text:
Genetic Counseling for Diabetes Mellitus
- First Online:
DOI: 10.1007/s40142-014-0039-5
- Cite this article as:
- Stein, S.A., Maloney, K.A. & Pollin, T.I. Curr Genet Med Rep (2014) 2: 56. doi:10.1007/s40142-014-0039-5
Most diabetes is polygenic in etiology, with (type 1 diabetes, T1DM) or without (type 2 diabetes, T2DM) an autoimmune basis. Genetic counseling for diabetes generally focuses on providing empiric risk information based on family history and/or the effects of maternal hyperglycemia on pregnancy outcome. An estimated one to five percent of diabetes is monogenic in nature, e.g., maturity onset diabetes of the young, with molecular testing and etiology-based treatment available. However, recent studies show that most monogenic diabetes is misdiagnosed as T1DM or T2DM. While efforts are underway to increase the rate of diagnosis in the diabetes clinic, genetic counselors and clinical geneticists are in a prime position to identify monogenic cases through targeted questions during a family history combined with working in conjunction with diabetes professionals to diagnose and assure proper treatment and familial risk assessment for individuals with monogenic diabetes.
KeywordsDiabetesGenetic counselingMonogenic diabetesType 1 diabetesType 2 diabetesGestational diabetes
Diabetes mellitus (commonly referred to as "diabetes" but distinguished from the far less common condition of diabetes insipidus) is a group of metabolic disorders characterized by elevated blood sugar levels that results from insulin deficiency, insulin resistance (defect in the body's ability to use insulin), or a combination of both. Insulin is secreted from the pancreas and enables cells to use glucose for energy. Diabetes is a major cause of morbidity and mortality, with 8.3 % of the US population (25.8 million people) affected as of 2011 [1]. Chronic hyperglycemia can result in damage to different organ systems including the eyes, heart, kidneys, nerves, and blood vessels. Diabetes is the leading cause of kidney failure, non-traumatic lower-limb amputations, and new cases of blindness among adults and is the seventh leading cause of death in the US, killing more than 1.4 million people worldwide in 2011 [2]. Diagnosing and treating diabetes effectively is paramount to preventing complications.
The etiology of diabetes is highly heterogeneous. The American Diabetes Association (ADA) has classified diabetes into four categories: type 1 diabetes mellitus (T1DM), caused by autoimmune destruction of the pancreatic β-cells; type 2 diabetes mellitus (T2DM), itself a highly heterogeneous group of disorders involving insulin resistance combined with relative insulin deficiency; gestational diabetes mellitus (GDM); and other specific types, another heterogeneous group which includes, among others, forms of diabetes resulting from the inheritance of a mutation in a single gene (monogenic diabetes) [3••].
Knowing the etiology is important so that therapy can be tailored, glycemic control obtained, and complications prevented or reduced in severity. Yet there is increasing evidence that subtype misdiagnosis is common, with a recent study published in 2013 showing that 94 % of children and adolescents with the most common forms of monogenic diabetes (maturity onset diabetes of the young, or MODY) were misdiagnosed, mostly as T1DM or T2DM, and 76 % were receiving the wrong treatment [4••].
Additionally and highly relevant here, since nearly all diabetes has a genetic component ranging from monogenic to polygenic, identifying the specific diabetes subtype allows for more precise risk assessment in family members and allows family members to benefit from a more tailored treatment approach. In this review, we provide a brief overview of the types of diabetes, how they are treated, how they are inherited, and what is currently understood about their genetic etiology and its current implications for use of genetic testing. We then propose a multidisciplinary approach to assuring that individuals with diabetes receive the correct genetic diagnosis and treatment.
Background, Etiology and Practical Genetics Issues by ADA Diabetes Category
T1DM, responsible for about 5–10 % of diabetes cases, results from absolute insulin deficiency, most commonly due to an autoimmune process destroying the pancreatic β-cells. Patients are characteristically young and thin, and many present with severe hyperglycemia in diabetic ketoacidosis. Insulin autoantibodies can be detected in the blood of about 85–90 % of individuals [3••]. More recently, it has become apparent that T1DM can have a later and more insidious onset, sometimes known as latent autoimmune diabetes of adulthood (LADA), which may be incorrectly diagnosed initially as T2DM [5]. T1DM was in the past known as insulin-dependent diabetes mellitus (IDDM) or juvenile diabetes, terms that have fallen out of favor in the quest to categorize diabetes by etiology rather than treatment and in recognition of the ability of T1DM to affect adults. Individuals with T1DM ultimately require insulin for treatment because of loss of β-cells and consequent lack of insulin production.
The largest known genetic contributor to T1DM susceptibility is variation at the human leukocyte antigen (HLA) locus, with some haplotypes having odds ratios (OR) as high as 11 [6], followed by over 40 other primarily genome-wide association study (GWAS)-derived loci with effect sizes ranging from 1.09 to 2.38 [7]. Discovery of these variants is enhancing the ability to understand the physiology of T1DM. However, attempts to build clinically useful models for predicting T1DM risk from these variants have not been successful, and it has been suggested that this would not change with the elucidation of the entire genetic architecture of T1DM [8]. There are ongoing efforts that utilize pre-symptomatic genotyping at the HLA locus to identify individuals at risk and evaluate environmental predictors [9], but to date genetic testing is not considered to be a useful clinical tool in T1DM. Thus, in cases of confirmed T1DM, genetic risk counseling appropriately focuses on empiric risk based on family history.
T2DM, responsible for about 90–95 % of diabetes cases, refers to a heterogeneous group of disorders characterized by a combination of insulin resistance (limitations in the ability to utilize insulin effectively) with a relative insulin deficiency. There is a strong complex and polygenic underlying genetic effect on susceptibility, and factors such as overweight/obesity, sedentary lifestyle and/or aging increase insulin resistance and promote the development of T2DM in susceptible individuals. T2DM is arguably a diagnosis of exclusion since all non-pregnancy diabetes not due to autoimmune processes or a specific known etiology falls into this category. T2DM was in the past known as non-insulin-dependent diabetes mellitus (NIDDM) or adult onset diabetes, terms that have fallen out of favor in the quest to categorize diabetes by etiology rather than treatment and in recognition of the increasing number of children diagnosed with T2DM.
