Michael.Massing + etiology   267

Early predictors of metabolic syndrome in healthy 7-9 year-olds identified -- ScienceDaily
Markers that may precede the metabolic syndrome and mechanisms that explain these relationships have yet to be identified. These mechanisms may originate in the intrauterine environment, be exacerbated in susceptible populations, such as African Americans and, be further promoted by a genetic predisposition, particularly among African American children. These abnormalities may work synergistically to create a childhood metabolic syndrome phenotype and may originate earlier in youth than previously proposed.

The purpose of the study was to explore potential correlates of insulin sensitivity, fasting insulin, and insulin resistance, and to determine the best model to predict them in young children. The study of more than 100 healthy children, ages 7-9, found that fat in the liver, abdominal fat, and fat oxidation predicted insulin resistance and appear to be early markers for the metabolic syndrome via a mechanism of impaired lipid metabolism and fat oxidation. Impaired metabolic function may be due, in part, to pre-and post natal factors that are modified by current physical activity. Therefore, race, low or high pregnancy weight and/or birth weight, and low physical activity collectively create a phenotype for poor metabolic function leading to increased risk for insulin resistance in young children.

"Although some of the risk factors cannot be changed, pregnancy weight, birth weight, and physical activity can all be modified and are targets for early intervention to prevent or delay insulin resistance and reduce the risk for metabolic syndrome," noted Dr. Sothern, who is the study's principal investigator.
low  birth  weight  risk  metabolic  syndrome  lipids  fats  blood  cholesterol  skeletal  fat  fatty  liver  epigenetic  insulin  resistance  child  development  children  youth  health  disparities  diabetes  teen  diet  body  disorder  etiology  T2D  research  correlation  type  2  factor  public  genetics  genetic  biomarkers  prognosis  diagnosis  screening  in  vivo  human  clinical  trial  prognostic  leg  prenatal  perinatal  breast  feeding  childhood  cause 
9 weeks ago by Michael.Massing
LSUHSC RESEARCHERS 1ST TO DOCUMENT EARLY SIGNS FOR DIABETES IN KIDS AS YOUNG AS 7
Insulin resistance/poor insulin sensitivity is closely associated with increased total body fat and may precede development of the metabolic syndrome and type 2 diabetes. Indicators of impaired insulin sensitivity have yet to be clearly identified in children prior to puberty.

The LSUHSC researchers found that the child’s current fat weight is the strongest predictor for poor insulin sensitivity which is a risk factor for type 2 diabetes. LDL (bad cholesterol) was also strongly associated with insulin sensitivity in the prediction model. Previously unidentified Metabolic Syndrome markers discovered by Dr. Sothern’s team include:

• Fat in the liver cells and fat in the skeletal (leg) muscle cells also predict poor insulin sensitivity and high insulin resistance (pre-diabetes) along with an impaired fat burning ability in the muscles.

• These relationships were only found after the researchers considered the child's current fat weight, so the strongest predictor is whether or not these young children are currently overweight or obese.

• The fat in the skeletal muscle became less important after Dr. Sothern’s team considered the mother’s weight prior to and during pregnancy, whether the child was breast-fed, and the current physical activity level of these young children.

“This means that if the mother has a healthy weight gain during pregnancy and the child is breast-fed and physically active, the fat may not accumulate in the skeletal muscle and/or liver and the child may not experience an impaired fat burning ability in the muscle. All of these factors are significantly associated with poor insulin sensitivity that may eventually lead to type 2 diabetes in adolescence or young adulthood. We hope to conduct future prospective studies in this cohort of healthy children to confirm this finding,” notes Dr. Melinda Sothern, LSU Health Sciences Center New Orleans Professor of Public Health and study leader.

Collectively, fat oxidation (how well the body is able to utilize fat as a fuel), blood pressure, and lipids (HDL and LDL) were identified as the best physiologic predictors of insulin sensitivity.

Arlette Soros, MD, an LSUHSC Pediatrics fellow who is a member of Dr. Sothern’s research team, is presenting results of the first study to examine why some children become hypoglycemic (low blood sugar) during insulin sensitivity testing. She will report that children who are lean and have less fat in their skeletal muscle are more likely to get hypoglycemia. Also those with the best insulin sensitivity were the most likely to get low blood sugar.

