbidity of type 2 diabetes. However, it is not known whether the severity of OSA is a predictor of glycemic control in patients with diabetes. Objectives : To determine the impact of OSA on hemoglobin A1c (HbA1c), the major clinical indicator of glycemic control, in patients with type 2 diabetes. Methods : We performed polysomnography studies and measured HbA1c in 60 consecutive patients with diabetes recruited from outpatient clinics between February 2007 and August 2009. Measurements and Main Results : A total of 77% of patients with diabetes had OSA (apnea–hypopnea index [AHI] >5). Increasing OSA severity was associated with poorer glucose control, after controlling for age, sex, race, body mass index, number of diabetes medications, level of exercise, years of diabetes and total sleep time. Compared with patients without OSA, the adjustedmeanHbA1cwas increased by 1.49% ( P 5 0.0028) in patients with mild OSA, 1.93% ( P50.0033) in patients with moderate OSA, and 3.69% (P,0.0001) in patients with severeOSA( P,0.0001 for linear trend). Measures of OSA severity, including total AHI ( P 5 0.004), rapid eye movement AHI ( P50.005), and the oxygen desaturation index during total and rapid eye movement sleep ( P 5 0.005 and P 5 0.008, respectively) were positively correlated with increasing HbA1c levels. Conclusions : In patients with type 2 diabetes, increasing severity of OSA is associated with poorer glucose control, independent of adiposity and other confounders, with effect sizes comparable to those of widely used hypoglycemic drugs. Keywords: sleep disordered breathing; glycemic control; diabetes Given the enormous public health burden of the type 2 diabetes epidemic, and growing concerns about the safety profiles of current pharmacologic treatments (1, 2), a better understanding of the impact of comorbidities on glucose control is needed to develop additional preventive and therapeutic strategies. Obstructive sleep apnea (OSA) is a treatable sleep disorder characterized by repetitive upper airway closures, leading to oxygen desaturations and sleep fragmentation. OSA has been identified as a highly prevalent comorbidity of type 2 diabetes (3–5). In particular, among obese patients with type 2 diabetes, who represent the vast majority of individuals with type 2 diabetes in the United States, the prevalence has recently been estimated at a staggering 86% (5). OSA is a well documented risk factor for cardiovascular disease and mortality (6–9). Multiple epidemiologic and clinical studies have revealed that individuals without diabetes suffering from OSA show alterations in glucose metabolism, including insulin resistance and impaired glucose tolerance, independent of adiposity (10–13). Despite these independent associations between OSA and abnormal glucose metabolism and the high prevalence of OSAin patients with type 2 diabetes, data on whether the presence and severity of OSA compromises glycemic control in patients with type 2 diabetes is lacking. The majority of patients with type 2 diabetes need multiple drugs, in addition to lifestyle modifications, to control glucose levels and avoid or delay the development of serious complications (14). Currently, both physicians and patients are challenged by rising concerns about the safety of widely used pharmacologic treatment options. Therefore, determining whether OSA has an adverse effect on glucose control in patients with diabetes has major clinical implications, because effective treatment of OSA could be a nonpharmacologic strategy to improve glucose control in the management of millions of patients with type 2 diabetes. In the present study, we therefore evaluated the impact of untreated OSA on hemoglobin A1c (HbA1c), the major clinical indicator of glycemic control, in patients with type 2 diabetes. Preliminary findings from this study have been previously reported in abstract form (15, 16). METHODS Participants and Study Design Patients with type 2 diabetes were consecutively recruited by one of the study investigators (R.S.A.), from the Primary Care and Endocrinology Clinics at the University of Chicago between February 2007 and August 2009. Sleep complaints or symptoms of OSA were not used as selection criteria. All participants were on stable medications for diabetes and other comorbidities for the preceding 3 months. Subjects were excluded if they: failed to meet the criteria for type 2 diabetes, based on physician diagnosis, in accordance with established guidelines (14); had unstable cardiopulmonary, neurological, or psychiatric disease; upper airway surgery; or used nocturnal oxygen, positive airway pressure AT A GLANCE COMMENTARY Scientific Knowledge on the Subject Obstructive sleep apnea (OSA) is associated with alterations in glucose metabolism in non-diabetic individuals and is a highly prevalent co-morbidity of type 2 diabetes, but its effect on glycemic control in patients with diabetes was not known. What This Study Adds to the Field In patients with type 2 diabetes, there is a robust graded relationship between the severity of OSA and glycemic control. ( Received in original form September 22, 2009; accepted in final form December 11, 2009) Supported by the National Institute of Health grants P01 AG11412 (E.V.C.), R01 HL086459 (E.T.), UL1RR024999, and P60 DK20595, and grants from the American Academy of Sleep Medicine/Pfizer Scholars Grant in Sleep Medicine, and the ResMed Foundation. Correspondence and requests for reprints should be addressed to Renee Aronsohn, M.D., Department of Medicine, MC 1027, University of Chicago, 5841 South Maryland Avenue, Chicago, IL 60637. E-mail: raronsoh@medicine. Am J Respir Crit Care Med Vol 181. pp 507–513, 2010 DOI: 10.1164/rccm.200909-1423OC Internet address: therapy, or oral appliances. The study was approved by the University of Chicago Institutional Review Board, and all participants gave written informed consent. During a 45-minutes interview, each patient completed surveys, including the University of Chicago Diabetes/Quality of Life Survey (17) (which includes self-report of medications, presence of diabetic complications [retinopathy, nephropathy, neuropathy, coronary artery disease, and peripheral vascular disease], and level of exercise [no 5 rarely, mild 5once or twice a week, moderate5three times a week, and heavy 5 more than three times a week]), the Berlin Questionnaire (18) (used to assess the presence of snoring), and the Center for Epidemiologic Studies Depression Scale (19) (score >16 indicates depression). Height and weight were measured in all patients. Waist circumference was measured in 58 patients. Subjects underwent 5 consecutive days of ambulatory wrist actigraphy to determine habitual sleep habits. An overnight laboratory polysomnogram (PSG) was then performed to establish the presence and severity of OSA. Bedtimes in the laboratory were individually designed based on the subject’s usual habits derived from actigraphy. However, each subject was recorded for a minimum of 7 hours. HbA1c values (%, defined as the proportion of hemoglobin that is glycosylated) were obtained from the patient’s chart if assessed during the previous 3 months, or a single blood sample was drawn on the morning after PSG. HbA1c was measured by Bio-Rad Variant Classic boronate affinity-automatedHPLC(Bio-Rad, Hercules, CA). The