T2DM can be treated with oral agents and in some cases diet and exercise alone, but some affected individuals require insulin depending on the degree of insulin resistance and deficiency and disease duration. Metformin is considered first-line therapy and works partly by reducing insulin resistance [10, 11]. T2DM is highly heterogeneous in etiology and finding the most efficacious treatment can be challenging; for example, not all individuals respond to metformin.
As with T1DM, the genetic architecture of T2DM is complex. To date, variants in at least 65 genetic loci have been implicated in T2DM susceptibility, which together explain approximately 10–11 % of the variance [12••]. Although genetic risk profiling for T2DM is offered by some companies, it does not currently have proven clinical utility [13, 14]. Thus, similar to T1DM, genetic counseling in cases of confirmed T2DM currently focuses on family history-based recurrence risk. The ADA recommends that early (before age 45) testing for T2DM [via fasting or random glucose, oral glucose tolerance test or HBA1c (glycosylated hemoglobin)] be considered in individuals who are overweight [body mass index (BMI) ≥25 kg/m2] and have one or more additional risk factors, one of which is a first-degree relative with diabetes [15].
Treatment, prognostic and genetic counseling implications of distinguishing selected high-penetrance single-gene forms of diabetes from other types of diabetes
Molecular diagnosis
Medical implications
Prognostic implications
Implications to family members
Low-dose sulfonylureas instead of insulin
Progressive, high complication risk
Autosomal dominant [16]
Low-dose sulfonylureas more effective than metformin
No treatment/diet only instead of insulin
Non-progressive, low complication risk
Autosomal dominant [16]
No treatment/diet only; oral agents not recommended
KCNJ11 or ABCC8
KATP channel-related permanent neonatal diabetes (PNDM)
T1DM or other form of PNDM
High-dose sulfonylureas instead of insulin; may be able to taper dose with time
Most remain stable over time; remit in 10 % of cases
Autosomal dominant, usually de novo [16]
Abnormality of 6q24 PLAG/HYMAI imprinted region
Transient neonatal diabetes (TNDM)
T1DM or other form of NDM
Insulin at diagnosis until remission; may require oral agents or insulin upon relapse
Watch for remission and ability to taper off insulin; watch for relapse in later childhood
Tiered testing/counseling approach depending on type of defect (paternal UPD, paternally derived duplication, global imprinting defect) [78, 79]
Maturity-onset diabetes of the young (MODY) is the most common type of monogenic diabetes and results from one of several single gene defects in β-cell function. It is inherited in an autosomal dominant manner. In the classic criteria, patients typically present with diabetes at a young age (<25 years), are not necessarily obese, continue to make insulin, lack T1DM-related autoantibodies, and have other family members with diabetes [17, 18]. However, these criteria are likely too narrow. MODY can often be mistaken for both T1DM and T2DM because of overlapping characteristic features. To date, 13 different genes have been implicated in causing MODY [19–23]. Most commonly, MODY results from mutations in transcription factor genes involved in the insulin secretion/β-cell development pathways. Mutations in HNF1A, encoding the transcription hepatic nuclear factor 1α (HNF1α), results in MODY3, the most frequent MODY subtype, responsible for 52 % of MODY cases [24, 25]. Mutations in GCK, encoding the enzyme glucokinase, are implicated in 32 % of MODY cases [26–29]. About 10 % of MODY cases are due to mutations in HNF4A (MODY1), encoding the transcription factor HNF4α. The other genes with mutations more rarely causing MODY include IPF-1 (MODY4), HNF1B (MODY5), NEUROD1 (MODY6), KLF11 (MODY7), CEL (MODY8), PAX4 (MODY9), INS (MODY10), BLK (MODY11), ABCC8 (MODY12), and KCNJ11 (MODY13) [22, 23, 30, 31]. Still, some families with MODY remain genetically unexplained (MODY-X), but with advancements in DNA sequencing techniques, additional genes will continue to be identified [23].
Patients with transcription factor MODY subtypes develop progressive hyperglycemia, typically in adolescence or early adulthood [32]. They are at risk for diabetes-related complications if not treated and so require appropriate monitoring including regular eye and foot exams and screening of the urine for microalbuminuria (the earliest detection for kidney disease) [33]. Patients with HNF1A (MODY3) and HNF4A (MODY1) mutations are especially sensitive to low doses of the sulfonylurea class of antidiabetic agents, which should be tried first, although some still may require insulin, especially at later stages [33–35]. This is in contrast to standard of care for T1DM, where insulin is started immediately upon diagnosis, and T2DM, for which metformin is the first-line treatment. Therefore, distinguishing at least these types of transcription factor diabetes from T1DM and T2DM is paramount.
GCK-MODY (MODY2) characteristically presents with stable, mildly elevated blood glucoses that do not progress or cause complications. Therefore, these patients' glucoses can be monitored intermittently but most do not necessitate treatment [36]. Since T1DM can present with mild hyperglycemia if diagnosed through routine screening, identifying a GCK mutation can prevent unnecessary invasive and possibly harmful treatment with insulin. As discussed below, GCK mutations increase the risk for GDM, and there appears to be value for optimal pregnancy management in knowing the maternal and fetal mutation status.
Those with MODY5, due to HNF1B mutations, can have developmental problems of the kidneys (most often cysts) and so require co-management by nephrologists [37]. Because of the coexisting renal problems, MODY5 is often classified instead as a syndrome (renal cysts and diabetes syndrome, or RCAD), and poor kidney function in the presence of good glucose control can be a clue to the presence of an HNF1B mutation [38].
Neonatal diabetes is a rare (1/100,000 newborns) monogenic diabetes subtype that presents in the first six months of life, and can be transient (TNDM) or permanent (PNDM) [39]. PNDM most often results from activating mutations in the KCNJ11 gene encoding the pore-forming Kir6.2 subunit of the potassium-sensitive ATP (KATP) channel (57, 58), which in some cases also cause developmental delay and seizures. Most patients with neonatal diabetes due to mutations in KCNJ11 and ABCC8, which encodes the sulfonylurea receptor (SUR) subunit of the KATP channel, can be successfully treated with high doses of the sulfonylurea class of antidiabetic agents. These should be chosen as first-line therapy [40–42], in contrast to other cases of neonatal diabetes, which are treated with insulin. Thus, it is essential for clinical care that any infant diagnosed with diabetes be tested for mutations in these genes, since such a diagnosis makes treatment less invasive and more effective.