“We are not sure why this is but think they may be more fit and less prone to diabetes,” concludes Dr. Sothern.
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American Diabetes Association 2009 Annual Scientific Session Meeting in New Orleans. Dr. Sothern’s group is the first to document previously unknown markers for obesity, heart disease and diabetes, collectively called the Metabolic Syndrome, in children [ages 7–9]. Posters will be presented on Saturday, June 6, 2009, and Brian Bennett, a Research Associate in Dr. Melinda Sothern’s laboratory will make the oral presentation, Early Markers for the Metabolic Syndrome in Youth, on Monday, June 8, 2009.
low  birth  weight  risk  metabolic  syndrome  lipids  fats  blood  cholesterol  skeletal  fat  fatty  liver  epigenetic  insulin  resistance  child  development  children  youth  health  disparities  diabetes  teen  diet  body  disorder  etiology  T2D  research  correlation  type  2  factor  public  genetics  genetic  biomarkers  prognosis  diagnosis  screening  in  vivo  human  clinical  trial  prognostic  leg  prenatal  perinatal  breast  feeding  cause 
9 weeks ago by Michael.Massing
Twitter
Diabetes. HIV. Now two cancers. Obstructing Medicaid expansion means underdiagnosis and consequent missed treatment…
Medicaid  morbidity  mortality  cost  benefit  expansion  risk  obstructionism  diagnosis  treatment  health  disparities  poverty  SDH  social  determinants  of  epidemiology  correlation  chronic  research  peer-reviewed  population  studies  etiology  diabetes  cause  factor  obstruction  public  disease  burden  data  access  care  healthcare  from twitter
may 2019 by Michael.Massing
Twitter
Rising HIV rates and falling intervention map to political obstruction of Medicaid expansion. [Diabetes also goes u…
diabetes  HIV  Medicaid  political  obstructionism  poverty  health  disparities  treatment  diagnosis  chronic  disease  morbidity  mortality  cost  benefit  risk  expansion  SDH  social  determinants  of  epidemiology  correlation  research  peer-reviewed  population  studies  etiology  cause  factor  obstruction  public  burden  data  access  care  healthcare  from twitter
april 2019 by Michael.Massing
Twitter
If you live in the US poverty/fast-food/diabetes belt, you are at greater risk of expression of your genetic risk f…
poverty  diabetes  risk  etiology  epidemiology  correlation  cause  factor  from twitter
june 2018 by Michael.Massing
Diet-induced insulin resistance precedes other aspects of the metabolic syndrome. - PubMed - NCBI
This study was designed to examine the effects of a high-fat refined-sugar (HFS) or a low-fat complex-carbohydrate (LFCC) diet on insulin-stimulated skeletal muscle glucose transport, plasma insulin, blood pressure, plasma triglycerides, plasma glycerol, body weight, and body fat in female Fischer rats. Insulin-stimulated glucose transport was significantly reduced in the HFS group at 2 wk, 2 mo, and 2 yr, whereas serum insulin was significantly elevated at all time points. Blood pressure was not significantly elevated in the HFS group until 12 mo, and all HFS animals were hypertensive by 18 mo. Glycerol, triglycerides, and abdominal fat cell size were not significantly different at 2 wk but were significantly elevated in the HFS rats at 2 and 6 mo. Body weight was similar in both groups until 20 wk on the diet, when the HFS rats started to gain more weight. These results demonstrate that insulin resistance and hyperinsulinemia occur before the other manifestations of the metabolic syndrome and that diet, not obesity, is the underlying cause.
insulin  resistance  metabolic  syndrome  factor  risk  etiology  diabetes  in  vivo  animal  peer-reviewed  research  diet  high  fat  sugar  complex  carbohydrate  low  symptoms  cause 
january 2018 by Michael.Massing
Diet-induced insulin resistance precedes other aspects of the metabolic syndrome | Journal of Applied Physiology
This study was designed to examine the effects of a high-fat refined-sugar (HFS) or a low-fat complex-carbohydrate (LFCC) diet on insulin-stimulated skeletal muscle glucose transport, plasma insulin, blood pressure, plasma triglycerides, plasma glycerol, body weight, and body fat in female Fischer rats. Insulin-stimulated glucose transport was significantly reduced in the HFS group at 2 wk, 2 mo, and 2 yr, whereas serum insulin was significantly elevated at all time points. Blood pressure was not significantly elevated in the HFS group until 12 mo, and all HFS animals were hypertensive by 18 mo. Glycerol, triglycerides, and abdominal fat cell size were not significantly different at 2 wk but were significantly elevated in the HFS rats at 2 and 6 mo. Body weight was similar in both groups until 20 wk on the diet, when the HFS rats started to gain more weight. These results demonstrate that insulin resistance and hyperinsulinemia occur before the other manifestations of the metabolic syndrome and that diet, not obesity, is the underlying cause.
insulin  resistance  metabolic  syndrome  factor  risk  etiology  diabetes  in  vivo  animal  peer-reviewed  research  diet  high  fat  sugar  complex  carbohydrate  low  symptoms  cause 
january 2018 by Michael.Massing
Dietary carbohydrate: relationship to cardiovascular disease and disorders of carbohydrate metabolism. - PubMed - NCBI
The nature of carbohydrate is of considerable importance when recommending diets intended to reduce the risk of type II diabetes and cardiovascular disease and in the treatment of patients who already have established diseases. Intact fruits, vegetables, legumes and wholegrains are the most appropriate sources of carbohydrate. Most are rich in nonstarch polysaccharides (NSPs) (dietary fibre) and other potentially cardioprotective components. Many of these foods, especially those that are high in dietary fibre, will reduce total and low-density lipoprotein cholesterol and help to improve glycaemic control in those with diabetes. There is no good long-term evidence of benefit when NSPs or other components of wholegrains, fruits, vegetables and legumes are added to functional and manufactured foods. Frequent consumption of low glycaemic index foods has been reported to confer similar benefits, but it is not clear whether such benefits are independent of the dietary fibre content of these foods or the fact that low glycaemic index foods tend to have intact plant cell walls. Furthermore, it is uncertain whether functional and manufactured foods with a low glycaemic index confer the same long-term benefits as low glycaemic index plant-based foods. A wide range of carbohydrate intake is acceptable, provided the nature of carbohydrate is appropriate. Failure to emphasize the need for carbohydrate to be derived principally from wholegrain cereals, fruits, vegetables and legumes may result in increased lipoprotein-mediated risk of cardiovascular disease, especially in overweight and obese individuals who are insulin resistant.
risk  benefit  industrialized  processed  lipids  vegetables  cardiovascular  blood  whole  grain  fruit  carbohydrate  legumes  glucose  peer-reviewed  research  response  insulin  fiber  comparison  overview  correlation  type  2  T2D  effect  diet  epidemiology  etiology  self  care  management  long  term  short  soluble  insoluble  metabolism  prevention  intact  integrity  diabetes  cause  factor 
september 2017 by Michael.Massing
Cereal grains, legumes and diabetes. - PubMed - NCBI
Epidemiological studies strongly support the suggestion that high intakes of whole grain foods protect against the development of type II diabetes mellitus (T2DM). People who consume approximately 3 servings per day of whole grain foods are less likely to develop T2DM than low consumers (<3 servings per week) with a risk reduction in the order of 20-30%. The role of legumes in the prevention of diabetes is less clear, possibly because of the relatively low intake of leguminous foods in the populations studied. However, legumes share several qualities with whole grains of potential benefit to glycaemic control including slow release carbohydrate and a high fibre content. A substantial increase in dietary intake of legumes as replacement food for more rapidly digested carbohydrate might therefore be expected to improve glycaemic control and thus reduce incident diabetes. This is consistent with the results of dietary intervention studies that have found improvements in glycaemic control after increasing the dietary intake of whole grain foods, legumes, vegetables and fruit. The benefit has been attributed to an increase in soluble fibre intake. However, prospective studies have found that soluble fibre intake is not associated with a lower incidence of T2DM. On the contrary, it is cereal fibre that is largely insoluble that is associated with a reduced risk of developing T2DM. Despite this, the addition of wheat bran to the diets of diabetic people has not improved indicators of glycaemic control. These apparently contradictory findings might be explained by metabolic studies that have indicated improvement in glucose handling is associated with the intact structure of food. For both grains and legumes, fine grinding disrupts cell structures and renders starch more readily accessible for digestion. The extent to which the intact structure of grains and legumes or the composition of foods in terms of dietary fibre and other constituents contribute to the beneficial effect remains to be quantified. Other mechanisms to help explain improvements in glycaemic control when consuming whole grains and legumes relate to cooking, type of starch, satiety and nutrient retention. Thus, there is strong evidence to suggest that eating a variety of whole grain foods and legumes is beneficial in the prevention and management of diabetes. This is compatible with advice from around the world that recommends consumption of a wide range of carbohydrate foods from cereals, vegetables, legumes and fruits both for the general population and for people with diabetes.
breakfast  blood  whole  grain  lsgumes  glucose  peer-reviewed  research  response  insulin  fiber  comparison  review  overview  correlation  type  2  T2D  effect  diet  epidemiology  etiology  self  care  management  long  term  short  soluble  insoluble  metabolism  prevention  diabetes  cause  factor  risk 
september 2017 by Michael.Massing
Matching Meals to Body Clocks—Impact on Weight and Glucose Metabolism
The prevalence of type 2 diabetes continues to rise worldwide and is reaching pandemic proportions. The notion that this is due to obesity, resulting from excessive energy consumption and reduced physical activity, is overly simplistic. Circadian de-synchrony, which occurs when physiological processes are at odds with timing imposed by internal clocks, also promotes obesity and impairs glucose tolerance in mouse models, and is a feature of modern human lifestyles. The purpose of this review is to highlight what is known about glucose metabolism in animal and human models of circadian de-synchrony and examine the evidence as to whether shifts in meal timing contribute to impairments in glucose metabolism, gut hormone secretion and the risk of type 2 diabetes. Lastly, we examine whether restricting food intake to discrete time periods, will prevent or reverse abnormalities in glucose metabolism with the view to improving metabolic health in shift workers and in those more generally at risk of chronic diseases such as type 2 diabetes and cardiovascular disease....