intraassay coefficient of variation was 0.5–1.0%, and the interassay coefficient of variation ranges from 2.2–2.4%. Polysomnography PSG (Neurofax EEG 1100 system; Nihon Kohden, Foothill Ranch, CA) included recordings of six electroencephalogram channels, bilateral electro-oculograms, chin and tibialis electromyogram, electrocardiogram, airflow by nasal pressure transducer and oronasal thermocouples, chest and abdominal wall motion by piezo electrodes, and oxygen saturation by pulse oximeter. Recordings were visually scored in 30 seconds in stages 1–4 of non–rapid eye movement (REM) sleep and in REM sleep, according to standard criteria (20). Respiratory events and microarousals were scored according to established criteria (21, 22). Total cessation of airflow for at least 10 seconds was defined as apnea (obstructive if respiratory efforts were present and central if respiratory efforts were absent). Hypopneas were identified if there was a discernable reduction in airflow lasting at least 10 seconds and associated with at least3%desaturation. The apnea–hypopnea index (AHI) was defined as the total number of obstructive apneas and obstructive hypopneas per hour of sleep. OSA severity categories were defined according to commonly used clinical cutoffs as follows: no OSA (AHI ,5); mild OSA(AHI >5 but,15); moderateOSA(AHI>15 but,30); and severe OSA(AHI >30). Total oxygen desaturation index (ODI) was defined as the total number of desaturations of at least 3% per total sleep time in hours. REM ODI was defined as number of desaturations of at least 3% duringREMsleep perREMsleep time in hours. The microarousal index was calculated as the total number of microarousals per hour of sleep. Actigraphy Habitual sleep duration was assessed at home by actigraphy using the Actiwatch (Mini-Mitter, Bend, OR) in accordance with previously described methods (23–25). Participants were asked to wear the Actiwatch for 5 consecutive days—3 weekdays and 2 weekend days—and to maintain their habitual bedtimes and fill out daily sleep logs. Of the 60 subjects who were included in the final analysis, 50 (83%) wore the Actiwatch for all 5 days, 7 (12%) wore the Actiwatch for 4 days, and 2 (3%) wore the Actiwatch for 3 days. One subject’s data could not be downloaded due to a technical failure, thus data on habitual sleep duration are reported in 59 subjects. Statistical Analysis Group data are expressed as means ( 6SD). Variables were examined for normality, and, if skewed, the log-transformed values were used. All categorical data were compared by Pearson’s x2 test. Pair-wise comparisons of continuous variables in patients with and without OSA were examined by t test and confirmed by the nonparametric Mann-Whitney test. Unadjusted group differences across OSA severity categories were assessed by analysis of variance. A linear contrast was used to test for trends.We performed multivariate regression analyses to characterize the independent associations between measures of OSA severity and the primary outcome variable, HbA1c. The primary independent predictor was the OSA severity category, and we also examined total AHI, REM AHI, totalODI, andREMODI.Potential confounding variables included in all multivariable models as covariates were: age; sex; race; body mass index (BMI);number of diabetesmedications; level of exercise; years since diabetes diagnosis; and total sleep time by PSG.After log transformation, the distribution of HbA1c values remained skewed due to one outlier subject, thus a sensitivity analysis excluding this outlier value was performed and confirmed the significance of the association between severity ofOSA andHbA1c.We also performed sensitivity analyses using waist circumference as covariate (instead of BMI) in all multivariate models. Data are presented in non–log-transformed values for ease of interpretation. All statistical analyses were performed using JMP version 6.0.3 statistical software (SAS Institute, Cary, NC). All reported P values are two sided. RESULTS Figure 1 shows the flow diagram of patient recruitment and selection. Patients who obtained less than 4 hours of total sleep time during the PSG, thus preventing accurate assessment of the degree of severity of OSA, were not included in the analysis ( n 5 6). One patient showed severe oxygen desaturations not explained by apneas or hypopneas (thus consistent with significant hypoventilation) and, in another patient, the PSG data could not be interpreted due to multiple artifacts in the airflow signal. Thus, 60 patients were included in the final analysis. Table 1 summarizes the demographic characteristics of the cohort, which comprised similar proportions of men and women and of whites and African Americans. The age range was 41–77 years. The BMI range was 20–57 kg/m 2. The sample included 7 lean, 14 overweight, and 39 obese patients. A total of 46 of the 60 patients (77%) had OSA (AHI >5). Only five patients had been previously evaluated for OSA, and none were receiving treatment. Mild, moderate, and severe OSA was found in 38.3% ( n 5 23), 25.0% (n 5 15), and 13.3% ( n 5 8) of the sample, respectively. Compared with patients without OSA, those with OSA were heavier and 6 years older on average (Table 1). Increasing severity of OSA was associated with increasing BMI (unadjusted Figure 1. Participant flow diagram 508 AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE VOL 181 2010 P 5 0.00042 for linear trend) and greater waist circumference (unadjusted P 5 0.00038 for linear trend). Patients without OSA had fewer diabetic complications than those with OSA. Out of 60 patients, 6 (10%) did not take any diabetes medications (i.e., insulin, oral agents, or incretin-based therapies), 18 (30%) were on 1 medication, 24 (40%) were on 2 medications, 11 (18%) were on 3 medications, and 1 (2%) patient was on 4 medications. Out of 60 patients, 20 (33.3%) reported no exercise, 11 (18.3%) reported mild exercise, 14 (23.3%) reported moderate exercise, and 15 (25.0%) reported heavy exercise. Sleep characteristics are summarized in Table 2. Habitual sleep duration was not significantly different between patients with and without OSA. In the laboratory, patients with OSA had shorter total sleep duration, decreased sleep efficiency, increased wake time after sleep onset, and less REM sleep than those without OSA. Increasing severity of OSA was associated with lower amounts of REM sleep (unadjusted P 5 0.012 for linear trend), more stage 1 sleep (unadjusted P 5 0.007 for linear trend), and more sleep fragmentation as assessed by the microarousal index (unadjusted P 5 0.0001 for linear trend). The predominant respiratory disturbances were obstructive apneas and hypopneas, rather than central apneas. Increasing severity ofOSAwas associated with poorer glucose control after controlling for age, sex, race, BMI, number of diabetes medications, level of exercise, years of diabetes, and total sleep time on PSG ( P , 0.0001 for linear trend). Figure 2 shows the adjusted mean values of HbA1c in each OSA category. Compared with patients without OSA, the adjusted mean HbA1c was increased by 1.49% ( P 5 0.0028) in patients with mild OSA, 1.93% ( P 5 0.0033) in patients with moderate OSA, and 3.69% ( P , 0.0001) in patients with severe OSA (P , 0.0001 for linear trend). Associations between OSA severity and HbA1c levels