Abnormalities leading to overexpression of the imprinted genes PLAGL1 and HYMAI on chromosome 6q are the most common cause of TNDM, accounting for about 70 % of cases, and may also result in accompanying macroglossia or umbilical hernia [43–45]. At onset, TNDM is treated with insulin. Spontaneous remission occurs at a mean age of 4.5 months, at which point therapy can be stopped. Relapses occur in about 50 % of cases during childhood or adolescence, and so these patients and their families need counseling on the symptoms of hyperglycemia and intermittent monitoring of their glucoses after initial remission [43, 45]. On relapse, some require insulin for treatment, whereas others can be managed on pills [39, 41]. Several other genes are implicated in neonatal diabetes including INS, GCK, PDX1, HNF1B, and EIF2AK3.
Genetic syndromes with diabetes as a key feature
Extra-pancreatic features
EIF2AK3 (2p11.2)
Epiphyseal dysplasia, renal, and/or hepatic impairment, intellectual disability, developmental delay
Usually within first 3 years of life
Autosomal recessive [80]
FOXP3 (Xp11.23)
Immunodysregulation, polyendocrinopathy, and enteropathy, X-linked (IPEX)
Only males, chronic diarrhea with villous atrophy, thyroid and pancreatic autoantibodies, thyroiditis, eczema, anemia
Median diagnosis of 6 weeks
Immunosuppresents ± steroids, insulin, antibiotics, bone marrow transplantation (can resolve symptoms if performed early)
X-linked [81]
KCNJ11 (11p15.1)
Developmental delay, epilepsy, and neonatal diabetes (DEND)
Developmental delay, generalized epilepsy, diabetic ketoacidosis (DKA)
Median diagnosis of 6 weeks
Sulfonylurea pills
Autosomal dominant [82]
WFS1 (4p16.1)
Wolfram/diabetes insipidus, diabetes mellitus, optic atrophy, and deafness (DIDMOAD)
Progressive optic atrophy, bilateral sensorineural deafness, truncal ataxis,
Under age 16 (mean 6 years)
SLC19A2 (1q24.2)
Thiamine responsive megaloblastic anemia (TRMA)/Roger's syndrome
Megaloblastic anemia, sensorineural deafness
Between infancy and adolescence
Insulin, large doses of thiamine (effective in some patients)
HNF1B (17q12)
Renal cysts and diabetes RCAD/MODY5
Renal cysts, renal dysplasia, uterine and genitalia developmental anomalies, hyperuricemia, gout, abnormal liver function tests
Before age 25
Insulin (not sensitive to sulfonylurea pills)
Autosomal dominant [87]
Mitochondrial genes (MTTL1 3243A > G most common)
Maternally inherited diabetes and deafness (MIDD)
Sensorineural deafness, short stature, stroke-like episodes
Mitochondrial (maternal) [88]
Loss of expression of paternally inherited genes (15q11.2-q13)
Prader-Willi syndrome
Hypotonia, poor suck, global developmental delay, small hands and feet, hyperphagia, cognitive impairment, hypogonadism
Dietary, ±growth hormone, glucagon-like peptide-1 (GLP-1) therapy
II: LMNA (1q22)
III: PPARG (3p25)
Familial partial lipodystrophy types II and III
Loss of total or partial subcutaneous fat, hirsutism, acanthosis nigricans
Congenital or adolescence
Metformin, U500
Autosomal dominant [92]
INSR (19p13.2)
Growth retardation, abnormal dentition, acanthosis nigricans, enlarged genitalia, coarse facies
Pharmacologic doses of human leptin
INSR (19p13.2)
Type A insulin resistance
Acanthosis nigricans, polycystic ovary syndrome (PCOS), hirsutism
Recombinant insulin-like growth factor I (IGF-1) helpful in some cases
INSR (19p13.2)
Leprechaunism (Donohue syndrome)
Abnormal facies, large genitalia, small for gestational age, and growth retardation
IGF-1 helpful in some cases
GDM is hyperglycemia first diagnosed during pregnancy, a time of insulin resistance induced by placental hormones [46]. Women diagnosed with GDM are at a significantly increased risk for developing T2DM later in life [47]. For some women, a diagnosis of GDM may be the first recognition of pre-existing T2DM, which can be asymptomatic. Maternal hyperglycemia in the third trimester is associated with adverse maternal, fetal, and neonatal outcomes including macrosomia and perinatal distress. It is also well-known that pre-existing maternal hyperglycemia increases the risk for certain congenital malformations. Therefore, diagnosis and effective treatment are essential [48]. Treatment of GDM can include lifestyle therapy with diet and exercise, or pharmacological therapy with antidiabetic pills or insulin, depending on the degree of hyperglycemia [49]. In addition, screening for diabetes is recommended 6 to 12 weeks postpartum given the increased risk.
GDM is often viewed not as a specific disease, but as a manifestation of underlying glucose intolerance brought out by the insulin sensitivity-challenging conditions of pregnancy, and this is borne out by the association of T2DM variants with GDM [50]. For example, the TCF7L2 rs7903146 variant conferred an increased risk (1.56- to 2.69-fold for heterozygotes, 2.05- to 3.25-fold for homozygotes compared with non-carriers) [51–53]. Numerous other T2DM-susceptibility variants have been associated with GDM as well [52, 54–58]. Similar to T2DM, these common variants do not currently lend themselves to clinically useful genetic testing. Thus, similarly, family history of both GDM and T2DM can be used as a guide to estimate the risk of GDM.
An area that brings relevance of genetic counseling and testing to GDM is the effect of maternal and fetal genotypes on birth weight, as has been observed with the GCK gene, in which mutations cause a monogenic form of diabetes called MODY2. As discussed in the preceding section, MODY2 is a mild condition that manifests as elevated fasting glucose beginning at birth, often does not present as overt diabetes, generally does not require treatment outside of diet, and is associated with a low rate of complications. However, women with GCK mutations but without overt diabetes have a high likelihood of developing gestational diabetes, often beginning early in pregnancy [59]. Based on the study of several large pedigrees, maternal GCK mutations not passed to the fetus resulted in large babies (86th percentile on average), as expected in GDM. In contrast, paternally inherited fetal GCK mutations resulted in small babies (24th percentile). GCK mutations passed from mother to fetus resulted in average weight babies (53rd percentile) [60]. These findings can be explained by fetal mutations causing reduced glucose sensing and insulin secretion and consequent growth retardation. Maternal mutations compensate by creating a hyperglycemic environment that stimulates increased fetal insulin secretion [60–62]. In a case report, aggressive treatment of GDM with insulin throughout two pregnancies in a GCK mutation carrier resulted in the birth of one baby who inherited the mutation and was in the lowest percentile for weight and a second baby who did not inherit the mutation but was of normal weight [63]. These findings suggest that determining the GCK-mutation status of women with GDM and their infants could be useful in deciding how aggressively to treat the maternal hyperglycemia.