There is a general belief that consumption of more energy throughout the day is preferable to evening consumption. Few studies have examined this prospectively in humans, or for any length of time. Nonetheless, time restricted feeding has shown promise as a tool to mitigate the metabolic sequelae of diet induced obesity in mouse models. Good quality evidence for TRF as a dietary approach to improve glucose control in humans is lacking. Controlled trials are necessary, and must determine if there is adaptation in the approach, whilst keeping in mind the practicality of translating this approach into the community.
opblood  protein  glucose  metabolism  peer-reviewed  research  response  insulin  meal  timing  in  vivo  animal  correlation  comparison  type  2  T2D  circadian  rhythms  social  factor  environmental  etiology  risk  shift  work  obesity  body  fat  diabetes  cause 
september 2017 by Michael.Massing
Twitter
So is type 2 diabetes in the US a disease both of poverty (as mapped by geography) AND of affluence (as mappable to…
poverty  diabetes  risk  etiology  epidemiology  correlation  cause  factor  from twitter
september 2017 by Michael.Massing
Pinboard: bookmarks for Michael.Massing tagged 'diabetes+self+treatment+remission'
Etiology ≠ destiny. I've advocated rigorous self-treatment—stricter than the standard of care—for 14 years.
hcsm  diabetes  etiology  cause  factor  risk  from twitter
july 2017 by Michael.Massing
State by state, diabetes prevalence—overwhelmingly type 2—and household income
State by state, diabetes prevalence—overwhelmingly type 2—and household income: disease of affluence & indulgence,…
diabetes  etiology  risk  factor  correlation  mapping  poverty  data  type  2  T2D  public  health  epidemiology  diet  cause  from twitter
may 2017 by Michael.Massing
Pinboard: bookmarks for michael.massing tagged 'diabetes+etiology+pollution'
Environment & disease literature is rich, e.g. Is carbon cycling new frontier for expanding…
diabetes  etiology  cause  factor  risk  from twitter
april 2017 by Michael.Massing
Gut bacteria may play a role in Alzheimer’s disease -- ScienceDaily
Gut bacteria may play a role in Alzheimer’s disease

#alzheimersdisease #GutBacteria #microbiome #hcsm #hcsmeu
gut  flora  bacteria  Alzheimer's  brain  correlation  peer-reviewed  research  in  vivo  animal  etiology  progression  GutBacteria  hcsmeu  hcsm  microbiome  alzheimersdisease 
february 2017 by Michael.Massing
How we ‘fixed’ our diabetic dad – and saved his life | Life and style | The Guardian
Weak on etiology? Keen on "diabetes reversal"? If doc shows remission requires sustained, hard effort, net good?
diabetes  etiology  cause  factor  risk  from twitter
january 2017 by Michael.Massing
Twitter
Diabetes diagnosis data—presumably a bellwether—show GOP-state obstruction of ACA's expanded Medicaid is already ki…
diabetes  Medicaid  political  obstructionism  poverty  health  disparities  treatment  diagnosis  chronic  disease  morbidity  mortality  cost  benefit  risk  epidemiology  correlation  research  peer-reviewed  population  studies  etiology  cause  factor  obstruction  expansion  public  burden  social  determinants  data  access  care  healthcare  from twitter
january 2017 by Michael.Massing
Diabetes Mystery: Why Are Type 1 Cases Surging? - Scientific American
For reasons that are completely mysterious, however, the incidence of type 1 diabetes has been increasing throughout the globe at rates that range from 3 to 5 percent a year. Although the second trend is less well publicized, it is still deeply troubling, because this form of the illness has the potential to disable or kill people so much earlier in their lives.
No one knows exactly why type 1 diabetes is rising. Solving that mystery—and, if possible, reducing or reversing the trend—has become an urgent problem for public health researchers everywhere. So far they feel they have only one solid clue.
“Increases such as the ones that have been reported cannot be explained by a change in genes in such a short period,” says Giu­seppina Imperatore, who leads a team of epidemiologists in the Division of Diabetes Translation at the U.S. Centers for Disease Control and Prevention. “So environmental factors are probably major players in this increase.”
diabetes  type  1  T1D  etiology  data  surge  incidence  global  risk  factor  environment  environmental  cause 
june 2016 by Michael.Massing
dLife Diabetes News - Diabetes | Type 1 Diabetes | Type 2 Diabetes - www.dlife.com
Previous research conducted by the same researchers at Lund University in 2009 showed a gene variant to melatonin receptor 1B increases risk for type 2 diabetes. The variant causes the level of the melatonin receptors in beta cells to increase, making them more sensitive to melatonin and stopping them from secreting insulin.
"A third of all people carry this specific gene variant," Hindrik Mulder, a professor at Lund University, said in a press release. "Our results show that the effect of melatonin is stronger in them. We believe that this explains their increased risk of developing type 2 diabetes."
For the study, researchers recruited 23 healthy carriers of the gene variant and 22 people without the variant, treating them with four milligrams of melatonin before bed for three months.
The researchers found insulin secretion was lower among participants with the genetic variation, and that blood glucose levels were higher among all participants after melatonin treatment -- but most significantly in those with the variation.
genetic  risk  etiology  factor  T2D  type  2  diabetes  melatonin  correlation  peer-reviewed  research  circadian  rhythms  hormone  drug  effects  contraindication  pancreas  insulin  beta  cells  light  body  clock  mutation  genetics  cause 
may 2016 by Michael.Massing
The Carb-Sane Asylum: Blood Sugar 140: Context is Everything I - Diabetic vs. Non
I can think of nothing more harmful to health than the insulin phobia rampant in the LC community.  While the frank type 2 diabetic is baseline hyperinsulinemic, they don't produce the appropriate acute insulin response.  Given the health issues accompanying improper insulin/signaling, it seems a no-brainer that establishing  as normal a level of both insulin and glucose as possible....

Normal individuals eating a "normal" diet will regularly exceed 140 mg/dL, though not necessarily by much, to no apparent detriment. Neuropathy would simply be far more common in occur in younger populations if BG's over 140 damaged nerves to any significant level.

In a diabetic, however, not only do postprandial glucose levels climb higher, they tend to stay elevated for longer periods of time, thus if the hyperglycemia is toxic per se, the exposure is greater. The glucose levels also may never fall below, say, 100 or even far higher depending on the degree of glycemic control. Therefore it is not surprising that IGT or diabetes was diagnosed by OGTT in 2/3rds of subjects presenting with neuropathy in this study. I shall discuss the implications of that finding in a separate post as well.

In someone with impaired insulin secretion (T1 = none/insignificant, T1.5 = insufficient, T2 = varying depending) if blood glucose goes over 140, it likely climbs considerably over that and takes longer to clear (and/or is added to by inappropriate endogenous glucose production). The more carbs ingested the higher the glucose spike in somewhat proportional fashion. This is because insulin is not secreted properly and the glucose will be cleared by non-insulin dependent mechanisms. A person with normal insulin secretion will almost never get a glucose spike over around 180 because their glucose stimulated insulin secretion (GSIS) is proportional to the glucose ingested. So a diabetic consumes 50g carb or 100g carb and their BG level climbs quite a lot higher after the 100g load, but a non-diabetic consumes 50g or 100g or 200g, and their BG level may climb 10 or 20 points higher at the high dose, but their GSIS will just increase proportionally to handle the load to avoid runaway glucose levels....

Eating sugar or carbohydrates in general does not cause diabetes. The pancreas has more than enough insulin making capacity to last more than a lifetime. It's not like eggs in your ovaries as I've seen the analogy drawn. Yes, with aging comes some declining function, just as sarcopenia can become an issue, but that decline is not due to having used up some insulin reservoir. Eating a low carb diet to avoid getting diabetes on this basis is, frankly, downright foolish. Equally foolish, IMO, is looking at thresholds and studies in diabetics and applying those same measures to the non-diabetic. A non-diabetic will simply rarely if ever exceed around 180 mg/dL no matter what, and this includes "compensators" -- those with IR for whom an exaggerated GSIS compensates for impaired transport to achieve normoglycemia. So long as one is not continually adding to whatever has caused the IR, there's little indication the pancreas can't keep on keeping on. Remember, the LIRKO mouse is hyperglycemic throughout most of its shortened life, but hyperinsulinemic to the bitter end. We can argue over the glucose and/or insulin being toxic in this mouse, but it's pretty clear that at least in the mouse, raging chronic hyperglycemia didn't kill off its beta cells.

