Foot disease in Icelandic patients with established type 2 diabetes

Neðst á síðunni er hægt að nálgast greinina í heild sinni með því að smella á hlekkinn View/OpenOBJECTIVE: To assess the prevalence of symptoms and signs of diabetic foot disease in patients with established type 2 diabetes (T2DM) in Iceland and compare it to controls without diabetes. MATERIALS AND METHODS: Participants were 41 individuals (age range 48 to 75 years), with diabetes of at least 8 years duration, birth date between 1925 and 1965 who were living in the greater Reykjavik area. The control group consisted of 34 spouses without diabetes (age range 43 - 77 years). RESULTS: The most common symptom was leg cramps which affected 37% of patients with T2DM and 29% of controls (difference not statistically significant). Moderate or severe symptoms indicating neuropathy were found in 39% of T2DM patients and in 27% of controls (difference not statistically significant). Intermittent claudication was present in 29% of patients with T2DM and 9% of controls (p<0.03). Based on both symptoms and signs, neuropathy was considered present in 12% of patients with T2DM but none of the controls (p<0.04). The most common sign was dry skin, present in 51% of patients with T2DM and in 18% of controls (p<0.003) while abnormal vibration perception was found in 34% of patients with T2DM and 12% of controls (p<0.003). Abnormal pressure sensation was found in 20% patients with T2DM and 3% of controls (p<0.003). Peripheral macrovascular disease was considered present in 15% of each group. CONCLUSION: Symptoms and signs from feet are common in adult individuals, regardless of diabetes. The observed prevalence of peripheral diabetic neuropathy is among the lowest published. The assessment of diabetic foot disease needs to be standardised, multimodal and take account of both symptoms and signs.Tilgangur: Að kanna algengi einkenna og teikna um fótamein hjá fullorðnum Íslendingum með þekkta sykursýki af tegund 2 og bera niðurstöður saman við sambærilegan hóp fólks án sykursýki. Efniviður og aðferðir: Þýðið var 41 einstaklingur á aldrinum 48-75 ára með þekkta sykursýki af tegund 2 (SS2) í að minnsta kosti 8 ár, fæðingardag á bilinu 1925-1965 og búsetu á höfuðborgarsvæðinu, auk 34 maka á aldrinum 43-75 ára án sykursýki (viðmið). Þátttakendur svöruðu stöðluðum spurningum og voru skoðaðir ítarlega af sama aðila með tilliti til einkenna og teikna sem talin eru einkenna fótamein hjá sykursjúkum. Niðurstöður: Algengasta einkennið var sinadráttur (37% einstaklinga með SS2 og 29% viðmiða) en þessi munur var ekki marktækur tölfræðilega og sama gilti um meðalsvæsin eða svæsin einkenni um taugakvilla sem fundust hjá 39% SS2 sjúklinga og 27% viðmiða. Claudicatio intermittens var til staðar hjá 29% SS2 sjúklinga og 9% viðmiða (p<0,03). Taugakvilli var til staðar, samkvæmt skilgreiningu sem byggir bæði á einkennum og teiknum, hjá 12% SS2 sjúklinga en engum í samanburðarhópi (p<0,04). Algengasta teiknið var þurr húð (51% einstaklinga með SS2 og 18% viðmiða, p<0,003). Óeðlilegt titringsskyn var til staðar hjá 34% SS2 hópsins og 12% viðmiða (p<0,003), en þrýstingsskyn var óeðlilegt hjá 20% SS2 sjúklinga og 3% viðmiða (p<0,003). Útæðasjúkdómur var talinn vera til staðar hjá 15% hvors hóps. Ályktun: Einkenni og teikn frá fótum eru algeng, hvort sem fólk hefur sykursýki eða ekki. Algengi taugakvilla hjá Íslendingum með sykursýki 2 er með því lægsta sem birt hefur verið. Mat á fótameini sykursjúkra þarf að vera staðlað og byggja á mörgum þáttum, bæði einkennum og kerfisbundinni skoðun

Latent autoimmune diabetes in adults in Iceland: prevalence, phenotype and relatedness