It is not known how prevalent GCK mutations are in GDM, but studies in various populations have estimated 5 % [64–66]. One study selecting 15 women on specific criteria (fasting hyperglycemia outside pregnancy, insulin required during but not outside pregnancy, limited 2 h glucose increase, and first-degree family history) found mutations in 80 % [67]. Very recently, a population-based study in Ireland found evidence that combined criteria of a BMI <25 kg/m2 and fasting glucose ≥5.5 mmol/l could identify women with GCK mutations with a sensitivity of 68 % and specificity of 98 % [68•]. It is not yet known how well these criteria apply to other populations, but the findings reported in the preceding paragraph indicate that knowing the maternal GCK status would be useful during pregnancy. While determining the baby's mutation status would currently require an invasive test such as amniocentesis, it has been suggested that serial fetal abdominal scans be used to monitor growth in women with GCK mutations [63]. Given that currently (based on a survey reported in 2004) fetal growth in GDM is monitored by ultrasound by only 7 % of OB/GYNs [69], knowledge that the fetus inherited GCK-mutation-induced delayed insulin release could serve as a potential tool for selecting women for more intensive monitoring and potential avoidance of aggressive glucose control during the current and future pregnancies in the presence of a GCK mutation. As the genetic architecture of diabetes continues to be elucidated, other genetic variants could serve as a source of information to guide pregnancy management as well.
Genetic Counseling and Testing in Diabetes
The Clinical Challenge
Anecdotal and survey evidence suggests that a personal or family history of diabetes is rarely a presenting indication for genetic counseling, other than for women with diabetes seeking to understand the risks to the pregnancy associated with exposure to maternal hyperglycemia. When diabetes is encountered in a family history taken for other genetic indications, counselors typically ask patients what type of diabetes, and, if not known, age of onset and whether insulin is used. Patients are then advised that there is an increased risk for diabetes in relatives of individuals with diabetes. Empiric risk figures based on the apparent type of diabetes (1 or 2), such as those presented in Harper [70], are sometimes provided along with an explanation of their limitations.
In the diabetes clinic, both MODY and neonatal diabetes are often misdiagnosed as T1DM and T2DM [4, 71]. When antibody-negative subjects diagnosed with diabetes at less than 20 years old were sequenced for mutations in the HNF1A, HNF4A, and GCK genes, 36 and 51 % were found to be previously misdiagnosed as having T1DM and T2DM, respectively [4••]; 67 % of those diagnosed with diabetes at less than six months old with KCNJ11, ABCC8, and INS gene mutations carried the wrong diagnosis of T1DM [72••]. The molecular diagnosis is often missed because they share similar characteristics with both T1DM and T2DM, and we do not have a validated screening tool to find cases. In addition, healthcare providers are not as well versed on these rarer subtypes as school curricula and medical training tend to focus on the more common T1DM and T2DM. Further compounding the problem is the lack of access to and cost of diagnostic testing.
In sum, current clinical practices do not favor the identification of patients with highly genetic forms of diabetes that may benefit from molecular diagnosis in either the genetics clinic or the diabetes care setting.
Improving the Pickup Rate for Monogenic Diabetes
Properly diagnosing highly genetic forms of diabetes is critical so that patients can potentially go on more optimal therapy (i.e., an oral sulfonylurea agent rather than insulin) for an improved quality of life and often improved glycemic control. Making the proper diagnosis also allows us to predict the clinical course, explain associated clinical features (i.e., renal disease with MODY5), and diagnose family members early to get them on treatment and hopefully prevent complications from developing. Since it appears that highly genetic forms of diabetes are currently unlikely to be identified in either a genetics or diabetes setting, a new model is needed in which each individual with diabetes has the opportunity to be considered for the possibility of diabetes.
Equal Opportunity for All: Screening and Testing for Monogenic Diabetes in the Diabetes Clinic
In the diabetes clinic, we propose a tiered screening approach in which the target population is all individuals with diabetes. We have begun to implement this approach in the University of Maryland Center for Diabetes and Endocrinology Personalized Diabetes Medicine Program (PDMP) on a research basis. Each new and returning patient with diabetes completes a quick survey consisting of seven yes/no questions that identify patients with a high likelihood of monogenic diabetes. Currently the survey is completed on paper, but development of an electronic version that can integrate with the electronic health record is planned. Patients referred by providers or screening positive on the questionnaire with one of the following profiles are selected for further evaluation: diabetes diagnosed <1 year of age, diagnosed with T1DM and having a parent with T1DM, diagnosed with T2DM at <30 years old and not obese at diagnosis, diagnosed with T2DM at <45 years of age and two or more first- or second-degree relatives diagnosed <50 years of age, or presence of diabetes plus an extrapancreatic feature that may be indicative of a syndrome. Further evaluation using a combination of laboratory testing (C-peptide and IA-2 antibodies) and family and medical history elicited by a genetic counselor is used to determine eligibility for testing.
Testing for the most well-known and clinically actionable forms of monogenic diabetes is currently available in several clinical laboratories. However, the cost of standard Sanger sequencing and sometimes lack of insurance coverage for sequencing several genes that may be implicated can discourage testing. Therefore, several groups outside the US [73•, 74•, 75•] have developed monogenic diabetes panels that utilize next-generation sequencing technologies to test patients suspected to have any type of monogenic diabetes simultaneously for coding mutations in 30 or more genes. We are currently developing such a panel.