In summary, then, application of thresholds and targets aimed at diabetics to non-diabetics should be qualified and are often so out of context as to be irrelevant. I would agree that maintaining more truly normal glycemic control in the diabetic -- keeping glucose spikes under 200 and 2 hr readings below 140 -- may well be a more effective means to prevent diabetic complications. I'd sure as heck aim for that myself were I diabetic. But I don't see any reason for a non-diabetic to worry or obsess over postprandial spikes exceeding that magic 140 mg/dL number. If your low carb diet has rendered your formerly non-diabetic metabolism into a functionally diabetic one, it may be time to rethink things a bit. Insulin does more than stimulate glucose transport into your cells....

The last [study cited by a correspondent] is very interesting [link] What Is the Best Predictor of Future Type 2 Diabetes?

"The insulin secretion/insulin resistance index is useful as a predictor of future development of type 2 diabetes."

I think I'll do a quick blog post on this paper in the next day or so. If insulin is a better predictor it *may* mean that it is the primary factor in the etiology. This is what I believe based on my reading of the literature (especially recently) demonstrating that postprandial insulin production is impaired early on in the progression of the disease.
insulin  normoglycemia  euglycemia  blood  glucose  excursions  cycle  postprandial  diabetes  type  2  T2D  normal  standards  threshold  eitiology  etiology  cause  factor  risk 
may 2016 by Michael.Massing
The future of medicine is food — Quartz
“We translate the preponderance of dietary evidence,” which Harlan told Quartz supports the oft-praised Mediterranean diet, “for the American kitchen.” That includes consideration of cost as well as nutritional value—diet-related illnesses like obesity are often linked to low income communities, including the New Orleans community that Tulane’s kitchen also serves. This also works out well for training would-be doctors, says Harlan, who are usually on a stringent budget themselves....

While it’s still early days for the Tulane program, two separate studies have shown its effectiveness—for both the patients and med students alike. (Both studies included authors from the Goldring Center.) The first, which looked at patients with Type 2 Diabetes, found, for example, that those that who participated in the program saw a major drop in total cholesterol, while those who did not participate saw an increase. The second found that medical students also benefited: They not only thought nutrition advice was important for their patients, but for themselves, too. By the second year, the participating med students were eating significantly more fruits and vegetables than they had previously.

Harlan expects a sea change to take place in the way doctors treat chronic illness—and the way insurance charges for it. At the conference, Kass described a future where doctors write recipes as prescriptions and insurance companies treat food as a reimbursable expense. (There is, of course, a strong economic argument in favor of a prevention-based approach to health.) Harlan predicts that care plans will eventually include menu planning, recipes and maybe even programming to get the ingredients delivered to patients. “Call me up in ten years and let’s see if that’s true.”
nutrition  food  diet  #MedEd  poverty  correlation  diabetes  type  2  T2D  neighborhood  service  earnest  insurance  etiology  epidemiology  cause  factor  risk 
may 2016 by Michael.Massing
Exaggerated effects of particulate matter air pollution in genetic type II diabetes mellitus (PDF Download Available)
Researchers found that exposure to air pollution, over a period of 24 weeks, exaggerates insulin resistance and fat inflammation. “[O]besity has reached epidemic proportions with 34% of adults in the US, ages 20 and over, meeting the criteria...Obesity and diabetes are very prevalent in urban areas and there have been no studies evaluating the impact of poor air quality on these related conditions until now.”
Type 2 diabetes...has soared worldwide with a projected 221 million people expected to suffer from this disease in 2010, a 46 percent increase compared to 1995...[S]cientists fed male mice a diet high in fat over a 10-week period to induce obesity and then exposed them to either filtered air or air with particulate matter for six hours a day, five days a week, over a 24-week period...The air pollution level inside the chamber containing particulate matter was comparable to levels a commuter may be exposed to in...many metropolitan areas in the U.S.
[description by Diabetes in Control - expired link]
in  vivo  animal  correlation  pollution  environment  risk  body  fat  inflammation  heart  circulation  insulin  epidemic  poison  etiology  resistance  T2D  diabetes  type  2  research  peer-reviewed  environmental  factor  public  health  genetic  genetics  cause 
april 2016 by Michael.Massing
Association Between Fine Particulate Matter and Diabetes Prevalence in the U.S.
OBJECTIVE Recent studies have drawn attention to the adverse effects of ambient air pollutants such as particulate matter 2.5 (PM2.5) on human health. We evaluated the association between PM2.5 exposure and diabetes prevalence in the U.S. and explored factors that may influence this relationship.

RESEARCH DESIGN AND METHODS The relationship between PM2.5 levels and diagnosed diabetes prevalence in the U.S. was assessed by multivariate regression models at the county level using data obtained from both the Centers for Disease Control and Prevention (CDC) and U.S. Environmental Protection Agency (EPA) for years 2004 and 2005. Covariates including obesity rates, population density, ethnicity, income, education, and health insurance were collected from the U.S. Census Bureau and the CDC.

RESULTS Diabetes prevalence increases with increasing PM2.5 concentrations, with a 1% increase in diabetes prevalence seen with a 10 μg/m3 increase in PM2.5 exposure (2004: β = 0.77 [95% CI 0.39–1.25], P < 0.001; 2005: β = 0.81 [0.48–1.07], P < 0.001). This finding was confirmed for each study year in both univariate and multivariate models. The relationship remained consistent and significant when different estimates of PM2.5 exposure were used. Even for counties within guidelines for EPA PM2.5 exposure limits, those with the highest exposure showed a >20% increase in diabetes prevalence compared with that for those with the lowest levels of PM2.5, an association that persisted after controlling for diabetes risk factors.

CONCLUSIONS Our results suggest PM2.5 may contribute to increased diabetes prevalence in the adult U.S. population. These findings add to the growing evidence that air pollution is a risk factor for diabetes.
diabetes  human  population  environmental  risk  factor  environment  etiology  particulate  matter  correlation  in  vivo  situ  peer-reviewed  research  public  health  insurance  cause 
april 2016 by Michael.Massing
UNC study helps clarify link between high-fat diet and type 2 diabetes — UNC School of Medicine
New research from the University of North Carolina at Chapel Hill School of Medicine adds clarity to the connection. The study published online April 10 in the journal Nature Immunology finds that saturated fatty acids but not the unsaturated type can activate immune cells to produce an inflammatory protein, called interleukin-1beta.

“The cellular path that mediates fatty acid metabolism is also the one that causes interleukin-1beta production,” says senior study co-author Jenny Y. Ting, PhD, William Kenan Rand Professor in the Department of Microbiology and Immunology.

“Interleukin-1beta then acts on tissues and organs such as the liver, muscle and fat (adipose) to turn off their response to insulin, making them insulin resistant.  As a result, activation of this pathway by fatty acid can lead to insulin resistance and type 2 diabetes symptoms.”  Ting is also a member of the UNC Lineberger Comprehensive Cancer Center, and the UNC Inflammatory Diseases Institute.
insulin  resistance  mechanism  risk  factor  diabetes  type  2  T2D  inflammation  correlation  etiology  saturated  fat  peer-reviewed  research  diet  food  earnest  liver  fatty  body  metabolic  syndrome  disorder  public  health  cause 
april 2016 by Michael.Massing
Type 2 Diabetes Genetic Predispositions
The study included 6,501 participants (81.1% non-Hispanic white, 12.7% non-Hispanic black, and 6.2% Mexican-American). 38 type 2 diabetes-related single nucleotide polymorphisms (SNPs) were genotyped. Association between aggregate genetic risk for type 2 diabetes and all-cause mortality was investigated.