remained robust when ‘‘number of diabetes medications’’ was replaced by ‘‘oral hypoglycemic medication use’’ ( P , 0.0001 for linear trend) or ‘‘insulin use’’ ( P 5 0.0002 for linear trend) in the regression model. Similar associations between the severity of OSA and glycemic control were found when the presence of diabetic complications was added to the regression model ( P , 0.0001 for linear trend). A sensitivity analysis including waist circumference (instead of BMI) in the regression model also showed similar linear associations between increasing severity of OSA and higher HbA1c levels ( P 5 0.0001 for linear trend). Other measures of OSA severity, including total AHI ( P 5 0.004), REM AHI ( P 5 0.005), total ODI (P 5 0.005), and REM ODI ( P 5 0.008), were positively correlated with increasing HbA1c levels after adjusting for age, sex, race, BMI, number of diabetes medications, level of exercise, years of diabetes, and total sleep time on PSG.Wedid not detect significant associations between HbA1c levels and the microarousal index ( P 5 0.75) or the amount of slow wave sleep ( P 5 0.67) after adjusting for age, sex, race, BMI, number of diabetes medications, level of exercise, years of diabetes, and total sleep time. DISCUSSION The present study indicates that OSA is highly prevalent in patients with type 2 diabetes, and demonstrates, for the first time, a clear, graded, inverse relationship between OSA severity and glucose control in patients with type 2 diabetes, after controlling for the degree of adiposity and multiple other potential confounders. A total of 46 of our 60 subjects (77%) had OSA. In nearly 90% of these patients, the presence of OSA had not been previously evaluated. Relative to patients without OSA, the presence of mild, moderate, or severe OSA increased mean adjusted HbA1c values by 1.49, 1.93, and 3.69%, respectively. These effect sizes are comparable to, if not exceeding, those of TABLE 1. SAMPLE CHARACTERISTICS: PATIENTS WITH DIABETES ACCORDING TO OBSTRUCTIVE SLEEP APNEA STATUS All Patients Patients without OSA Patients with OSA Characteristic ( n 5 60) (n 5 14) (n 5 46) P Value* Age, yr 57.0 6 9.2 52.4 6 7.6 58.4 6 9.2 0.03 Male sex, % 45 43 46 0.85 Race, % African American 58 64 57 White 42 36 43 0.61 BMI, kg/m 2 33.8 6 7.7 28.9 6 5.8 35.3 6 7.6 0.005 Waist circumference, inches † 43.0 6 6.6 39.8 6 5.6 43.9 6 6.6 0.05 HbA1c, % 7.7 6 1.8 7.2 6 1.4 7.8 6 1.9 0.28 Diabetes diagnosis, yr 9.6 6 8.0 9.9 6 9.0 9.6 6 7.8 0.91 Diabetic complications, % † 55 21 65 0.004 Diabetic medications, % † Insulin 35 50 30 0.18 Oral hypoglycemic 76 71 78 0.60 Incretin based 20 14 22 0.54 Exercise, % † 67 79 63 0.28 Hypertension, % † 70 64 72 0.59 Depression, % † 35 21 39 0.22 Snoring* 33 32 21 0.42 Definition of abbreviations: BMI 5 body mass index (calculated as weight in kilograms divided by height in meters squared); HbA1c 5 hemoglobin A1c; OSA 5 obstructive sleep apnea defined by five or more obstructive apneas and hypopneas per hour of sleep. Data are given as mean 6 SD or percentage. * P values for unadjusted comparisons between patients with and without OSA are determined by t test for continuous variables or Pearson’s x2 test for categorical variables. † Data forwaist circumference are reported in n558 subjects; presence of diabetic complications is based on self-report of one or more of the following: retinopathy, nephropathy, neuropathy, coronary artery or peripheral vascular disease; use of all diabetic medications are dichotomous variables (yes or no) by self-report; use of oral hypoglycemic agents is defined as use of at least one of the following medications: metformin, sulfonylurea, thiazolidinedione; exercise is a dichotomous variable (yes or no) based on self-report of exercising at least one to two times per week; the presence of hypertension is based on either self-report and/or use of medications; presence of snoring is by self-report using the Berlin Questionnaire. Aronsohn, Whitmore, Van Cauter, et al.: Sleep Apnea and Type 2 Diabetes 509 widely used hypoglycemic medications (26–28). Our findings have important clinical implications, as they support the hypothesis that reducing the severity of OSA may improve glycemic control. Thus, effective treatment of OSA may represent a novel nonpharmacologic intervention in the management of millions of patients with type 2 diabetes. Obstructive apneas and hypopneas were more frequent during REM sleep than during other sleep stages, indicating that the prevalence and the degree of severity of OSA in patients with type 2 diabetes may be underestimated when recording times are too short to allow for sufficient amounts of REM sleep to occur. Our findings contrast with the negative results of the only previous study that examined associations between the severity of OSAand HbA1c in patients with type 2 diabetes (4). It is possible that the lack of association in the previous study was due to the short duration ofPSGrecording (reported to be as low as 4 h), and thus perhaps insufficient to detect an association between OSA severity and HbA1c. In contrast, our study design specified a minimum duration of PSG recording of 7 hours, and our subjects achieved 6.6 hours of sleep on average. Of note, in an exploratory reanalysis of our own data set using only the first 4 hours of recording, the robust relationship between severity of OSA and HbA1c found with a PSG recording time of at least 7 hours was much weaker. Compared with patients without OSA (mean adjustedHbA1c 5 7.05%), when only 4 hours of recording were analyzed, the adjusted meanHbA1c levelswere not different in patients with mild OSA (mean adjusted HbA1c 5 6.83%; P 5 0.67), moderate OSA(mean adjusted HbA1c 57.79%; P5 0.28), and severe OSA (mean adjusted HbA1c 5 8.53%; P 5 0.10), indicating that the shorter duration of PSG recording, which precludes observing normal amounts of REM sleep, fails to detect the robust relationship observed with the longer recording time. These findings highlight the importance of obtaining PSG recordings longer than the commonly used minimum of 4 hours to examine associations between OSA severity and metabolic variables. Figure 2. Adjusted mean hemoglobin A1c (HbA1c) values for patients with no, mild, moderate and severe obstructive sleep apnea (OSA). Data were adjusted for age, sex, race, body mass index, number of diabetes medications, level of exercise, years of diabetes, and total sleep time on polysomnogram. Bars represent SEM; P , 0.0001 for linear trend. TABLE 2. SLEEP CHARACTERISTICS: PATIENTS WITH DIABETES ACCORDING TO OBSTRUCTIVE SLEEP APNEA STATUS All patients Patients without OSA Patients with OSA Characteristic ( n 5 60) (n 5 14) (n 5 46) P Value* Actigraphy Sleep duration, h † 6.1 6 1.2 5.7 6 1.0 6.2 6 1.3 0.18 Polysomnography Total sleep time, h 6.6 6 1.1 7.2 6 1.1 6.5 6 1.0 0.02 Sleep efficiency, % 83.1 6 11.6 89.7 6 7.7 81.1 6 11.9 0.01 Sleep latency, min 14.9 6 18.6 9.3 6 7.8 16.7 6 20.5 0.19 Wake after sleep onset, min 66.1 6 50.0 42.0 6 34.0 73.5 6 52.0 0.04 REM, % 22.3 6 7.8 27.0 6 7.2 20.9 6 7.5 0.01 Stage 1 sleep, % 8.5 6 5.3 6.1 6 2.4 9.2 6 5.7 0.06 Stage 2 sleep, % 62.9 6 8.7 59.0 6 9.0 64.1 6 8.3 0.06 Slow wave sleep, % 6.4 6 7.8 7.9 6 8.6 5.9 6 7.5 0.40 Microarousal index per hour of sleep 25.6 6 13.4 20.1 6 10.7 27.3 6 13.8 0.07 Total AHI per hour of sleep 15.2 6 14.8 2.0 6 1.2 19.2 6 14.8 ,0.0001 REM AHI per hour of sleep 27.3 6 21.0 3.4 6 3.4 34.6 6 18.5 0.003 Total obstructive events 96.5 6 89.1 14.8 6 9.1 121.3 6 87.7 ,0.0001 Number of obstructive events in REM sleep 36.5 6 33.9 5.9 6 4.6 45.8 6 33.5 ,0.0001 Total central events 1.7 6 3.8 0.8 6 1.4 2.0 6 4.2 0.30 Total ODI per hour of sleep 11.0 6 12.0 1.1 6 0.6 14.0 6 12.2 0.0002 REM ODI per hour of sleep 22.1 6 18.2 2.3 6 2.2 28.2 6 16.6 , 0.0001 Total no. of desaturations: >3% 69.7 6 71.5 8.0 6 4.8 88.5 6 71.8 0.0001 No. of desaturations in REM sleep: >3% 29.1 6 28.3 3.9 6 2.6 36.7 6 28.1 ,0.0001 Definition of abbreviations: AHI 5 apnea–hypopnea index; ODI 5 oxygen desaturation index; OSA 5 obstructive sleep apnea defined by five or more obstructive apneas and hypopneas per hour of sleep; REM 5 rapid eye movement. Data are given as mean 6 SD. * P values for unadjusted comparisons between patients with and without OSA are determined by t test for continuous variables. † Data for sleep duration measured by wrist actigraphy are reported in n 5 59 subjects. 