Besides the screening and testing algorithm and panel, we are developing protocols for incorporating molecular diagnosis into the electronic health record and using it to inform patient care. Thus, as with any screening program, there are three main goals to our PDMP: to provide the entire target population access to personalized diabetes care; to facilitate accurate follow-up diagnostic testing; and to educate and make available appropriate intervention when a diagnosis is made. We are in the process of extending this approach into primary care settings, where many patients with diabetes are seen for most of their care, and collecting outcome data on the PDMP in order to determine efficacy of this approach so that it can be implemented on a more widespread basis and more specific clinical practice recommendations can be developed. While a genetic counselor is part of the clinical team in our current approach, we recognize that this is unlikely to be possible in all specialty and primary care clinics where people with diabetes are diagnosed and treated. Thus, an important component of a more widespread screening and testing program will be the development of guidelines for referring to genetic counselors and clinical geneticists for evaluation and counseling once a diagnosis has been made. For example, in cases of suspected mitochondrial disorder, we recommend that the patient/family be referred to a clinical geneticist for further evaluation and a thorough discussion of maternal inheritance. We believe that most effective will be a team approach, in which practitioners in diabetes care and genetics engage each other in a reciprocal relationship to assure the optimal diagnosis and treatment of these patients.
The Genetic Counseling Session: A Golden Opportunity for Case Identification
Individuals who have neither neonatal onset nor a syndrome can be evaluated for scenarios that, based on published guidelines or research [15, 76, 77••], are consistent with monogenic diabetes: (1) diagnosis of T1DM in a parent and child, (2) diagnosis of T2DM before age 30 in the absence of obesity, and (3) diagnosis of diabetes before age 45 and two first-degree relatives in the same lineage diagnosed with diabetes before age 50. We have developed this third criterion as a starting point to use family history to increase the pickup rate over more strict age and obesity criteria. For family members meeting these criteria, the genetic team could work with the diabetes team to determine whether the individual was antibody negative and C-peptide positive, in which case MODY testing would be considered. Finally, those not meeting any of the criteria above would be considered to have T1DM or T2DM based on history, and empiric risk counseling could be provided. While, as stated earlier, common genetic variant susceptibility panels have not proven to be a useful approach for modifying risk for T1DM and T2DM, the polygenic burden approach, in which models constructed from several hundred thousand SNPs currently under study may prove useful in the future, particularly in the absence of available or extensive family history information.
Education is key
In order to increase recognition of these rarer subtypes of diabetes, it is important to include information about monogenic diabetes and features that distinguish it from T1DM and T2DM in medical school, genetic counseling, residence, and fellowship curricula. Primary care physicians, endocrinologists, diabetes educators, genetic counselors, and geneticists are especially likely to see these patients in their clinics and need to be ready to recognize them.
The etiology of diabetes is extremely heterogeneous. While most individuals have T1DM or T2DM and complex inheritance, some diabetes results from a mutation in a single gene. Many of the relevant genes have been known for nearly two decades, but these forms of diabetes remain vastly underdiagnosed. Properly diagnosing monogenic diabetes can have a profound impact on health and quality of life. It is hoped that the information provided in these pages will arm both genetics and diabetes professionals with the tools to begin to work cooperatively to identify, diagnose, and provide these individuals with optimal care.
We thank Dr. Alan Shuldiner, Ms. Kathleen Palmer and the Personalized Diabetes Medicine Program (PDMP) staff and participants for making the PDMP and insights gained from it possible.
SA Stein declares no conflicts of interest. KA Maloney declares no conflicts of interest. TI Pollin has received a speaker honorarium and reimbursed travel expenses from the American Diabetes Association.
Human and Animal Rights and Informed Consent
All studies by the authors involving animal and/or human subjects were performed after approval by the appropriate institutional review boards. When required, written informed consent was obtained from all participants.


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Travelodge Newport Area/Middletown places you within 2 miles (3 km) of Prescott Farm and Newport Vineyards. This 77-room motel welcomes guests with free breakfast and conveniences like an outdoor pool and free in-room WiFi. Naval War College Museum and Touro Synagogue are also nearby.
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Renovated in 2014, Travelodge Newport Area/Middletown offers an outdoor pool, free WiFi in public areas, and a business center. There's free parking if you drive. The 24-hour front desk has staff standing by to help with dry cleaning/laundry and securing valuables. Additional amenities include a seasonal outdoor pool, coffee/tea in a common area, and a computer station.
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Travelodge Newport Area/Middletown1185 W Main Rd Middletown RI 02842
Hotel Amenities
Hotel Amenities
A computer station is located on site and high-speed wireless Internet access is complimentary. This motel offers access to a business center. A complimentary breakfast is offered each morning. This Middletown motel also offers an outdoor pool, coffee/tea in a common area, and complimentary newspapers in the lobby. Complimentary self parking is available on site. A total renovation of this property was completed in March 2014.
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- Number of floors - 2
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- Free WiFi
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Available in all rooms: Free WiFi
Available in some public areas: Free WiFi
Free self parking, RV, bus, truck parking, Free RV, bus, truck parking
Room Amenities
- Free WiFi
- Free cribs/infant beds
- Free newspaper
- Refrigerator
- Coffee/tea maker
- Phone
- Private bathroom
- Hair dryer
- Iron/ironing board
- Television
- Desk
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- Separate bathtub and shower
- Access via exterior corridors
- Air conditioning
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Where to Eat
Guests are offered a complimentary continental breakfast each morning.
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The recreational activities listed below are available either on site or nearby; fees may apply.
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by Nelson Mandela
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Read by Danny Glover, with an introduction by Kofi Annan. Nelson Mandela is one of the great moral and political leaders of our time: an international hero whose lifelong dedication to the fight against racial oppression in South Africa won him the Nobel Peace…
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Contiene sus alegatos desde el banquillo de los acusados: "Un hombre negro en un tribunal blanco" y "Estoy dispuesto a morir." Sección de fotos de 16 páginas.
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Skip to comments.Closer Scrutiny Reveals the Lies Surrounding Katrina Evacuation and Recovery - CORRECTED
Posted on 09/05/2005 7:24:35 PM PDT by WriterInTX
Having lived on Long Island for most of my life, I weathered only the most minor effects of hurricanes. Typically, their devastating strength drained along the coastline as they churned northwards. When I was a child, my father comforted me through Hurricane Belle; not by holding me and telling me everything would be alright, but by his activity in securing our house, his purchase of supplies and preparations, and his explanations of hurricanes and their threats.
While the storm whipped overhead, my piqued curiosity prompted me to ask about all different kinds of natural disasters. We passed the time discussing typhoons, tornadoes, earthquakes, and floods. I never thought I would use this information, but I did; twice.
