Michael.Massing + diabetes   1088

Glycemic index and glycemic load: measurement issues and their effect on diet-disease relationships. - PubMed - NCBI
Meta-analyses suggest that foods with a low GI or GL may confer benefit in terms of glycemic control in diabetes and lipid management. However, low GI and GL foods can be energy dense and contain substantial amounts of sugars or undesirable fats that contribute to a diminished glycemic response. Therefore, functionality in terms of a low glycemic response alone does not necessarily justify a health claim. Most studies, which have demonstrated health benefits of low GI or GL involved naturally occurring and minimally processed carbohydrate containing cereals, vegetables and fruit. These foods have qualities other than their immediate impact on postprandial glycemia as a basis to recommend their consumption. When the GI or GL concepts are used to guide food choice, this should be done in the context of other nutritional indicators and when values have been reliably measured in a large group of individuals.
glycemic  index  load  whole  foods  grains  fruit  processed  food  vegetables  cereals  diet  choices  glucose  management  diabetes  sugars  fats  dietary  postprandial  blood 
4 weeks ago by Michael.Massing
Nutmeg Uses, Benefits & Dosage - Drugs.com Herbal Database
Nutmeg has shown insulin-like activity in vitro. 38 Inhibitory effects on protein tyrosine phosphate 1B, involved in insulin cellular signaling, have been demonstrated. 39

Animal data
Serum glucose and lipid profiles improved in mice when mace lignan was administered. 40 In rabbits given an ethanolic extract of nutmeg, total and low-density lipoprotein (LDL) cholesterol and triglyceride were reduced; however, high-density lipoprotein levels were not changed. 41....

Other effects
Screening and in vitro experiments in nutmeg components demonstrated ultraviolet-protectant effects and inhibition of melanin biosynthesis. 65 , 66 Anti-inflammatory and analgesic activities of nutmeg have been recorded in mice, as well as antithrombotic activity. 67 , 68 Other studies document hepatoprotective properties, 69 effects on osteoblast differentiation, 70 and reduced acidity and volume of gastric secretion. 71 , 72
nutmeg  mace  diabetes  insulin  cholesterol  blood  glucose  lipids  peer-reviewed  research  in  vitro  vivo  animal  triglyceride 
5 weeks ago by Michael.Massing
The Effects of Breakfast Consumption and Composition on Metabolic Wellness with a Focus on Carbohydrate Metabolism. - PubMed - NCBI
Findings from epidemiologic studies indicate that there are associations between breakfast consumption and a lower risk of type 2 diabetes mellitus (T2DM) and metabolic syndrome, prompting interest in the influence of breakfast on carbohydrate metabolism and indicators of T2DM risk. The objective of this review was to summarize the available evidence from randomized controlled trials assessing the impact of breakfast on variables related to carbohydrate metabolism and metabolic wellness. Consuming compared with skipping breakfast appeared to improve glucose and insulin responses throughout the day. Breakfast composition may also be important. Dietary patterns high in rapidly available carbohydrate were associated with elevated T2DM risk. Therefore, partial replacement of rapidly available carbohydrate with other dietary components, such as whole grains and cereal fibers, proteins, and unsaturated fatty acids (UFAs), at breakfast may be a useful strategy for producing favorable metabolic outcomes. Consumption of fermentable and viscous dietary fibers at breakfast lowers glycemia and insulinemia. Fermentable fibers likely act through enhancing insulin sensitivity later in the day, and viscous fibers have an acute effect to slow the rate of carbohydrate absorption. Partially substituting protein for rapidly available carbohydrate enhances satiety and diet-induced thermogenesis, and also favorably affects lipoprotein lipids and blood pressure. Partially substituting UFA for carbohydrate has been associated with improved insulin sensitivity, lipoprotein lipids, and blood pressure. Overall, the available evidence suggests that consuming breakfast foods high in whole grains and cereal fiber, while limiting rapidly available carbohydrate, is a promising strategy for metabolic health promotion.
carbohydate  protein  breakfast  blood  whole  grain  unsaturated  fatty  acids  lipids  UFA  glucose  peer-reviewed  research  response  insulin  fiber  high  low  glycemic  index  correlation  type  2  T2D  effect  diet  self  care  management  long  term  short  viscous  soluble  fermentable  insoluble  metabolism  risk  reduction  harm  prevention  diabetes  metabolic  syndrome 
12 weeks ago by Michael.Massing
Timing of Peak Blood Glucose after Breakfast Meals of Different Glycemic Index in Women with Gestational Diabetes
There was no significant difference in subjective satiety throughout the test period. In conclusion, the low GI breakfast produced lower postprandial glycemia, and the peak PBGL [postprandial blood glucose level] occurred closer to the time recommended for PBGL monitoring (i.e., 1 h postprandial) in GDM than a macronutrient matched high GI breakfast.