After adjusting for age, sex, BMI, smoking, alcohol, and hypertension, increased mortality risk was observed for every type 2 diabetes allele an individual had, independent of BMI (OR 1.04, 95% CI 1.00 – 1.07, P = 0.05). These findings were consistent with non-Hispanic whites and non-Hispanic blacks, but not with Mexican Americans. Mexican Americans showed a negative trend even after adjustments. The analysis was repeated with Cox regression that showed generally similar results. Association of increased risk of mortality was evaluated by ethnicity, which yielded similar results for non-Hispanic whites, and non-Hispanic blacks, but not for Mexican Americans (OR 0.95, 95% CI 0.89 – 1.01, P = 0.01).

When BMI was accounted for, the mortality risk per allele was higher among obese non-Hispanic whites as compared to normal-weight non-Hispanic whites. There was a negative trend observed in normal-weight Mexican Americans (BMI <25 kg/m2, OR 0.91, 95% CI 0.82 – 1.00)....

Individuals with diabetes carrying type 2 diabetes alleles have an increased risk of mortality.
High BMI (> 25 kg/mm3) is associated with increased risk of mortality in individuals with high genetic predisposition to type 2 diabetes.
Individuals with diabetes should maintain a normal-body weight to reduce the risk of mortality, especially the ones genetically predisposed to type 2 diabetes.
Researched and prepared by Sabair Pradhan, Doctor of Pharmacy Candidate USF College of Pharmacy, reviewed by Dave Joffe, BSPharm, CDE
mortality  risk  factor  race  ethnicity  peer-reviewed  research  genetic  etiology  genetics  diabetes  cause 
april 2016 by Michael.Massing
Diabetes prevalence and socioeconomic status: a population based study showing increased prevalence of type 2 diabetes mellitus in deprived areas -- Connolly et al. 54 (3): 173 -- Journal of Epidemiology & Community Health
Abstract
OBJECTIVE To establish the relation between socioeconomic status and the age-sex specific prevalence of type 1 and type 2 diabetes mellitus. The hypothesis was that prevalence of type 2 diabetes would be inversely related to socioeconomic status but there would be no association with the prevalence of type 1 diabetes and socioeconomic status.

SETTING Middlesbrough and East Cleveland, United Kingdom, district population 287 157.

PATIENTS 4313 persons with diabetes identified from primary care and hospital records.

RESULTS The overall age adjusted prevalence was 15.60 per 1000 population. There was a significant trend between the prevalence of type 2 diabetes and quintile of deprivation score in men and women (χ2 for linear trend, p<0.001). In men the prevalence in the least deprived quintile was 13.4 per 1000 (95% confidence intervals (95% CI) 11.44, 15.36) compared with 17.22 per 1000 (95% CI 15.51, 18.92) in the most deprived. For women the prevalence was 10.84 per 1000 (95% CI 9.00, 12.69) compared with 15.48 per 1000 (95% CI 13.84, 17.11) in the most deprived. The increased prevalence of diabetes in the most deprived areas was accounted for by increased prevalence of type 2 diabetes in the age band 40–69 years. There was no association between the prevalence of type 1 diabetes and socioeconomic status.

CONCLUSION These data confirm an inverse association between socioeconomic status and the prevalence of type 2 diabetes in the middle years of life. This finding suggests that exposure to factors that are implicated in the causation of diabetes is more common in deprived areas.
diabetes  prevalence  socioeconomic  status  SES  correlation  peer-reviewed  research  poverty  education  risk  etiology  epidemiology  cause  factor 
march 2016 by Michael.Massing
Socioeconomic Status and Risk of Diabetes-Related Mortality in the U.S.
Results

Having less than a high school education was associated with a twofold higher mortality from diabetes, after controlling for age, gender, race/ethnicity, marital status, and body mass index, compared with adults with a college degree or higher education level (relative hazard [RH] = 2.05, 95% confidence interval [CI] 1.78, 2.35). Having a family income below poverty level was associated with a twofold higher mortality after adjustments compared with adults with the highest family incomes (RH=2.41, 95% CI 2.05, 2.84).....

Conclusion

Findings from this nationally representative cohort demonstrate a socioeconomic gradient in diabetes-related mortality, with both education and income being important determinants of the risk of death.
diabetes  mortality  socioeconomic  status  SES  correlation  peer-reviewed  research  poverty  education  risk  etiology  epidemiology  cause  factor 
march 2016 by Michael.Massing
Antidepressant Medication as a Risk Factor for Type 2 Diabetes and Impaired Glucose Regulation
Antidepressant Medication as a Risk Factor for Type 2 Diabetes and Impaired Glucose Regulation
Systematic review
Katharine Barnard, PHD1⇑, Robert C. Peveler, FRCPSYCH2 and Richard I.G. Holt, FRCP1
diabetes  depression  risk  comorbidities  affective  mood  disorders  correlation  stress  distress  factor  peer-reviewed  research  clinical  in  vivo  situ  human  antidepressant  SSRI  systematic  review  etiology  public  health  cause 
march 2016 by Michael.Massing
Depression, Diabetes Linked in Women
For depression and incident diabetes, they found:

There were 2,844 new cases of diabetes over the 10 years of follow-up.
Compared with the reference group, participants with Mental Health Index scores of 76 through 85, 53 through 75, or 52 and below had a monotonic elevated risk of developing diabetes, and the trend was significant at P=0.002 in the multivariate analysis.
Participants with scores of 52 or less had an adjusted relative risk of developing diabetes of 1.17, with a 95% confidence interval from 1.05 to 1.30.
Those using antidepressants were at higher relative risk after adjustment for covariates — of 1.25, with a 95% confidence interval from 1.10 to 1.41.
On the other hand, the parallel analysis showed:

There were 7,415 new cases of clinical depression over the decade of follow-up.
Compared with the reference group, those with diabetes had a relative risk of developing clinical depression — after controlling for covariates – of 1.29, with a 95% confidence interval from 1.18 to 1.40.
The relative risks rose with disease severity: 1.25 and 1.24 for those without medications or using oral hypoglycemic agents, respectively, and 1.53 for those on insulin. The associations remained significant after adjusting for diabetes-related comorbidities.
Hu and colleagues noted that the study’s strengths include its large size and prospective design. On the other hand, much of the data was self-reported and the participants were registered nurses and most were white, so the results might not apply to different populations.

Practice Pearl:

Point out that this study, in conjunction with prior studies, indicates the importance of screening for depression in patients with diabetes, and screening for diabetes in patients with depression.

Pan A, et al “Bidirectional association between depression and Type 2 diabetes mellitus in women” Arch Intern Med 2010; 170(21): 1884-1891.
diabetes  depression  risk  comorbidities  affective  mood  disorders  correlation  stress  distress  factor  peer-reviewed  research  clinical  in  vivo  situ  human  antidepressant  population  prospective  etiology  cause 
march 2016 by Michael.Massing
A Link Between Antidepressants and Type 2 Diabetes
What she found was the risk of diabetes almost doubled for the patients who were using two types of therapies at the same time, tricyclic antidepressants (TCAs) and selective serotonin reuptake inhibitors (SSRIs). Brown says people are usually prescribed multiple medications "if they have severe depression or if they are having a problem finding the right therapy."