At 19, my passenger and I found ourselves caught in the only flash flood in the history of Long Island. What started as a heavy rain became an overwhelming downpour within minutes. Not unlike the City of New Orleans, the patch of road on which I traveled was nestled in a natural funnel. In the space of minutes, we experienced more rain in that small bit of road alongside Eisenhower Park than all of Long Island had received in a year. With traffic surrounding me, I had not choice but to inch forward to the overpass that would take me to higher ground. Just moments before my car cleared the water now pouring in under my doors, the engine stalled, and my Monte Carlo sank back down the embankment, eventually to be completely submerged.
We had to wait until the water rose inside the car and the pressure stabilized before we could get out.
The gas pumps at the corner station began bubbling up, turning the water so black you couldnt see your hand just two inches under the surface. An elderly man, trapped in his car, didnt want to leave. Plodding through chest deep water, my passenger and I managed to get his door open and help him slog back to safety.
Everyone caught in that mess experienced a loss, but it is nothing compared to Katrina.
The second time I used my fathers sage advice came when I moved to Texas. In the bottom tip of the tornado belt, I knew what to do when the sky turned an ominous shade of green, the clouds started rotating above my head, and where to seek shelter to maximize my potential for living. It was in those few moments, when the doors and windows rattled and I imagined that my new house would be reduced to kindling around me, that all my priorities changed forever.
The folks in Louisiana and Mississippi experienced wide scale devastation during Katrina. New Orleans, and other parts of the coast, experienced a second, even more devastating blow from the horrible flooding. One is bad enough, but both? Its a catastrophe beyond comprehension, and our fellow Americans need our compassion, our generosity, and our understanding as they rebuild their entire lives.
We should be coming together, as we did after other catastrophic events in the last decade, to help and heal.
Sadly, that is not the case.
What I find astonishing is the almost immediate response from Bush Bashers to blame everything that happened, from the actual hurricane itself, to the anarchy that quickly erupted, on the President and his administration. When they do so, they not only distort the truth, they outright lie to the public, and they are doing so daily through any media venue that will give them the opportunity.
Lie #1: President Bush doesnt care about the people of New Orleans.
This outrageous lie is thoroughly debunked by the fact that it was President Bush who pushed for a mandatory evacuation of New Orleans.(1) Governor Blanco issued only a voluntary evacuation order, but admitted that she received a call from the President on August 27, 2005, urging her to make it a mandatory one. He wanted as many people as possible out of the path of the storm.
So much for the President not caring.
Despite the fact that New Orleans own Emergency Response Guidelines call for a mandatory evacuation of the City if a strike by a Category 3 Hurricane is projected, with 72 hours advance notice to all residents, Mayor Nagin didnt order a mandatory evacuation until Sunday. Further, he only did so after Max Maxfield, the National Hurricane Director, called Nagin at his home to plead that he empty the City. (2)
Why did Nagin wait so long? He was worried about the legalities. If people want to affix blame, perhaps they can look at lawyers.
How ironic, that The Drudge Report (3) and Free Republic (4) have pictures of dozens of New Orleans submerged and now useless school buses, buses that could have been used to transport residents out of the City prior to the storm, bring in supplies after the storm, and help evacuees escape the flooding. Meanwhile, Governor Blanco issued a request to the State of Louisiana to provide her with buses from local school districts.
According to a Washington Post report on Sunday, September 4, Shortly before midnight Friday, the Bush administration sent her a proposed legal memorandum asking her to request a federal takeover of the evacuation of New Orleans, a source within the state's emergency operations center said Saturday.
Bushs offer to have the federal government takeover the evacuation was rejected. (5)
Lie #2: The Bush Administration was slow in coordinating help.
Mike Brown, Under Secretary of the Department of Homeland Security for Emergency Response and Preparedness, received the order from President Bush on August 27, two full days before the storm hit the region, to prepare for Katrina disaster relief. (6) The President also declared the entire region under a State of Emergency, so that FEMA could coordinate efforts at the request of the Governors. (7) Under the Emergency Management Assistance Compact, the Federal Government and FEMA are not allowed to interfere with local operations unless they are authorized by state and local leaders.
Blanco did not authorize this until September 1, 2005.
Further, according to an Association Press report on August 30, The federal government began rushing baby formula, communications equipment, generators, water and ice into hard-hit areas of Louisiana, Mississippi and Alabama, along with doctors, nurses and first-aid supplies. The U.S. Defense Department sent experts to help with search-and-rescue operations. (8) FEMA was there and helping, in the capacity that was allowed by local officials, but could not swing into full gear until after Blanco gave them permission.
Lie #3: The Bush Administration did nothing to control the anarchy.
The local and state governments have control over law enforcement activities in their state, and such activities could only be coordinated through the federal government with their permission. It was not until terrible reports of rapes and violence, videos of looting, and reports of shoots being fired at rescue workers did Governor Blanco relinquish any claim of control on an out-of-control city.
An August 31, 2005 Fox News Report reveals, The looting prompted authorities to send more than 70 additional officers and an armed personnel carrier into the city. One police officer was shot in the head by a looter but was expected to recover, authorities said. Blanco said she will ask President Bush for military troops to help keep looting under control. (9) Almost immediately thereafter, FEMA, the military, and the Bush Administration began to restore order.
Further, on September 2, 2005, the Bush administration sought unified control over all local police and state National Guard units reporting to the governor. Louisiana officials rejected the request after talks throughout the night, concerned that such a move would be comparable to a federal declaration of martial law. (10)
Lie #4: The Bush Administration did nothing to prevent the flooding.
Predictions of wide spread devastation have been known since Hurricane Camille in 1969. Despite these, it was local officials who reportedly appropriated funds designated for levee improvements towards such necessary purchases as a casino, hotel, and other projects.
Amazing, isnt it?
From the carnage inside the Superdome, to the massacre of the truth on television, this is a sad time for all of America.
Just dont forget who helped all this to happen .because despite what the media wants you to believe, it wasnt President Bush.