510 AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE VOL 181 2010 In our sample,OSAwas characterized by a clear predominance of obstructive, rather than central, disease. This is in contrast with findings from the Sleep Heart Health Study (SHHS) (3), in which self-reported diabetes was associated with a significant increase in periodic breathing, an abnormality reflecting disruption of central control of breathing, and a nonstatistically significant increase in the occurrence of central apneas. By contrast, we did not observe periodic breathing pattern in any participant in our study. Consistent with our findings, two previous studies in patients with diabetes with autonomic neuropathy have reported a high frequency of obstructive, rather than central, respiratory events (29, 30). The finding of predominantly obstructive disease in patients with diabetes has important clinical implications, as it would indicate that the available therapies to improve obstructive disease, such as positive airway pressure therapy, oral appliances, and surgical options (31), could have a significant effect on glucose control in patients with type 2 diabetes and OSA. To date, six studies, including a total of 120 patients, have examined the impact of continuous positive airway pressure (CPAP) treatment ofOSA on measures of glucose tolerance in type 2 diabetes (32–37). The study by Babu and colleagues (32) involving 25 obese patientswith diabetes showed beneficial effects of 3 months of CPAP use on HbA1c and postprandial glucose levels, and two other studies (33, 36) reported improvements in nocturnal glucose levels after CPAP. Two earlier studies, including only a total of 10 subjects (34, 35), showed no change in HbA1c levels, but reported improvements in insulin sensitivity (by hyperinsulinemic eugylcemic clamps) after 3–4 months of CPAP. The only randomized controlled study, by West and colleagues (37), which included 20 obese patients with diabetes randomized to the active CPAP arm, found no effect of active CPAP on HbA1c levels or insulin sensitivity, but reported significant improvements in sleepiness measures. Of note, in this study, the average nightly CPAP use over a 3-month period was only about 3.3 hours. By contrast, the positive study by Babu and colleagues found that, in patients who usedCPAP formore than 4 hours per night (average nightly use of z 6.6 h/night), the reduction in HbA1c levels was strongly correlated with CPAP use, suggesting that the negative findings on HbA1c in the study byWest and colleagues could be explained, at least in part, by low CPAP adherence. It is also possible that the efficacy of CPAP varies according to the outcome (i.e., sleepiness versus glucose control), such that the duration and nightly use of CPAP needed to observe significant benefits may not be the same for cognitive versus metabolic outcomes. Our findings regarding the prevalence of OSAin patients with type 2 diabetes are consistent with those of the most recent and largest study, the SleepAHEAD(Action for Health in Diabetes) study, which included 306 obese patients with diabetes, and reported a prevalence of 86% (5). Two earlier studies had estimated the prevalence of OSA in patients with type 2 diabetes using full overnight PSG. First, the SHHS involving older individuals (about 50% .65 yr of age), in whom the diagnosis of diabetes was based on self-report only, found an OSAprevalence of 58% (3). Furthermore, in the SHHS, the definition of hypopneas was based on at least 4% desaturation, whereas, in our study, we used a cutoff of 3% desaturation, which could explain the difference in prevalence estimations (38). The second study (4), which did not specify respiratory event definitions, reported a prevalence of 71%, similar to our findings. Of note, in an exploratory reanalysis of our data using a definition of hypopneas based on a minimum of 4% desaturation, the prevalence of OSA was58%(versus77%with a cutoff of3%desaturation), similar to that reported in the SHHS. Importantly, the associations between OSA severity and HbA1c levels that we observed with a cutoff of 3% desaturation remained significant, albeit somewhat weaker, when the 4% desaturation criterion was used ( P 5 0.007 and P 5 0.013 for total AHI and REM AHI, respectively). These findings suggest that the reliance on strict criteria in definingOSAmay fail to detect patients with milder disease who could nonetheless potentially benefit from treatment. Our study was not designed to examine the mechanisms linking OSA and glucose control in type 2 diabetes. Although it remains possible that hyperglycemia may promote sleep disturbances, the current evidence supports the hypothesis that OSA, and its inherent characteristics, such as intermittent hypoxia, elevated sympathetic nervous activity (39, 40), sleep fragmentation and low amounts of slow wave sleep (41), and cumulative sleep loss (42, 43), has adverse effects on glucose tolerance. Multiple prospective epidemiologic studies have indicated that short sleep and/or poor sleep quality, as is typical of OSA, is associated with an increased incidence of diabetes over time (44– 49). In a recent prospective population study, the presence of moderate to severe OSA was found to be a significant risk factor for incident diabetes during a 4-year follow-up period (50). The present study reveals that the majority of patients with type 2 diabetes have undiagnosed OSA, and that untreated OSA is associated with poorer glucose control, which may instigate the need for more intensive pharmacotherapy. Conversely, treating OSA may have clinically significant beneficial effects on glucose control and reduce the number of drugs needed and/or their dose regimen. Pharmacotherapy of type 2 diabetes with drugs that promote weight gain may have the undesirable consequence of promoting the development of OSA or exacerbating the severity of existing OSA, thereby compromising glycemic control and elevating cardiovascular risk. The high prevalence of OSA and its cardiovascular consequences in type 2 diabetes may help in understanding possible adverse effects of antidiabetic pharmacotherapy. Noteworthy examples are the recent findings of the Action to Control Cardiovascular Risk in Diabetes and Action in