Neðst á síðunni er hægt að nálgast greinina í heild sinni með því að smella á hlekkinn View/OpenINTRODUCTION: Ninety percent of diabetic individuals in Iceland suffer from type 2 diabetes mellitus. Antibodies against ss-cell components characterise type 1 diabetes, but these antibodies are also found in type 2 diabetic individuals, defined as latent autoimmune diabetes in adults or LADA. The purpose of this investigation was to estimate the prevalence of LADA in Iceland and to describe the phenotype and relatedness of these individuals. MATERIAL AND METHODS: A list of individuals diagnosed with type 2 diabetes was generated from outpatient clinic lists and the Reykjavik Study of the Icelandic Heart Association. A genealogy database (Book of Icelanders; deCODE Genetics) was used to identify all individuals related to these index cases within six meioses. This method identified 950 type 2 diabetic individuals during the years 1998-2000. We analyzed their phenotype and measured glutamic acid decarboxylase antibody (GAD). Kinship coefficient was used to compare the relatedness of those with antibodies to GAD to the relatedness of all type 2 diabetic individuals in the study. RESULTS: 10.1% of men and 9.3% women had measurable antibodies against GAD (non-significant difference). The mean age of GAD positive and GAD negative individuals was comparable (67.1 +/- 10.7 and 68.0 +/- 11.3; years +/- SD). Body mass index was significantly lower (p=0,02) for the GAD positive individuals or 28.2 kg/m(2) (27.2-29.2; 95% CI) vs. 29.7 (29.3-30.1). Of the GAD positive individuals, 47% +/- 9% (95% CI) had the metabolic syndrome as defined by WHO compared with 60 +/- 4% of the GAD negative individuals (p=0.02). The kinship coefficient for GAD positive individuals (n=94) was 6.00x10(-4) compared with 3.93x10(-4) +/- 8.3x10(-5) for 500 random samples (each of 94 individuals) of the whole cohort (p=0.008). CONCLUSION: About 10% of Icelandic type 2 diabetic individuals have antibodies against GAD, which is comparable to the results of other investigators. Icelandic GAD positive type 2 diabetic individuals have less frequently the metabolic syndrome than other type 2 diabetic individuals and GAD positive individuals are significantly more related to each other than type 2 diabetic individuals in general.Tilgangur: 90% sykursjúkra á Íslandi eru með tegund 2 sykursýki (SS2). Meirihluti sjúklinga með tegund 1 sykursýki (SS1) hafa ß-frumumótefni en hafi sjúklingur með SS2 slík mótefni er hann sagður hafa mótefnatengda sykursýki af tegund 2 (MTSS2, latent autoimmune diabetes in adults eða LADA). Tilgangur rannsóknarinnar var að ákvarða algengi MTSS2 á Íslandi og jafnframt að lýsa svipgerð og skyldleika þessara sjúklinga. Efniviður og aðferðir: Búinn var til listi yfir SS2 sjúklinga úr sjúkraskrám og Reykjavíkurrannsókn Hjartaverndar. Ættfræðigagnagrunnur Íslenskrar erfðagreiningar „Íslendingabók“ var notuð til að finna alla sem skyldir voru þessum sjúklingum í sex ættliði. Á árunum 1998-2000 fundust 950 sjúklingar sem greindir voru með SS2. Svipgerð sjúklinganna var ákvörðuð og ELISA notuð til að mæla mótefni gegn Glutamic Acid Decarboxylase (GAD). Skyldleikastuðull var notaður til að bera saman innbyrðis skyldleika GAD-jákvæðra (GADAb+) og skyldleika allra SS2 sjúklinga. Niðurstöður: 10,1% karla og 9,3% kvenna voru GADAb+ (ómarktækur munur). Meðalaldur GADAb+ og GADAb- sjúklinga var sambærilegur (67,1 ± 10,7 og 68,0 ± 11,3; ár ± staðalfrávik). Holdastuðull var marktækt lægri (p=0,02) hjá GADAb+ sjúklingum eða 28,2 kg/m2 (27,2-29,2; 95% öryggismörk) miðað við 29,7 (29,3-30,1) hjá GADAb-. Efnaskiptavilla var til staðar hjá 47 ± 9% (95% öryggismörk) GADAb+ sjúklinganna saman­borið við 60 ± 4% GADAb- sjúklinganna (p=0,02). Skyldleikastuðullinn fyrir GADAb+ sjúk­lingana (n=94) var 6,00×10-4 samanborið við 3,93×10-4 ± 8,3×10-5 fyrir fimm hundruð 94 manna slembi­úr­tök úr öllum SS2 sjúklingahópnum (p=0,008). Ályktun: Um 10% íslenskra SS2 sjúklinga eru GADAb+ sem er sambærilegt við niðurstöður annarra. Íslenskir GADAb+ SS2 sjúklingar eru sjaldnar með efnaskiptavillu og eru marktækt skyldari innbyrðis en SS2 sjúklingahópurinn í heild