1. Associated Press, Mandatory Evacuation Ordered for New Orleans, August 28, 2005, 10:48 a.m. CT.
2. Knight Ridder Newspapers, National Hurricane Director had to call Nagin at home Saturday night to plead: "Get people out..." by Marc Caputo, David Ovalle, and Erika Bolstad, August 28, 2005
3. www.drudgereport.com
4. www.freerepublic.com
5. Washington Post, Many Evacuated, but Thousands Still Waiting, White House Shifts Blame to State and Local Officials, Manuel Roig-Franzia and Spencer Hsu, Washington Post Staff Writers, Sunday, September 4, 2005; Page A01
6. FEMA Press Release, Emergency Aid Authorized For Katrina Emergency Response In LA August 27, 2005
7. Associated Press, Bush Declares Emergency in Louisiana, August 27, 2005
8. Associated Press, Federal Government sent emergency supplies to Louisiana as early as Tuesday, August 30, 2005
9. Fox News.com, Its Not Safe In New Orleans, August 31, 2005
10. Washington Post, Ibid
Although my "born on" date indicates a new arrival to FR, I have actually been on the board since 1998. Two new computers, two changes in service providers, and a recent trojan horse forced me to change my login. You may know me as "TheWriterInTx," or "TheWriterTX" or simply, "TheWriter."
Health issues and a complicated pregnancy prompted to stop writing for almost the entire last year, but the mud slinging around Hurricane Katrina brought me to my breaking point. During the wee hours of Sunday morning, I hammered out the original of this piece and did something I almost never do...sent it right away without looking it over. After many years of writing solid articles for many internet magazines, most editors don't give my stuff a second look before posting.
Egg, major egg.
Many thanks to Cbolt and others for pointing out a serious error in the original article. I don't mind the egg on my face, saying I was wrong, and correcting it. Unlike the MSM, I actually do want the facts out there. The corrected version should also hit Enter Stage Right shortly.
Thanks, FReepers, for keeping me on my toes.
He said Florida was very prepared for the next hurricane and so they were able to send resources to New Orleans to help out.
It's obvious that Louisana was not prepared to help themselves, let alone help anyone else.
Congressman Billybob
Latest column: "Tide of Lies Swamps NY Times: Employees Riot and Steal Office Supplies"
It's unbelievable how people can equate President Bush with the forces of nature. It is just plain absurb.
There were not just "200 buses". There were 200 buses in just one photo and Freepers studying the post-Katrina satellite images have counted over 400 buses altogether at other city parking.
At 70 people per bus that is 28,000 people per round trip that could have been taken out of the storm surge area in the 48 hours prior the Katrina striking.
After the storm hit, what makes you think that buses sent from outside of New Orleans could drive through the flooded mess any better than the 145 New Orleans city buses that were parked 1.2 miles away from the Superdome?
Was Scotty supposed to beam the outside buses to the Superdome and them beam them back out so that they would not have to drive through impassable roads?
The time to evacuate those 200,000 low-income people on public buses OUT OF THE STORM SURGE ZONE was BEFORE the Category 4 storm struck.
That was what the Southern Louisiana Evacuation Plan for New Orleans specifically called for.
The Democrat Governor and the Democrat Mayor did NOTHING to carry out that portion of the plan. They left 200,000 low-income resident abandoned and they now blame the Federal Government for not having Scotty beam down a massive logistics effort after a human disaster of their own making.
Once my baby is successfully brought into this world, my health should improve and I can start focusing on writing seriously again. Until now, only cases of extreme vexation bring out the beast in me, as was this case.
Welcome back TxWriter. Thanks for the timeline & info. Take care.
Not only did the lousy Democrat Mayorand Democrat Gvernor NOT carry out their duties to help their citizens, but they then BLAMED the President!!! NEVER....EVER trust a Liberal Democrat with your life.
du bump
Not to mention, what kind of idiot doesn't evacuate hospitals and nursing homes! That was just plain stupid!
Can you imagine what the situation would be if Katrina had made a direct strike on NOLA, including the levee breaches? Considering the current estimated projected death toll of 10,000, can you imagine the deaths if Katrina had done to NOLA what she did to MS ?
Bump for a good article.
Funny and smart = sexy and cute
I am bookmarking this post! Thanks!
It is fairly obvious the Dem machine jumped in once they had public opinion turned against the White House - you don't suppose Blanco's actions were studied and intentional BEFORE the levee break, do you?
And thank YOU and Cbolt for prompting me to examine the article, my research articles, and sources anew. Believe me, I don't like the egg on my face, but I won't ignore it at the expense of the truth.
Thanks again, TCO.
(8) FEMA was there and helping, in the capacity that was allowed by local officials, but could not swing into full gear until after Blanco gave them permission.
That would be Wednesday September 1, 2005
She is SOOOOOOOOOOO screwed.
Join here, upload your photos and you can post them anywhere!
For the life of me, I just cannot understand why every single "official" in the state of Louisiana came out of the shute blaming Bush, practically before any of the really bad news came out.
Unless they knew that the really bad stuff was coming earlir than that admitted that and didn't tell people in time.
Whatever it is, they are really hiding something. Something big, IMO, is all that would explain the vitrol from people who have been through hurricanes before and know how long aid takes.
Isn't that the truth!
And those media elites just keep on pretending George sent the wind and rain!
My favorite, the self described "smartest woman in world" Hillary doesn't seem to be able to tell the difference either! :-)
If you don't mind, please share with us your "scheduled launch date". And, please know that many of us will be praying for you and all of yours!
Oh, yes -- thanks for a great article!!!
TXnMA (Back home in the northeast Texas Piney Woods)
Right now, Justin's official due date is December 11; however, they are scheduling to take him on November 18 due to my existing risk of premature abruption and his two-vessel umbillical cord. If left unchecked, he has a 25% chance of being stillborn.
They are monitoring me for toxemia now, and may have to take him sooner; believe me, I will let folks know. Many thanks for the prayers. We can sure use them!
read later
Well done.
These posts need to be made more public. I am glad to see that the public isn't rushing to drink out of the trough the dems are!
Don't you know we just don't talk about busing in the South. It's bad manners! /sarcasm off
What would Democrats have to do if they didn't have lying and finger pointing available?
Why would anybody trust a Democrat with anything?
I have asked the same question on other threads. This has all the earmarks of the Clintons trying to set this up as Campaign 08.
Oh, wow.......you are so right.
That is even worse, isn't it? (I knew I should have looked at a calendar!
Thanks for the re-ping. Bookmarked.
I completely agree.