breakfast  glucose  metabolism  appetite  diabetes  gestational  peak  postprandial  blood  SMBG  self  care  glycemic  index  high  timing  monitoring  excursion  spike  peer-reviewed  research 
12 weeks ago by Michael.Massing
Targeting glucose metabolism for healthy aging. - PubMed - NCBI
Advancing age is the greatest single risk factor for numerous chronic diseases. Thus, the ability to target the aging process can facilitate improved healthspan and potentially lifespan. Lack of adequate glucoregulatory control remains a recurrent theme accompanying aging and chronic disease, while numerous longevity interventions result in maintenance of glucoregulatory control. In this review, we propose targeting glucose metabolism to enhance regulatory control as a means to ameliorate the aging process. We highlight that calorie restriction improves glucoregulatory control and extends both lifespan and healthspan in model organisms, but we also indicate more practical interventions (i.e., calorie restriction mimetics) are desirable for clinical application in humans. Of the calorie restriction mimetics being investigated, we focus on the type 2 diabetes drug acarbose, an α-glucosidase inhibitor that when taken with a meal, results in reduced enzymatic degradation and absorption of glucose from complex carbohydrates. We discuss alternatives to acarbose that yield similar physiologic effects and describe dietary sources (e.g., sweet potatoes, legumes, and berries) of bioactive compounds with α-glucosidase inhibitory activity. We indicate future research should include exploration of how non-caloric compounds like α-glucosidase inhibitors modify macronutrient metabolism prior to disease onset, which may guide nutritional/lifestyle interventions to support health and reduce age-related disease risk.

[Note mention of metformin in graphical abstract.]
hyperglycemia  diabetes  type  2  T2D  blood  glucose  diet  foods  legumes  berries  sweet  potatoes  SMBG  self  care  risk  cardiovascular  kidney  neuropathy  nephropathy  chronic  disease  progression  aging  caloric  calorie  restriction  acarbose  metformin  peak  excursion  spike  peer-reviewed  research 
12 weeks ago by Michael.Massing
Postprandial glucose regulation: new data and new implications. - PubMed - NCBI
Type 2 diabetes is characterized by a gradual decline in insulin secretion in response to nutrient loads; hence, it is primarily a disorder of postprandial glucose (PPG) regulation. However, physicians continue to rely on fasting plasma glucose (FPG) and glycosylated hemoglobin (HbA1c) to guide management.
The objectives of this article are to review current data on postprandial hyperglycemia and to assess whether, and how, management of type 2 diabetes should change to reflect new clinical findings.
Articles were selected from MEDLINE searches (key words: postprandial glucose, postprandial hyperglycemia, and cardiovascular disease) and from our personal reference files, with emphasis on the contribution of postprandial hyperglycemia to overall glycemic load or cardiovascular (CV) risk.
About 33% of people diagnosed as having type 2 diabetes based on postprandial hyperglycemia have normal FPG. PPG contributes > or =70% to the total glycemic load in patients who are fairly well controlled (HbA1c <7.3%). Furthermore, there is a linear relationship between the risk of CV death and the 2-hour oral glucose tolerance test (OGTT). Increased mortality is evident at OGTT levels of approximately 90 mg/dL (5 mmol/L), which is well below current definitions of type 2 diabetes. Biphasic insulin aspart was shown to be more effective at reducing HbA1c below currently recommended levels than basal insulin glargine (66% vs 40%; P < 0.001), and it reduced endothelial dysfunction more effectively than regular insulin (P < 0.01). Repaglinide achieved regression of carotid atherosclerosis (intima-media thickness) in 52% of patients versus 18% for glyburide (P < 0.01) over 1 year, although levels of HbA1c and CV risk factors were similar for both treatment groups. Finally, acarbose reduced the relative risk of CV events by 49% over 3.3 years versus placebo in patients with impaired glucose tolerance (2.2% vs 4.7%; P = 0.03) and by 35% over > or =1 year in patients with type 2 diabetes (9.4% vs 6.1%; P = 0.006).
All components of the glucose triad (ie, FPG, HbA1c, and PPG) should be considered in the management of type 2 diabetes. Therapy targeted at PPG has been shown to improve glucose control and to reduce the progression of atherosclerosis and CV events; therefore, physicians should consider monitoring and targeting PPG, as well as HbA1c and FPG, in patients with type 2 diabetes.