Overall, 41.9% were taking a tricyclic antidepressant only, 38.7% were taking an SSRI only, 7.7% were taking one of each, and 11.8% were taking at least three medications, at least one of which was not a tricyclic antidepressant or SSRI.
After adjusting for age, sex, number of physician visits, and use of augmentation therapy, only use of one each of a tricyclic antidepressant and an SSRI was associated with an increased risk for type 2 diabetes compared with use of a tricyclic antidepressant alone (adjusted OR 1.89, 95% CI 1.35 to 2.65, P0.001).

Brown L, et al "Type of antidepressant therapy and risk of type 2 diabetes in people with depression"Diabetes Research and Clinical Practice 2008; DOI: 10.1016/j.diabres.2007.07.009.
diabetes  depression  risk  comorbidities  affective  mood  disorders  correlation  stress  distress  factor  peer-reviewed  research  clinical  in  vivo  situ  human  antidepressant  tricyclic  SSRI  population  retrospective  etiology  cause 
march 2016 by Michael.Massing
Depressive disorder and incident diabetes mellitus: the effect of characteristics of depression. - PubMed - NCBI
At baseline, 379 case subjects with depression were identified. The risk of incident diabetes mellitus was higher among subjects with depression when compared with nondepressed subjects, and the association remained significant after controlling for potential confounders, including diabetes risk factors. The estimated rate of diabetes mellitus attributable to depression was 6.87%. An increased risk of diabetes mellitus was also associated with the following characteristics of depression: nonsevere depression, persistent depression, and untreated depression. Treatment with antidepressants was not associated with an increased risk of diabetes mellitus.
CONCLUSIONS:
Clinically significant depression is associated with a 65% increased risk of diabetes mellitus. Characteristics of depression frequently found in the community, namely nonsevere depression, persistent depression, and untreated depression, may play a role in the development of diabetes in a predominantly elderly adult population.
diabetes  depression  risk  comorbidities  affective  mood  disorders  correlation  stress  distress  factor  peer-reviewed  research  clinical  in  vivo  situ  human  etiology  public  health  cause 
march 2016 by Michael.Massing
More Info on Depression Linked to Increased Risk of Diabetes
A random sample of 4,803 adults from the Zaragoza Dementia and Depression Project were identified and interviewed at baseline. After excluding patients with dementia and those with diabetes at baseline, a total of 3,521 participants older than 55 years were included in this study. Of these, 379 were diagnosed as having depression (80.5% female; mean age, 73.6 years), and 3,142 were found to be nondepressed (51.9% female; mean age, 71.8 years).

Diabetes was assessed using a risk factors questionnaire, and follow-up evaluations 2.5 and 5 years later were completed to determine the incidence of diabetes.

Results showed that “the risk of incident diabetes mellitus was higher among those with depression when compared with nondepressed subjects, and the association remained significant after controlling for potential confounders, including diabetes risk factors (P = 0.04).”

The incidence rate was 19.70 per 1000 person-years for the depressed patients compared with 12.36 per 1000 person-years for the nondepressed patients.

Although the community characteristics of nonsevere, persistent, and untreated depression were associated with a significantly increased risk of diabetes compared with nondepression, treatment with antidepressants was not.

Am J Psychiatry. Published online February 1, 2010. [print edition May 2010]
diabetes  depression  risk  comorbidities  affective  mood  disorders  correlation  stress  distress  factor  peer-reviewed  research  clinical  in  vivo  situ  human  etiology  public  health  cause 
march 2016 by Michael.Massing
The Effects of Depression on Metabolic Control and Quality of Life in Indigent Patients with Type 2 Diabetes
In the study sample (n = 201), approximately 20% (n = 40) were depressed. In unadjusted analyses, subjects with depression had significantly lower SF-12 physical component summary (PCS) scores (30.4 ± 7.3 vs. 39.6 ± 11.8, P < 0.001) and mental component summary (MCS) scores (32.8 ± 10.5 vs. 48.9 ± 9.2, P ≤ 0.001) and significantly higher total cholesterol (209.3 ± 72.1 vs. 186.6 ± 50.9, P = 0.024) compared to those without depression. No significant differences were observed by depression status in hemoglobin A1C, LDL cholesterol, and HDL cholesterol. After adjustment for relevant covariates, depressed individuals continued to have lower SF-12 PCS (36.1 vs. 39.0, P ≤ 0.001) and MCS (41.6 vs. 46.8, P ≤ 0.001) scores, but the difference in total cholesterol levels was no longer significant.

Conclusions

In an indigent sample with type 2 diabetes, depression is significantly associated with decreased physical and mental components of QOL. This finding further reinforces the importance of addressing depression in all populations with type 2 diabetes.
diabetes  depression  risk  comorbidities  affective  mood  disorders  correlation  stress  distress  factor  peer-reviewed  research  etiology  public  health  cause 
march 2016 by Michael.Massing
Treatment for diabetes and depression improves both, researchers say -- ScienceDaily
Of patients receiving integrated care combined with a brief period of intervention to assist with adherence to prescribed medication regimens, more than 60 percent had improved blood sugar test results and 58 percent had reduced depression symptoms, compared to only 36 percent and 31 percent, respectively, of patients receiving usual care.

The full results of the study are published in the January/February issue of The Annals of Family Medicine.

There is a link between depression and diabetes - as depression is a risk factor for diabetes, diabetes also increases the risk for the onset of depression....

After 12 weeks of monitoring for medication adherence, 60.9 percent of patients who received the integrated approach were found to achieve improved blood sugar test results, compared to only 35.7 percent patients who received only the usual primary care. Additionally, patients in the integrated care group were also more likely to show signs of remission of depression in comparison with patients in the usual care group (58.7 percent vs. 30.7 percent, respectively)....

H. R. Bogner, K. H. Morales, H. F. de Vries, A. R. Cappola. Integrated Management of Type 2 Diabetes Mellitus and Depression Treatment to Improve Medication Adherence: A Randomized Controlled Trial. The Annals of Family Medicine, 2012; 10 (1): 15 DOI: 10.1370/afm.1344
diabetes  depression  comorbidities  treatment  self  care  adherence  integrated  etiology  demographics  epidemiology  risk  glucose  efficacy  youth  peer-reviewed  research  T2D  medical  correlation  support  factor  stress  distress  drug  public  health  cause 
march 2016 by Michael.Massing
Diabetes correlates better with vitamin D deficiency than with obesity
[Headline corrected from:] Vitamin D deficiency linked more closely to diabetes than obesity
diabetes  type  2  T2D  correlation  peer-reviewed  research  vitamin  D  etiology  factor  risk  cause 
march 2016 by Michael.Massing
Bacterial molecules discovered in processed foods could unlock key to healthier diets -- ScienceDaily
February 9, 2016
Source:
University of Leicester
Summary:
Our favorite foods could be made healthier thanks to a new technique which has identified harmful bacterial molecules in certain processed foods such as burgers and ready meals. The study identifies a particular kind of contaminating molecule known as 'pathogen-associated molecular patterns' (PAMPs), which are released by certain types of bacteria as they grow during some food processing and refrigeration processes, and may increase our risk of developing conditions such as coronary artery disease and Type 2 diabetes.