Early life residency associated with the risk of developing type 2 diabetes - the population-based Reykjavík study

Neðst á síðunni er hægt að nálgast greinina í heild sinni með því að smella á hlekkinn View/OpenInngangur: Kyrrseta og ofneysla orkuríkrar fæðu tengjast aukinni áhættu á að fá sykursýki af tegund 2 en áhrif aðbúnaðar í uppvexti á slíka áhættu síðar á ævinni hafa lítt verið athuguð. Tilgangur þessarar rannsóknar var að kanna tengsl búsetu í dreifbýli fyrstu 20 æviárin við áhættu á að fá sykursýki 2 miðað við búsetu í Reykjavík frá fæðingu. Efniviður og aðferðir: Í lýðgrunduðu þýði 17.811 karla (48%) og kvenna, meðalaldur 53 ár (aldursbil 33-81), sem tóku þátt í Reykjavíkurrannsókn Hjartaverndar á árunum 1967-1991, bjuggu 29% í sveit og 35% í sjávarþorpum að meðaltali í 20 ár áður en þeir fluttu til Reykjavíkur, en 36% bjuggu í Reykjavík frá fæðingu. Reiknuð var hlutfallsleg áhætta á að fá sykursýki 2 eftir búsetu. Niðurstöður: Hlutfallsleg áhætta á að fá sykursýki 2 var 43% lægri í körlum (RR 0,57; 95% CI 0,43-0,77) og 26% lægri í konum (RR 0,74; 95% CI 0,56-0,99) sem bjuggu í sveit fyrstu 20 ár ævinnar í samanburði við þá sem bjuggu í Reykjavík frá fæðingu. Hið lága algengi meðal þeirra sem ólust upp í sveit fannst bæði í aldurshópunum 55-64 ára og 65 ára og eldri. Ályktanir: Niðurstöður okkar benda til þess að þeir sem bjuggu í sveit á fyrri hluta 20. aldar á Íslandi voru í minni hættu á að fá sykursýki 2 síðar á ævinni, en jafnaldrar þeirra sem bjuggu í Reykjavík frá fæðingu. Við vörpum fram þeirri tilgátu að aðbúnaður snemma á ævinni hafi langvarandi áhrif á sykurefnaskipti líkamans.Sedentary lifestyle and energy rich food have been associated with the risk of developing type 2 diabetes; limited data are available on environmental conditions in childhood on this risk later in life. The objective was to study if residency in the first 20 years of life affected the risk of developing type 2 diabetes. In a cohort of 17811 men (48%) and women, mean age 53 years (range 33-81) participating in the population-based Reykjavík Study from 1967-91, 29% grew up in rural and 35% in coastal areas for an average of 20 years before moving to urban Reykjavík, but 36% lived in Reykjavík from birth. The prevalence of type 2 diabetes according to residency in early life was examined. The relative risk of developing type 2 diabetes was 43% lower in men (RR 0.57; 95% CI 0.43-0.77) and 26% lower (RR 0.74; 95% CI 0.56-0.99) in women living in rural areas for the first 20 years of their life compared with those living in urban Reykjavík from birth. The low prevalence among those that grew up in rural areas was maintained through the age categories of 55-64 years and 65 years and older. Our findings indicate that persons growing up in rural areas in early 20th century Iceland had lower risk of developing type 2 diabetes later in life when compared with peers living in Reykjavík from birth. We postulate a prolonged effect of early development on glucose metabolism and risk of developing type 2 diabetes

The Third Workshop on Population of the RDBES Data Model (WKRDB-POP3)

The aims of this workshop were to explain the data model developed for the commercial fisheries Regional Database and Estimation System (RDBES), assist in populating it with real data for the second test data call for the RDBES, and encourage participants to take part in ongoing testing of the RDBES data submission system. This report documents the progress that participants have done to prepare their institutes for future use of the RDBES system. Some issues with data conversion have been identified and are documented in this report. None of the identified issues are thought to be serious impediments to moving forward with the RDBES development according to the roadmap decided by the Steering Committee of the Regional Fisheries Database in 2020. The RDBES Core Group (the group of people developing the RDBES data model) and ICES Data Centre will look at the results of this workshop and either respond to individual questions or adapt the data model and documentation as required. The workshop concluded and reported before the deadline of the test data call. For a complete test of the data model, all participants were encouraged to complete the data call. A report on the degree of completion of the data call may be expected from WGRDBESGOV which convenes after the data call deadline

New genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk.