Diabetes and Vascular Disease trials that examined the impact of intensive glucose lowering on cardiovascular risk (51, 52). Based on the data from our study, it is likely that OSA was present in most participants in both trials, and that this unrecognized comorbidity may explain the failure of near-normal glucose control to decrease the incidence of major macrovascular events. Consistent with a putative role of OSA in these findings, the ACCORD trial, which had to be terminated early due to unexpected mortality (particularly from cardiovascular causes), enrolled participants who were on average 15 kg heavier at baseline (thus, more likely to have OSA as well as more severe OSA) than those participating in theADVANCEtrial, which did not observe increased mortality or higher incidence of cardiovascular disease. Furthermore, those in the intensive treatment arm of ACCORD gained substantially more weight ( .10 kg in about one-third of the patients) than those in the standard therapy arm, whereas the difference in weight gain between the two treatment arms of ADVANCEwas less than 1 kg. It is well documented that weight gain increases the severity of OSA (53, 54) and thus obese participants in the intensive treatment arm of ACCORD may have been at increased risk for more severe OSA, and thus at increased risk for major cardiovascular events and death. Our findings are also noteworthy in the context of recent reports discussing a possible link between the use and dose of insulin glargine and cancer risk (2). Although the evidence is inconclusive, the questions raised by these reports clearly highlight the importance of developing additional, nonpharmacologic alternatives to offer patients with type 2 diabetes. There is a relentless increase in type 2 diabetes worldwide. Diligent control of glucose levels is needed to prevent or delay the development of life-threatening complications. Most patients are treated with multiple drugs, and a substantial proportion requires insulin injections. This pharmacotherapy is not without risk, and Aronsohn, Whitmore, Van Cauter, et al.: Sleep Apnea and Type 2 Diabetes 511 may promote further weight gain. Our findings indicate that the role of OSA in the management of type 2 diabetes is in urgent need of further rigorous assessment. Current practice approaches should be updated to include systematic evaluation and treatment of OSA in patients with type 2 diabetes. Conflict of Interest Statement : R.S.A. received $50,001–$100,000 as an investigator- initiated research grant from the ResMed Foundation, more than $100,001 as an investigator-initiated research grant from Respironics/Philips, and more than $100,001 (pending) as an investigator-initiated research grant from Amylin, Inc.; H.W. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript; E.V.C. received more than $100,001 as an investigator-initiated research grant from Respironics/Philips, $50,001–$100,000 as an investigator-initiated research grant from the ResMed Foundation, more than $100,001 (pending) as an investigator-initiated research grant from Amylin, Inc.; E.T. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. 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  4. When they say you don't have a current diagnosis, the last time you were diagnosed was over five years ago. Get rediagnosed with all your issues. Also you need to get a nexus letter done for all your issues. Have the provider site all the examples you say you submitted to include your service medical records. If an event took place during active duty such as a rape and you reported it, then you need to get a copy of the investigation or the report you submitted. The VA is reluctant to grant service connection on the basis of your saying it took place w/o any tangable evidence. You need to look in your VCAA letter and your rating decision letter to see if all the evidence you submitted they used. If not, resubmit it because they didn't use it. Last, if you submitted more than eight items, more than likely the VA ignored them. The adjudicator has 20-30 minutes to make a determination on all your issues. To assist the adjudicator, make a list of all issues, then made a file for each issue. Cite all the sources of your information you have used and they have acknowledged. Also cite any new information (and provide that new information). Where possible, do not use 21-4142's. Give them only the information that they ask for. You can go to to access your c&p exams. These are the same exams used for everyone. Also, you can write a statement in support of your claim. Stick to the facts like you did here! Draw conclusions like you were talking about someone else. Emotional issues turn off the VA. Should you not be aware of it, but your entitled to a second opinion. If the VA or it's contractor didn't do the C&P exam properly you can request a second C&P exam (use the exmples from the web site listed earlier). You can fax your C&P to the RO that is adjudicating your claim (always keep a the fax receipt showing it went thru to If you need a copy of the NEXUS letter that you can get your doctor, NP or PA or any or all of your medical providers to write, email me and I'll provide it to you. My email is
  5. I would fax to 540-597-1792 that you request the claim be expidited due to age. Inform the DVA the veteran is 88 yrs old. You will need to put his name, Address, Claim #, dated and signature on it. If the man is near death, a letter from his doctor stating he has less than 30 days to live so the DVA can expidite the claim. He will need to have one of the cancers listed below to qualify for the radiation-exposed veteran. They might not have to do a C&P exam if you/he provided medical evidence he as an active cancer(s). If he is near death, he can have his claim adjudicated in less than 30 days, but if the veteran is only going to use age, then it would probably take about six to seven months from time of filing (at least for the state of Virginia). Best of luck for your friend. PS. Your friend probably is either housebound or needs help in feeding himself, bathing himself and taking his own medicine, then he should apply for what most people call is Aid & Attendence (21-2680) d) Diseases specific to radiation-exposed veterans. (1) The diseases listed in paragraph (d)(2) of this section shall be service-connected if they become manifest in a radiation-exposed veteran as defined in paragraph (d)(3) of this section, provided the rebuttable presumption provisions of § 3.307 of this part are also satisfied. (2) The diseases referred to in paragraph (d)(1) of this section are the following: (i) Leukemia (other than chronic lymphocytic leukemia). (ii) Cancer of the thyroid. (iii) Cancer of the breast. (iv) Cancer of the pharynx. (v) Cancer of the esophagus. (vi) Cancer of the stomach. (vii) Cancer of the small intestine. (viii) Cancer of the pancreas. (ix) Multiple myeloma. (x) Lymphomas (except Hodgkin's disease). (xi) Cancer of the bile ducts. (xii) Cancer of the gall bladder. (xiii) Primary liver cancer (except if cirrhosis or hepatitis B is indicated). (xiv) Cancer of the salivary gland. (xv) Cancer of the urinary tract. (xvi) Bronchiolo-alveolar carcinoma. (xvii) Cancer of the bone. (xviii) Cancer of the brain. (xix) Cancer of the colon. (xx) Cancer of the lung. (xxi) Cancer of the