"In a study of 11 healthy human volunteers, adherence to the specially designed low PAMP diet for just one week caused a significant 18% reduction in LDL (bad) cholesterol and an 11% reduction in white blood cell count. Volunteers also lost weight (on average 0.6 kg) and their waist circumference was reduced (average 1.5 cm), during the low PAMP diet. These are key risk factors for coronary artery disease and Type II diabetes," according to Dr Clett Erridge, University of Leicester....

PAMPs are undetectable in non-processed and fresh foods, suggesting that they develop during the manufacturing process....

M. Herieka, T.A. Faraj, C. Erridge. Reduced dietary intake of pro-inflammatory Toll-like receptor stimulants favourably modifies markers of cardiometabolic risk in healthy men. Nutrition, Metabolism and Cardiovascular Diseases, 2015; DOI: 10.1016/j.numecd.2015.12.001
environment  diet  culture  etiology  diabetes  contamination  processed  food  foods  PAMP  pathogen  associated  molecular  patterns  earnest  peer-reviewed  research  clinical  trial  in  vivo  human  cardiovascular  risk  crossover  industrialization  correlation  environmental  factor  public  health  cause 
february 2016 by Michael.Massing
Twitter
Complex etiology for diabetes: check. Commonalities across types include compromised beta cells: news to me, thanks!
diabetes  etiology  cause  factor  risk  from twitter
february 2016 by Michael.Massing
A New Proposed Classification of Diabetes: No More Type 1 or Type 2 Diabetes
Based on new research performed by Stanley Schwartz and affiliates, there is a new proposition for using a β-cell centered model for diabetes, which supports the notion that all diabetes originates from an abnormal pancreatic β-cell. Type 1 diabetes has been thought of as an ailment of low insulin production, while type 2 has usually been of insulin resistance. This discrepancy is not clear or helpful. Schwartz and colleagues suppose all diabetes is a product of impairment to beta cells (which produce insulin) and according to this theory, insulin resistance just reveals the rudimentary deficiency in insulin production. Only one-third of individuals with insulin resistance will go on to develop diabetes. The basis of the new classification system is treatment of patients as individuals though currently most prescribers will initiate treatment based on a diagnosis instead of the person. Schwartz believes that diabetes is rooted to β-cell and because of this, classification of diabetes types should be based on causes of that damage so physicians will know how to go about treatment. This “β-cell centric” criterion recognizes that β-cell damage can be caused by inflammation, immune actions, gut biome, high fatty acids, high glucose levels, genetics and other causes; categorization founded on these sources can help cultivate an improved treatment strategy, as opposed to simply knocking down an individual’s glucose level. Defining key markers and the processes of care in using them will allot appropriate patient-centric approaches with either currently established medications or an up-and-coming drug.
diabetes  type  1  2  T1D  T2D  etiology  classification  beta  cell  treatment  strategy  autoimmune  immune  system  disorder  gut  biome  high  fatty  acids  glucose  blood  genetics  β-cell  factor  risk  genetic  cause 
february 2016 by Michael.Massing
Modifiable clinical and lifestyle factors are associated with [an NAFLD biomarker] in newly diagnosed type 2 diabetes patients
BACKGROUND:
Current literature lacks data on markers of non-alcoholic fatty liver disease (NAFLD) in newly diagnosed type 2 diabetes mellitus (T2DM) patients. We therefore, conducted a cross-sectional study to examine modifiable clinical and lifestyle factors associated with elevated alanine aminotransferase (ALT) levels as a marker of NAFLD in new T2DM patients.
METHODS:
Alanine aminotransferase levels were measured in 1026 incident T2DM patients enrolled in the nationwide Danish Centre for Strategic Research in Type 2 Diabetes (DD2) cohort. We examined prevalence of elevated ALT (>38 IU/L for women and >50 IU/L for men) and calculated prevalence ratios associated with clinical and lifestyle factors using Poisson regression. We examined the association with other biomarkers by linear regression.
RESULTS:
The median value of ALT was 24 IU/L (interquartile range: 18-32 IU/L) in women and 30 IU/L (interquartile range: 22-41 IU/L) in men. Elevated ALT was found in 16% of incident T2DM patients. The risk of elevated ALT was increased in patients who were <40 years old at diabetes debut [adjusted prevalence ratio (aPR): 1.96, 95% confidence interval (CI): 1.15-3.33], in those with alcohol overuse (>14/>21 drinks per week for women/men) (aPR: 1.60, 95% CI: 1.03-2.50), and in those with no regular physical activity (aPR: 1.42, 95% CI: 1.04-1.93). Obesity and metabolic syndrome per se showed no association with elevated ALT when adjusted for other markers, whereas we found positive associations of ALT with increased C-peptide (β = 0.14, 95% CI: 0.06-0.21) and fasting blood glucose (β = 0.07, 95% CI: 0.03-0.11).
CONCLUSIONS:
Among newly diagnosed T2DM patients, several modifiable clinical and lifestyle factors are independent markers of elevated ALT levels.
biomarker  NAFLD  ALT  peer-reviewed  research  risk  factor  diabetes  correlation  type  2  T2D  etiology  cause 
january 2016 by Michael.Massing
Tissue Renin-Angiotensin systems: a unifying hypothesis of metabolic disease. - PubMed - NCBI
The actions of angiotensin peptides are diverse and locally acting tissue renin-angiotensin systems (RAS) are present in almost all tissues of the body. An activated RAS strongly correlates to metabolic disease (e.g., diabetes) and its complications and blockers of RAS have been demonstrated to prevent diabetes in humans. Hyperglycemia, obesity, hypertension, and cortisol are well-known risk factors of metabolic disease and all stimulate tissue RAS whereas glucagon-like peptide-1, vitamin D, and aerobic exercise are inhibitors of tissue RAS and to some extent can prevent metabolic disease. Furthermore, an activated tissue RAS deteriorates the same risk factors creating a system with several positive feedback pathways. The primary effector hormone of the RAS, angiotensin II, stimulates reactive oxygen species, induces tissue damage, and can be associated to most diabetic complications. Based on these observations, we hypothesize that an activated tissue RAS is the principle cause of metabolic syndrome and type 2 diabetes, and additionally is mediating the majority of the metabolic complications. The involvement of positive feedback pathways may create a self-reinforcing state and explain why metabolic disease initiate and progress. The hypothesis plausibly unifies the major predictors of metabolic disease and places tissue RAS regulation in the center of metabolic control.
metabolic  disorder  disease  complications  RAS  etiology  progression  risk  mechanism  endocrine  theory  hypothesis  renin-angiotensin  systems  factor  diabetes  cause 
january 2016 by Michael.Massing
Screening for type 2 diabetes: literature review and economic modelling. - PubMed - NCBI
The case for screening for undiagnosed diabetes is probably somewhat stronger than it was at the last review, because of the greater options for reduction of CVD, principally through the use of statins, and because of the rising prevalence of obesity and hence type 2 diabetes. However, there is also a good case for screening for IGT, with the aim of preventing some future diabetes and reducing CVD. Further research is needed into the duration of undiagnosed diabetes, and whether the rise in blood glucose levels is linear throughout or whether there may be a slower initial phase followed by an acceleration around the time of clinical diagnosis. This has implications for the interval after which screening would be repeated. Further research is also needed into the natural history of IGT, and in particular what determines progression to diabetes. An RCT of the type required by NSC criterion 13 is under way but will not report for about 7 years.
diabetes  diagnosis  type  2  T2D  standards  glucose  risk  underdiagnosis  screening  reduction  harm  factor  etiology  public  health  cause 
january 2016 by Michael.Massing
[Guidelines on diagnosis of type 2 diabetes. Investigation, diagnosis and glucose measurement]. - PubMed - NCBI
Abstract
World wide the prevalence of type 2 diabetes is increasing and 30-50% of patients are undiagnosed. Early detection and intervention may decrease the risk of late diabetic complications, and thus clear guidelines for early detection and diagnosis of type 2 diabetes are needed. We recommend those individuals with either previous gestational diabetes; obesity (BMI > 30 kg/m2) and/or two or more relatives with diabetes should be considered eligible for testing for diabetes. In order to make the diagnosis two diabetic glucose values on separate days are required. The diagnosis may be made using plasma glucose or capillary whole blood, but quality control measures are essential for glucose measurements in general practice as well as in departments of clinical biochemistry.
PMID: 12715659 [PubMed - indexed for MEDLINE]
diabetes  diagnosis  type  2  T2D  standards  glucose  risk  underdiagnosis  complications  late-stage  symptoms  factor  etiology  cause 
january 2016 by Michael.Massing
Molecular link between diabetes and schizophrenia connects food and mood -- ScienceDaily
Galli's group was among the first to show that insulin -- the hormone that governs glucose metabolism in the body -- also regulates the brain's supply of dopamine -- a neurotransmitter with roles in motor activity, attention and reward. Disrupted dopamine signaling has been implicated in brain disorders including depression, Parkinson's disease, schizophrenia and attention-deficit hyperactivity disorder.