Levels of circulating glucose are tightly regulated. To identify new loci influencing glycemic traits, we performed meta-analyses of 21 genome-wide association studies informative for fasting glucose, fasting insulin and indices of beta-cell function (HOMA-B) and insulin resistance (HOMA-IR) in up to 46,186 nondiabetic participants. Follow-up of 25 loci in up to 76,558 additional subjects identified 16 loci associated with fasting glucose and HOMA-B and two loci associated with fasting insulin and HOMA-IR. These include nine loci newly associated with fasting glucose (in or near ADCY5, MADD, ADRA2A, CRY2, FADS1, GLIS3, SLC2A2, PROX1 and C2CD4B) and one influencing fasting insulin and HOMA-IR (near IGF1). We also demonstrated association of ADCY5, PROX1, GCK, GCKR and DGKB-TMEM195 with type 2 diabetes. Within these loci, likely biological candidate genes influence signal transduction, cell proliferation, development, glucose-sensing and circadian regulation. Our results demonstrate that genetic studies of glycemic traits can identify type 2 diabetes risk loci, as well as loci containing gene variants that are associated with a modest elevation in glucose levels but are not associated with overt diabetes

Genetic fine mapping and genomic annotation defines causal mechanisms at type 2 diabetes susceptibility loci.

We performed fine mapping of 39 established type 2 diabetes (T2D) loci in 27,206 cases and 57,574 controls of European ancestry. We identified 49 distinct association signals at these loci, including five mapping in or near KCNQ1. 'Credible sets' of the variants most likely to drive each distinct signal mapped predominantly to noncoding sequence, implying that association with T2D is mediated through gene regulation. Credible set variants were enriched for overlap with FOXA2 chromatin immunoprecipitation binding sites in human islet and liver cells, including at MTNR1B, where fine mapping implicated rs10830963 as driving T2D association. We confirmed that the T2D risk allele for this SNP increases FOXA2-bound enhancer activity in islet- and liver-derived cells. We observed allele-specific differences in NEUROD1 binding in islet-derived cells, consistent with evidence that the T2D risk allele increases islet MTNR1B expression. Our study demonstrates how integration of genetic and genomic information can define molecular mechanisms through which variants underlying association signals exert their effects on disease

An Expanded Genome-Wide Association Study of Type 2 Diabetes in Europeans.

To characterize type 2 diabetes (T2D)-associated variation across the allele frequency spectrum, we conducted a meta-analysis of genome-wide association data from 26,676 T2D case and 132,532 control subjects of European ancestry after imputation using the 1000 Genomes multiethnic reference panel. Promising association signals were followed up in additional data sets (of 14,545 or 7,397 T2D case and 38,994 or 71,604 control subjects). We identified 13 novel T2D-associated loci (P < 5 × 10(-8)), including variants near the GLP2R, GIP, and HLA-DQA1 genes. Our analysis brought the total number of independent T2D associations to 128 distinct signals at 113 loci. Despite substantially increased sample size and more complete coverage of low-frequency variation, all novel associations were driven by common single nucleotide variants. Credible sets of potentially causal variants were generally larger than those based on imputation with earlier reference panels, consistent with resolution of causal signals to common risk haplotypes. Stratification of T2D-associated loci based on T2D-related quantitative trait associations revealed tissue-specific enrichment of regulatory annotations in pancreatic islet enhancers for loci influencing insulin secretion and in adipocytes, monocytes, and hepatocytes for insulin action-associated loci. These findings highlight the predominant role played by common variants of modest effect and the diversity of biological mechanisms influencing T2D pathophysiology.Please refer to the manuscript or visit the publisher's website for funding infomation

Large-scale association analysis provides insights into the genetic architecture and pathophysiology of type 2 diabetes

To extend understanding of the genetic architecture and molecular basis of type 2 diabetes (T2D), we conducted a meta-analysis of genetic variants on the Metabochip involving 34,840 cases and 114,981 controls, overwhelmingly of European descent. We identified ten previously unreported T2D susceptibility loci, including two demonstrating sex-differentiated association. Genome-wide analyses of these data are consistent with a long tail of further common variant loci explaining much of the variation in susceptibility to T2D. Exploration of the enlarged set of susceptibility loci implicates several processes, including CREBBP-related transcription, adipocytokine signalling and cell cycle regulation, in diabetes pathogenesis

Species composition and diversity of moss communities in geothermal areas with and without Campylopus introflexus (Heath star moss).