ovary. Note: For the purposes of this section, the term “urinary tract” means the kidneys, renal pelves, ureters, urinary bladder, and urethra. (Authority: 38 U.S.C. 1112©(2)) (3) For purposes of this section: (i) The term radiation-exposed veteran means either a veteran who while serving on active duty, or an individual who while a member of a reserve component of the Armed Forces during a period of active duty for training or inactive duty training, participated in a radiation-risk activity. (ii) The term radiation-risk activity means: (A) Onsite participation in a test involving the atmospheric detonation of a nuclear device. (B) The occupation of Hiroshima or Nagasaki, Japan, by United States forces during the period beginning on August 6, 1945, and ending on July 1, 1946. © Internment as a prisoner of war in Japan (or service on active duty in Japan immediately following such internment) during World War II which resulted in an opportunity for exposure to ionizing radiation comparable to that of the United States occupation forces in Hiroshima or Nagasaki, Japan, during the period beginning on August 6, 1945, and ending on July 1, 1946. (D)( 1 ) Service in which the service member was, as part of his or her official military duties, present during a total of at least 250 days before February 1, 1992, on the grounds of a gaseous diffusion plant located in Paducah, Kentucky, Portsmouth, Ohio, or the area identified as K25 at Oak Ridge, Tennessee, if, during such service the veteran: ( i ) Was monitored for each of the 250 days of such service through the use of dosimetry badges for exposure at the plant of the external parts of veteran's body to radiation; or ( ii ) Served for each of the 250 days of such service in a position that had exposures comparable to a job that is or was monitored through the use of dosimetry badges; or ( 2 ) Service before January 1, 1974, on Amchitka Island, Alaska, if, during such service, the veteran was exposed to ionizing radiation in the performance of duty related to the Long Shot, Milrow, or Cannikin underground nuclear tests. ( 3 ) For purposes of paragraph (d)(3)(ii)(D)(1) of this section, the term “day” refers to all or any portion of a calendar day. (E) Service in a capacity which, if performed as an employee of the Department of Energy, would qualify the individual for inclusion as a member of the Special Exposure Cohort under section 3621(14) of the Energy Employees Occupational Illness Compensation Program Act of 2000 (42 U.S.C. 7384l(14)). (iii) The term atmospheric detonation includes underwater nuclear detonations. (iv) The term onsite participation means: (A) During the official operational period of an atmospheric nuclear test, presence at the test site, or performance of official military duties in connection with ships, aircraft or other equipment used in direct support of the nuclear test. (B) During the six month period following the official operational period of an atmospheric nuclear test, presence at the test site or other test staging area to perform official military duties in connection with completion of projects related to the nuclear test including decontamination of equipment used during the nuclear test. © Service as a member of the garrison or maintenance forces on Eniwetok during the periods June 21, 1951, through July 1, 1952, August 7, 1956, through August 7, 1957, or November 1, 1958, through April 30, 1959. (D) Assignment to official military duties at Naval Shipyards involving the decontamination of ships that participated in Operation Crossroads. (v) For tests conducted by the United States, the term operational period means: (A) For Operation TRINITY the period July 16, 1945 through August 6, 1945. (B) For Operation CROSSROADS the period July 1, 1946 through August 31, 1946. © For Operation SANDSTONE the period April 15, 1948 through May 20, 1948. (D) For Operation RANGER the period January 27, 1951 through February 6, 1951. (E) For Operation GREENHOUSE the period April 8, 1951 through June 20, 1951. (F) For Operation BUSTER-JANGLE the period October 22, 1951 through December 20, 1951. (G) For Operation TUMBLER-SNAPPER the period April 1, 1952 through June 20, 1952. (H) For Operation IVY the period November 1, 1952 through December 31, 1952. (I) For Operation UPSHOT-KNOTHOLE the period March 17, 1953 through June 20, 1953. (J) For Operation CASTLE the period March 1, 1954 through May 31, 1954. (K) For Operation TEAPOT the period February 18, 1955 through June 10, 1955. (L) For Operation WIGWAM the period May 14, 1955 through May 15, 1955. (M) For Operation REDWING the period May 5, 1956 through August 6, 1956. (N) For Operation PLUMBBOB the period May 28, 1957 through October 22, 1957. (O) For Operation HARDTACK I the period April 28, 1958 through October 31, 1958. (P) For Operation ARGUS the period August 27, 1958 through September 10, 1958. (Q) For Operation HARDTACK II the period September 19, 1958 through October 31, 1958. ® For Operation DOMINIC I the period April 25, 1962 through December 31, 1962. (S) For Operation DOMINIC II/PLOWSHARE the period July 6, 1962 through August 15, 1962. (vi) The term “occupation of Hiroshima or Nagasaki, Japan, by United States forces” means official military duties within 10 miles of the city limits of either Hiroshima or Nagasaki, Japan, which were required to perform or support military occupation functions such as occupation of territory, control of the population, stabilization of the government, demilitarization of the Japanese military, rehabilitation of the infrastructure or deactivation and conversion of war plants or materials. (vii) Former prisoners of war who had an opportunity for exposure to ionizing radiation comparable to that of veterans who participated in the occupation of Hiroshima or Nagasaki, Japan, by United States forces shall include those who, at any time during the period August 6, 1945, through July 1, 1946: (A) Were interned within 75 miles of the city limits of Hiroshima or within 150 miles of the city limits of Nagasaki, or (B) Can affirmatively show they worked within the areas set forth in paragraph (d)(3)(vii)(A) of this section although not interned within those areas, or © Served immediately following internment in a capacity which satisfies the definition in paragraph (d)(3)(vi) of this section, or (D) Were repatriated through the port of Nagasaki.
  6. If you wish to appeal, I would write the following: I wish to file a NOTICE of DISAGREEMENT with the rating decision dated MM/DD/YYYY. I wish to appeal the following issues: I wish to have the Decision Review Officer (DRO) adjudicate my appeal. In support of my claim, I have been going to the (give name of the VAMC) since to present. These records will describe the nature and severity of my condition. In my denial, it states there is no current diagnosis of this issue. You will see that I have been diagonsed with the following for my feet (list the diagnosis). If necessary, I am available for an examanation for rating purposes. Your attention to this issue is appreciated. ********************************************************** You can fax this on a 21-4138 to 540-597-1792. You have one year after the rating decision to have this decision adjudicated. Otherwise you will loss all back pay and you will have a higher bar to meet. Best of luck.