Now, Galli, Niswender, and colleagues have pieced together the molecular pathway between perturbed insulin signaling in the brain and dopamine dysfunction leading to schizophrenia-like behaviors....

They also showed how defects in insulin signaling disrupt neurotransmitter levels in the brain -- the mice have reduced dopamine and elevated norepinephrine in the prefrontal cortex, an important area for cognitive processes. These changes resulted from elevated levels of the transporter protein (NET) that removes norepinephrine and dopamine from the synaptic space between neurons.

"We believe the excess NET is sucking away all of the dopamine and converting it to norepinephrine, creating this situation of hypodopaminergia (low levels of dopamine) in the cortex," Galli explained. Low dopamine function in the cortex is thought to contribute to the cognitive deficits and negative symptoms -- depression, social withdrawal -- associated with schizophrenia.
diabetes  correlation  schizophrenia  insulin  neurotransmitter  endocrine  molecular  diseaseome  link  genetics  etiology  neuroendocrine  cause  causation  in  vivo  animal  peer-reviewed  research  dopamine  regulation  psychotropic  attention  reward  norepinephrine  depression  cognition  food  foods  risk  factor  genetic 
october 2015 by Michael.Massing
Incident diabetes and pesticide exposure among licensed pesticide applicators: Agricultural Health Study, 1993-2003. - PubMed - NCBI
They found seven specific pesticides (aldrin, chlordane, heptachlor, dichlorvos, trichlorfon, alachlor, and cyanazine) for which the odds of diabetes incidence increased with both ever use and cumulative days of use. Applicators who had used the organochlorine insecticides aldrin, chlordane, and heptachlor more than 100 lifetime days had 51%, 63%, and 94% increased odds of diabetes, respectively. The observed association of organochlorine and organophosphate insecticides with diabetes is consistent with results from previous human and animal studies. Long-term exposure from handling certain pesticides, in particular, organochlorine and organophosphate insecticides, may be associated with increased risk of diabetes.
diabetes  type  2  T2D  pesticide  environment  environmental  pollution  risk  factor  etiology  epidemiology  agriculture  incidence  prevalence  peer-reviewed  research  NIH  correlation  exposure  incidental  worker  safety  agricultural  occupational  farming  food  human  in  vivo  situ  public  health  cause 
august 2015 by Michael.Massing
Pesticide use and incident diabetes among wives of farmers in the Agricultural Health Study
The Agricultural Health Study (AHS), a large prospective cohort of pesticide applicators and their spouses in Iowa and North Carolina, presents a unique opportunity to conduct longitudinal studies of diabetes incidence among individuals with a known history of pesticide use. A previous prospective analysis[4] among predominantly male licensed pesticide applicators in the AHS found elevated risk of diabetes associated with ever-use of eight pesticides (two organochlorines: chlordane and heptachlor; four organophosphates: coumaphos, phorate, terbufos, and trichlorfon; and two herbicides: alachlor and cyanazine). Diabetes risk also increased with cumulative lifetime days of use of seven pesticides: aldrin, chlordane, heptachlor, dichlorvos, trichlorfon, alachlor, and cyanazine.

Among women in the AHS cohort with at least one pregnancy in the 25 years prior to enrollment, gestational diabetes was twice as likely in those who reported mixing or applying any pesticides during the first trimester of pregnancy[17]. Gestational diabetes also increased with lifetime ever-use of seven specific pesticides (two organophosphates, diazinon and phorate; the carbamate insecticide carbofuran; and four herbicides, atrazine and butylate, as well as the historically dioxin-contaminated herbicides 2,4,5-T and 2,4,5-TP)[17].
diabetes  type  2  T2D  pesticide  environment  environmental  pollution  risk  factor  etiology  epidemiology  agriculture  incidence  prevalence  peer-reviewed  research  NIH  correlation  exposure  incidental  familial  women's  health  gestational  agricultural  farming  worker  safety  occupational  food  human  in  vivo  situ  public  cause 
august 2015 by Michael.Massing
Exposure to Organochlorine Pollutants and Type 2 Diabetes: A Systematic Review and Meta-Analysis
This meta-analysis provides quantitative evidence supporting the conclusion that exposure to organochlorine pollutants is associated with an increased risk of incidence of T2DM.
diabetes  type  pesticide  environment  environmental  pollution  risk  factor  etiology  epidemiology  agriculture  incidence  prevalence  peer-reviewed  research  NIH  correlation  exposure  2  T2D  agricultural  farming  worker  safety  occupational  food  human  in  vivo  situ  overview  systematic  review  meta-analysis  public  health  cause 
august 2015 by Michael.Massing
Strong associations between the pesticide hexachlorocyclohexane and type 2 diabetes in Saudi adults. - PubMed - NCBI
Among various HCH isomers, serum concentrations of the pesticides β and γ-HCH were most strongly and consistently linked to T2DM in our studied subjects. Associations of HCH varied across five components of the metabolic syndrome. It positively and significantly associated with four out of the five components, especially elevated triglycerides, high fasting glucose, high blood pressure and HOMA-IR but negatively and significantly with HDL-cholesterol.
diabetes  type  2  T2D  pesticide  environment  environmental  pollution  risk  factor  etiology  epidemiology  incidence  prevalence  peer-reviewed  research  NIH  correlation  exposure  human  in  vivo  situ  public  health  cause 
august 2015 by Michael.Massing
Epidemiology of Childhood Type 1 Diabetes Mellitus in Nile Delta, Northern Egypt - A Retrospective Study
In a recent preliminary study conducted for the first time in pediatric patients (age group 1.2-10 years) at our unit for evaluation of the possible association between T1DM in children and exposure to pesticides, the authors demonstrated measurable levels of several pesticide residues in the sera of newly diagnosed T1DM Egyptian children and malathion was reported as the most prevalent pesticide encountered (35).
diabetes  type  1  T1D  pesticide  environment  environmental  pollution  risk  factor  etiology  epidemiology  agriculture  incidence  prevalence  peer-reviewed  research  NIH  correlation  exposure  human  in  vivo  situ  food  cause 
august 2015 by Michael.Massing
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