Hæruburst er mosategund sem uppgötvaðist fyrst á Íslandi 1983 og hefur síðan fundist víðar á landinu. Hæruburst hefur aukið dreifingu sína hér á landi og er skráð ágeng. Ekkert hefur verið kannað hérlendis hvort hæruburst hafi raunverulega neikvæð áhrif. Safnað var sýnum úr tveiumur sambærilegum svæðum í Grændal á Hengilssvæði, með og án hæruburstar og tegundir greindar ásamt því að meta hversu mikil þekja einstakra tegunda var. Hæruburst reyndist vera alls ráðandi þar sem hana var að finna og aðeins eitt sýni innihélt aðra tegund en hæruburst á þeim reit. Á viðmiðunarsvæðinu var að finna ýmsar ólíkar tegundir og tegundarfjölbreytnin mun hærri en á hæruburstarsvæðinu. Niðurstöðurnar gefa því vísbendingu um að tegundin ryðji frá innlendum mosum. Þannig getur hún dregið úr tegundafjölbreytni á þessum sjaldgæfu vistgerðum. Mikilvægt er að kanna þetta enn frekar enda jarðhitasvæði allfarið með hátt verndargildi og hlýtur lífríki sem tengist bæði hverum eða öðrum heitum uppsprettum sérstakrar verndar. Það lítur út fyrir að hæruburst ógni þessu lífríki sem ber að vernda.Heath star moss was first discovered in Iceland in 1983 and since then has been found in various new locations. Heath star moss has been spreading and is considered an invasive alien species. No local studies have investigated the potential negative impact of heath star moss. Samples were collected in from two comparable areas, with and without the heath star moss, in Grændalur in the Hengil area. Species were identified and the coverage of individual species was estimated. Heath star moss was found to dominate its area. In the reference area various differend species were found and species diversity was greater than in the heath star moss area. It appears that the species is displacing native mosses, thus reducing species diversity in these rare habitats. It‘s important to further investigate this as geothermal areas have high enviromentally protection values and the ecosystem connected to hot springs and other geothermal souces are protected. It seems that heath star moss poses a threat to this protected ecosystem

Verðlagning langlífisáhættu

Aðgangur opnaður 4. janúar 2018 með leyfi höfundar.Í fyrri hluta verkefnisins er fjallað um þróun aldursbundinnar dánartíðni hérlendis á undanförnum áratugum og einkenni þróunarinnar. Dánartíðnin hefur farið stöðugt lækkandi sem er í takt við þróunina annars staðar á Vesturlöndum. Í framhaldi af því er þróað dánartíðnilíkan með bayesískri aðferðafræði sem byggir á Lee-Carter hugmyndinni og lýsir dánartíðni íslenskra kvenna annars vegar og karla hins vegar. Bornar eru saman tvær mismunandi dreifingarforsendur Lee-Carter-líkansins þar sem annars vegar er gert ráð fyrir lognormal-dreifingu dánartíðni en hins vegar þeirri forsendu að fjöldi dánartilfella lúti poisson-dreifingu. Það sem einkennir íslensk lýðfræðigögn, eins og lýðfræðigögn fámennra þjóða, er mikill breytileiki í dánartíðni þar sem sérhvert dauðsfall hefur mikil áhrif og virðist poisson-dreifingarútfærsla Lee-Carter-líkansins ná með trúverðugri hætti að höndla þann breytileika. Í síðari hlutanum er fjallað um langlífisáhættu sem tekur á óvissu í verðlagningu lífeyrisgreiðslna og stafar af óvissri þróun dánartíðni og þar af leiðandi langlífis. Verðlagningin er metin annars vegar miðað við áframhaldandi lækkandi (breytilega) dánartíðni og hins vegar fasta (óbreytta) dánartíðni með notkun poisson Lee-Carter-líkansins. Niðurstaðan er mismunandi eftir aldurshópum en verðlagningin er frá því að vera um 19% lægri fyrir eldri aldurshópa til um 28% lægri fyrir yngri aldurshópa þegar miðað er við forsendu um fasta dánartíðni meðan þróun hennar fer lækkandi skv. líkaninu. Lífeyrisréttindi sem byggja á fastri dánartíðni meðan þróun hennar fer lækkandi skv. líkaninu leiða til ofmats á réttindum og greiðsluþrots í nánast 100% tilfella.Landssamtök lífeyrissjóð