  7. If your husband died of a Service Connected Disability or a Presumptive Illness, you should file for DIC. You will need a copy of his WD 53-55 or DD 214 or Statement of Service (if you don't have one, go on line to Google and type in DD214. Go to Archives and fax in a SF 180 requesting a copy). You will need a copy of the Marriage certificate, Death Certificate and if either one of you has been divorced, copy of your divorce decrees for each spouse each time they/you have been married. If your husband did not die of a service connected disability or a presumptive illness but you believe what he died of was service connected or should have been, then you will need a NEXUS letter. Email me at and I will send you one. If you also have problems getting out of your house (you only go out for church, buying food, doctors visits with a few odds and ends) then you should file for House Bound Status. You will need to complete a 21-2680 (you can go to, go to the right hand side click on forms and down load this form. Have your doctor fill it out. If it is going to take a while to gather all this information together, you should file an INFORMAL Claim. You can do this with the following information: Your Name Your Husbands Name Your SSN Your Husbands SSN Your mailing address Dated Signature Write the following: I wish to file a INFORMAL CLAIM for DIC. Fax this to 540-597-1792. This is the Roanoke Va RO. It doesn't matter where you fax it to so long as it gets in the system. This will give you one year to send in your claim and they will pay you from 10/1/2012. There is NO time limit on when you can file for a DIC or Pension claim. Anyone who tells you that is giving you bad information. I hope this helps you out. If you have further questions email me with your phone number and I'll call you and we can talk. Robert F. White Veteran Claims Agent Virginia Department of Veteran Services 5520 Cherokee Ave, Ste 100 Alexandria, Va 22312 Office: 703-813-1544 VBA-21-2680-ARE.pdf VBA-21-534-ARE.pdf VBA-21P-8416-ARE.pdf Nexus Letter.doc
  8. Your husband is wasting his time filing for an increase for Tinnitus. The US Supreme Court ruled in January 2008 that the rating is only 10%. The Court of Appeals for Veterans Claims was the only court that agreed with the DAV that it should be 20%. Between 1992 and 1999 you could get a rating of 0%, 10% or 20% but you had to have a head injury. Then in 1999 congress changed it to 10%. You have a better chance with an increase for Bilateral Hearing Loss. Best of luck.
  9. Rpowell, You should also look at filing for SSDI. If you were in OEF/OIF, let SS know about this and you will go faster. Also let them know about your VA claim so SS can use this information to help adjudicate your claim. Should you be turned down, get an attorney. They will not take the case if they don't think they can win. It is better to get 80% of something than have 100% of nothing. Best of luck.
  10. Westcoast, My record speaks for itself. I am sought out among all the offices in Northern Virginia. May veterans will not go to the DAV and are ignored by the VFW and AL since all they want to do is BDD and Quickstart claims. Having done well over 7350 claims and have very few claims come back totally rejected. I don't feel like I'm being arrogant by pointing out opinions listed as facts. Carlie went into to Hadit to see that I had not been log into it since April, yet their privacy statement says that no one will use my personal information. Yet she did. Fact is, with the best of intentions there is allot of mis information passed that needs to be corrected. Sure there is a lot of good information. That is why I suggested people do their research before opening up an new topic on a topic that has been explored extensively. As for your veteran, has he filed for SSDI, I'm told he has. Has he told DVA that he has filed and they are using that information for his claim. Also to get IU, you can get either the state Voc Rehab agency, the federal Voc Rehab or a private Voc Rehab specialist to state he isn't retrainable and the DVA will grant IU. Still if you can, try and get him 100% schedular. There are a lot of state benefits (depending on which state your in) that a veteran can get in addition to federal benefits. If someone disagrees on this forum and points out that opinions passed as facts are wrong and that is considered arrogant, then maybe your right. ON the other hand, maybe your so used to listening to a mishmas of facts and opinions you rebel against someone that points out what is the facts. You can find an exception to every policy. The problem, the exception a lot of time is reported w/o notifying everyone that this was the 1 in 100,000 chances of winning. Everyone complains that they can't get the exception and they get upset. Everything is in the details. People don't tell the truth. They tell you what they want you to hear. A lot of the truth is personal and no one is going to blast a lot of personal information into one of these forums since it will be there for years to come. So, with limited information, people give advice and it usually will work in a general environment. But for the specific issue, it usually will not work since each persons case is different and unique. That is why I insist on sitting down with my veterans and reviewing all the paperwork with them. I also write up all the correspondence and review it with them. They can request I revise the paperwork and if it works, I will. If they want me to lie, I will not. I will site case law, regulations and laws. By all means, I don't know everything. I have superiors to turn to for advice and I am constantly learning. Someone that does this part time on their own can not keep up with all the changes in the regulations and desires of the DVA. It is hard for someone working in an organization. Please do not see someone who strives to be "all you can be" as arrogant. I find a lot of good information, but I also find old and outdated information since the rules are constantly changing. Best of luck in your helping people.
  11. SPECIAL MONTHLY COMPENSATION isn't +!!!! You put down 100% + SMC. Again, giving an opinion not facts shows you don't know how to present information. As for getting people their IU back when they are working it was because it was marginal employment and if they get audited, the next person could state it isn't marginal employment. Also, it the individual works in the marginal employment too long, the DVA will state that is gainful employment. You have helped people w/o credentials. Try and do a 21-22 now if your not credentialed. It will be rejected. Look up the latest 21-22. Since you can't represent veterans, your providing opinions and your opinions have no facts to support them. You can't interface with the VA for these veterans. I can if they are respesented by either the VFW or American Legion, Red Cross, Marine Corps League, and Fleet Reserve. Also the State of Viriginia too. Can you say something simular? I don't think so. The veteran will have to sign a 21-22a for you to represent them. The call center will only give you a correct answer 36% of the time per a study done 6 yrs ago. I have a network of people that, if necessary, will talk with the individual that makes the decision (the team coach). Allot has changed in the last six months with the VA. You need to update what you know with all the NEW information. What worked a year ago doesn't necessarly work today. A good example would be a FDC. You know about that? How do you use it? When you can't use it? What you need to put into it? Since this is new, I'm sure you don't know all the in's and out of how it is applied. I'm constantly learning about it. You really need to know the rules before you give advice. As for working off the books, I advised people to sell hotdogs at a church function or at an auction. That is what I advised. Sporatic/intermittent work. This type of work is what most people with IU can do anyhow. They also need to check you SSDI to supliment their income. Have you been telling your clients that too! I doubt it. Do you know the different priority levels with the DVA? There are 12. Can you name them? This is seperate from FDC and congressional/presidental complaints. The wealth of information out there is usually gained by experience in working in the system or with the system and not reading rules and providing opinions. There is always an exception, but it isn't the rule.