See MissMarple's post Here
See MissMarple's post Here
Disclaimer: Opinions posted on Free Republic are those of the individual posters and do not necessarily represent the opinion of Free Republic or its management. All materials posted herein are protected by copyright law and the exemption for fair use of copyrighted works.


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Rick Scott Is Not Happy About the End of the Government Shutdown
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Scott took to writing a statement to say how supergrumpy he is that sanity has been restored (at least for the next few months, anyway).
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Scott is governor thanks, basically, to two reasons: Alex Sink is a bore, and Scott has always been openly opposed to health-care laws of any kind.
Also, because Florida.
But during the shutdown, Scott refused to answer questions about the situation and didn't write any statements at all. Instead, he tweeted out photos of his grandchildren.
But he did use the questions asked him to take shots at Obama. Because, OBAMA.
"What I agree with is that the buck stops with the president; I'm disappointed he doesn't know how to compromise," he said.
And he's been doing everything he can to keep Florida from participating in Obamacare.
Such as using fake math, and throwing a hissy fit at Congress to keep Affordable Care Act navigators from doing their jobs in the state.
And, during the shutdown, he told state parks and agencies not to use Florida money to help fund federal programs while his party kept the country hostage.
So, it's pretty much official (if it wasn't already).
Rick Scott has aligned himself with the Tea Party. You know, the same reps, congressmen, and senators who believe that you balance a budget and create jobs with Jesus Power, the American flag, and questioning if the president of the United States is a secret Muslim or not.
This is the guy who wants to keep running our state come 2014.
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The man accused of killing trainer Bob Camac and his wife at their Salem County, N. J. farm last Thursday was being evaluated as to whether he should be transferred from the county jail to a mental health facility after authorities said he was threatening to kill himself, it was reported Tuesday by Today's Sunbeam, a local newspaper.Wade M. Russell, 36, Camac's stepson, had threatened to jump from a second floor railing in the jail and corrections officers found a sheet "hanging in an unusual manner in his cell," according to the newspaper. Russell currently is in an "administrative segregation watch," meaning that he has no interaction with other inmates and is under close observation by officers and medical staff. He had been on a suicide watch over the weekend but was taken off.Bob and Maryann Camac were found dead early Thursday morning on the back porch of their home, located on their farm in Oldmans Township. Russell was charged with the double homicide on Friday.
Report: Man Charged in Camac's Death Threatens Suicide
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Reply to comment
class of 56 or 57
My dad graduated from reading high up on the hill in Reading. I am trying to find a yearbook or an image from the yearbook to see what my dad looked like when he graduated high school. If anyone in this picture looks at this site and remembers a Lester Boady, would you please email me. I would like to communicate with you to hear your memories of him. Unfortunately, he is deceased now; but I want to do something special for my mom at Christmas.


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Lido del Faro
Bathing Establishments BeachesLocalità Punta Carena - Anacapri - See map
Lido del Faro
+39 081 8371798
+39 081.8372657 (Fax)
Official website:
Lido del Faro
- The "sunniest" beach club of Capri: enjoy the sun till the sunset
- A dip in the blue sea or in the swimming pool: it's your choice!
- A great restaurant for lunch just on the seashore
Lido del Faro - AnacapriGo to the top
One of Capri's best-loved beach resorts, Anacapri's Lido del Faro occupies a series of sun-drenched terraces, carved into the rocks at the foot of the island's lighthouse.
At Lido del Faro you'll find everything you might possibly need for a perfect day by the sea: a salt water swimming pool with hydromassage, private sun decks, a gourmet restaurant specializing in fish and seafood...and the glorious Mediterranean sun, from dawn until dusk.
Typical island treats, from "caponata" to "insalata caprese" and "white wine with peaches", are served at the Snack Bar. And, if you can't bear the idea of missing a single ray of sun, on request staff will deliver drinks and nibbles direct to your lounger. What more could you want?
Lido del Faro: TripAdvisor reviews®Back to the top
Il posto migliore dove rilassarsi
Location meravigliosa dove prendere il sole fino al tramonto, mare cristallino, ormai sono anni che trascorro la mia giornata di riposo al Lido del Faro e non riesco a smettere! Il cibo è la giusta more »
Un must. Fare il bagno li e godersi il tramonto è obbligatorio, davvero il top. Occhio a non scivolare sugli scogli, e godetevi lo spettacolo. more »
My Favourite Spot in Capri
The problem with making such a recommendation is that I want to keep this place to myself ! However, it has already been discovered, and yes they KNOW it! Unlike the beach-club and restaurant at Il... more »
Lido del Faro: LocationBack to the top
Lido del Faro is located on Carena Point, and just a 10 minute bus ride away from the center of Anacapri.
Other suggestionsBack to the top
da Antonio
- Atmosphere like in the 50s at the "Faro di Punta Carena"
- Try the famous "caponata" made by Antonio
- Enjoy the sunset drinking a glass of wine
da Gelsomina Migliera
- A hidden spot in the heart of Capri
- A swimming pool near the Migliera scenic overlook, the prettiest view on Capri
- Traditional island specialties in the excellent restaurant
Torre Saracena
- Swim towards the Faraglioni
- Sunbathe in the hidden cove
- Taste the fresh seafood
da Gioia
- One of the fewest beach of Capri
- Enjoy a relaxing and comfortable day on the beach
- Taste the sea specialties of the restaurant


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San Angelo Resident
Needing someone to come clean our house.
Flexible hours
Not given.
Call Jim at 949-7024.
Employer: Leos Enterprises Posted: August 16
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Shannon Medical Center
Leos Enterprises
Employer: ServiceMaster By Texas Best Posted: August 12
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The Bighorn Elk Antler Chandelier
Item # WX2-122685
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The Bighorn Elk Antler Chandelier. Made with 7 intertwined elk antlers and 8 lights to add an impressive touch of the wild to your decor!
You'd never guess that the antlers on this Chandelier weren't the real thing! In fact, each of the 7 incredibly life-like elk antlers were professionally handcrafted from medium-density polyethylene and individually hand-stained and painted to look exactly like the real deal! The only difference you'll probably notice between these antlers and the genuine article is a much lower price!The details:
- Holds 8 lights (25 watt bulb recommended, not included)
- Antique brass canopy
- 36" of antique brass chain
- Hardware included
- 26 x 40".