  12. Interests:I enjoy researching and debate of claims for Clear and Unmistakable Error (C&UE). Service Connected Disability: 100+ Branch of Service: USA YOUR RIGHT. So why do you state your 100%+?
  13. In January of 2008, the US Supreme Court ruled on a DAV suit that Tinnitus is only a 10% rating. Appealing for more is a waste of time. It is my experience that people don't know what is expected of them when they do a C&P exam and they talk TOO much and give out information that is determental to their claim. See the link below and look up every issue the DVA will do a C&P exam on. If you feel the exam was done incorrectly, get the local fax number to your RO (or fax to the Roanoke RO at 540-597-1792) with a statement from you as to why you should get a second C&P exam. Don't give opinions, give facts. They didn't do such an such. The doc spent five minutes with you and was constantly interupted, the doc voiced the opinion from the get go that you were faking it etc. You will stand a much better chance of getting the best possible outcome. Also when it comes to your limbs, you need to move extremely slow and stop at the beginning of pain. If your talking about headaches, and you take off work early and return to work the next day, you didn't take off for a couple of hrs but instead took off for a day. They are looking at severity and how it affects your ability to work. USE their rules, not yours.
  14. You guys missed the point. I do this for a living. I used to do development for the BVA prior to the Appeals Management Center. I also have done claims since 9/2005. I've also worked for the Army Wounded Warrior Program (AW2) at Walter Reed. I've seen a lot and I don't give advice that is based upon opinion. Carlie does. If you read her profile it says so. It also says she is 100%+. There is no 100%+. Also, I stated, if you do your research yourself, you will find that the questions asked on this forum are repeatedly asked. On both HADIT and YUKU. Why not read these answeres. You will find a consistant answer for the question. Many people give opinions, but the people who give facts are right. YES, you can continue to work. You can also go to federal prison. There are rules. Abide by the rules and you will be much safer than if you ignore them. You must learn to play the VA game by their rules, not yours. 2. At the same time your applying for IU, why not apply for SSDI. You can double dip. If you have served in OEF/OIF, then let them know, your claim will be given priority. 3. Always know the rules. If your going to do a C&P exam, study what the examiner is going to look for. See the link: 4. Go to a compentent VSO/NSO not a post service officer. No matter how much experience they say they have, unless they do it full time, they don't know anything. Also pick a VSO/NSO that will return your calls and if they give you advice, ask them to produce the regulation to support their advice. If they can't, find another. 5. Last, DO NOT rely of barracks lawyers. You will find many in these forums. They give opinion's as facts instead, ask for them to provide the facts. You will quickly note they don't have facts and will tell you it's their experience. Experience w/o facts is an opnion. Ignore opinions, everyone one has one and it stinks!
  15. carlie You don't know what your talking about. As I have posted, you can also read the information that has posted on HADIT's sister site. You all really need to read the old postings. These subject keep on coming up over and over again. Really, if you read the old postings, you wouldn't get the same wrong answers from people who don't know what they are talking about. If you need to look up the CFR, go to google, type in ecfr, go to 38 CFR then Ch 3. Instead of asking baracks lawyers, why not do some research first, then ask the moderators (who USED to work for the DVA). When I have a technical question, I contact a fromer DRO who works for my state agency. He is very conservative and since he will give me a conservative answer, I know that if he say's it will work, I will work anywhere. Someone who gives your a liberal answer is doing you a disservice. Check out YUKU. This is the sister site for HADIT. Individual Unemployability Regs - A Must Read Lead [-] Posts: 3725 05/08/03 02:37:14 Admin Emeritus This is the regulation relating to Individual Unemployability. Pay close attention to the part I have highlighted, especially if you are thinking about trying to hold down a part time job. Veterans who show earned income of $6,000 of more, will be reported to the VA duing the IRS computer match. If the income is determined to be enough ( generally above the poverty level) the VA will then schedule the vet for a C&P exam for the purpose of determining if the IU status should remain in effect. Just putting it out front so there are NO surprises! MOM **************************************** 38 CFR §4.16 Total disability ratings for compensation based on unemployability of the individual. (a) Total disability ratings for compensation may be assigned, where the schedular rating is less than total, when the disabled person is, in the judgment of the rating agency, unable to secure or follow a substantially gainful occupation as a result of service-connected disabilities: Provided, That, if there is only one such disability, this disability shall be ratable at 60 percent or more, and that, if there are two or more disabilities, there shall be at least one disability ratable at 40 percent or more, and sufficient additional disability to bring the combined rating to 70 percent or more. For the above purpose of one 60 percent disability, or one 40 percent disability in combination, the following will be considered as one disability: (1) Disabilities of one or both upper extremities, or of one or both lower extremities, including the bilateral factor, if applicable, (2) Disabilities resulting from common etiology or a single accident, (3) Disabilities affecting a single body system, e.g. orthopedic, digestive, respiratory, cardiovascular-renal, neuropsychiatric, (4) Multiple injuries incurred in action, or (5) Multiple disabilities incurred as a prisoner of war. It is provided further that the existence or degree of nonservice-connected disabilities or previous unemployability status will be disregarded where the percentages referred to in this paragraph for the service-connected disability or disabilities are met and in the judgment of the rating agency such service-connected disabilities render the veteran unemployable. Marginal employment shall not be considered substantially gainful employment. For purposes of this section, marginal employment generally shall be deemed to exist when a veteran&#146;s earned annual income does not exceed the amount established by the U.S. Department of Commerce, Bureau of the Census, as the poverty threshold for one person. Marginal employment may also be held to exist, on a facts found basis (includes but is not limited to employment in a protected environment such as a family business or sheltered workshop), when earned annual income exceeds the poverty threshold.Consideration shall be given in all claims to the nature of the employment and the reason for termination. (Authority: 38 U.S.C. 501(a)) (b) It is the established policy of the Department of Veterans Affairs that all veterans who are unable to secure and follow a substantially gainful occupation by reason of service-connected disabilities shall be rated totally disabled. Therefore, rating boards should submit to the Director, Compensation and Pension Service, for extra-schedular consideration all cases of veterans who are unemployable by reason of service-connected disabilities, but who fail to meet the percentage standards set forth in paragraph (a) of this section. The rating board will include a full statement as to the veteran&#146;s service-connected disabilities, employment history, educational and vocational attainment and all other factors having a bearing on the issue.