hyperglycemia  diabetes  type  2  T2D  blood  glucose  postprandial  spike  peak  SMBG  self  care  risk  cardiovascular  excursion  damage  vessel  wall  epithelial  atherosclerosis  morbidity  mortality  threshold  peer-reviewed  research 
12 weeks ago by Michael.Massing
Postprandial hyperglycaemia: noxious effects on the vessel wall. - PubMed - NCBI
In recent years postchallenge or postprandial hyperglycaemia has been found to be an independent risk factor for cardiovascular comorbidities and all-cause mortality in impaired glucose tolerance (IGT) and type 2 diabetes. With the database of the Risk Factors in IGT for Atherosclerosis and Diabetes (RIAD) study, it was also shown that atherosclerosis as measured by intima-media thickness of the common carotid arteries was associated with 2-hour postchallenge glucose level when HbA1c was normal. Taken together there are now comprehensive and consistent data from pathophysiological as well as epidemiological studies that excessive post-load glucose excursions have acute and chronic harmful effects on the endothelium and vessel wall. This is supported by four outcome studies that included control of postprandial glucose to prevent cardiovascular disease: Diabetes Intervention Study (DIS), Kumamoto study, DIGAMI study, and STOP-NIDDM trial. Therefore, in addition to HbA1c and fasting blood glucose, postprandial glucose monitoring should be an integral part of treatment to prevent acute and chronic complications.
hyperglycemia  diabetes  type  2  T2D  blood  glucose  postprandial  spike  peak  SMBG  self  care  risk  cardiovascular  excursion  damage  vessel  wall  epithelial  atherosclerosis  peer-reviewed  research 
12 weeks ago by Michael.Massing
Postprandial peaks as a risk factor for cardiovascular disease: epidemiological perspectives. - PubMed - NCBI
A key issue in diabetes care is selecting glucose parameters to monitor and control. The recommendations of the American Diabetes Association for glycaemic control do not address postprandial glucose (PPG), but patients with type 2 diabetes experience wide variations in glucose levels after meals. We have observed a remarkable increase in plasma glucose two hours after breakfast and/or lunch in most non-insulin-treated patients; for up to 40% of them the increase is >40 mg/dl (2.2 mmol/l). As many as 70% of patients with an HbA1c <7% have PPG values >160 mg/dl (8.9 mmol/l) after meals. Fasting plasma glucose (FPG) is a poor indicator of plasma glucose at other times. The coefficient of correlation of FPG with plasma glucose at other times ranges from 0.50-0.70. Nor is the correlation of FPG with HbA1c very strong: in hundreds of determinations of HbA1c and FPG in our patients, the coefficient of correlation was not greater than 0.73. For the same FPG value, HbA1c varied markedly, and vice versa; further, the correlation between PPG and HbA1c was no higher than that between FPG and HbA1c (r = 0.65). Thus, monitoring in type 2 diabetes should include PPG along with FPG and HbA1c. Recent data provide direct and indirect evidence suggesting that PPG is independently related to cardiovascular disease (CVD), and supporting the idea that PPG should be assessed and glucose excursions with meals should be controlled: 1. Studies conducted by other investigators and ourselves in patients with type 2 diabetes have shown that the incidence of CVD is independently related to postprandial or post-OGTT (oral glucose tolerance test) blood glucose at baseline. In addition, data collected in the general population show an association between 2-hour OGTT plasma glucose (a surrogate of PPG) and cardiovascular morbidity and mortality that is independent of FPG. Also, subjects with impaired glucose tolerance (IGT) and isolated post-challenge hyperglycaemia have an increased cardiovascular risk over subjects with normal glucose tolerance (NGT). We found that IGT subjects had a risk of carotid stenosis 3-fold higher than subjects with NGT, even after adjustment for several confounders. Thus, a modest increase in post-OGTT plasma glucose and, by extrapolation, PPG seems to have a major detrimental effect on the arteries. 2. When FPG and/or HbA1c were the targets of glucose control in studies of patients with type 2 diabetes (the UGDP, VACSDM, and UKPDS) the effects on CVD were minimal. However, when the targets of glucose control included PPG (the Kumamoto Study and DIGAMI Study) favorable effects on CVD were observed. 3. There is experimental data suggesting that acute hyperglycaemia can exert deleterious effects on the arterial wall through mechanisms including oxidative stress, endothelial dysfunction, and activation of the coagulation cascade. This evidence prompted the European Diabetes Policy Group to set postprandial targets for blood glucose control: postprandial peaks should not exceed 135 mg/dl (7.5 mmol/ml) to reduce arterial risk and should not exceed 160 mg/dl (8.9 mmol/l) to reduce microvascular risk. Thus, glucose care in diabetes is not only "fasting glucose care" or "HbA1c care" but is also "postprandial glucose care."
hyperglycemia  diabetes  type  2  T2D  blood  glucose  postprandial  spike  peak  SMBG  self  care  risk  cardiovascular  excursion  peer-reviewed  research 
12 weeks ago by Michael.Massing
Peak-time determination of post-meal glucose excursions in insulin-treated diabetic patients. - PubMed - NCBI
The mean peak time after breakfast was 72+/-23 min, which was reached in less than 90 min in 80% of the patients. The apparent glucose rate of increase from pre-meal to the maximum postprandial value was 1.23+/-0.76 mg/dL/min, while the glucose rate of decrease was 0.82+/-0.70 mg/dL/min. Peak time correlated with the amplitude of postprandial excursions, but not with the peak glucose value. Also, peak times were similar after breakfast, lunch and dinner, and in type 1 and type 2 diabetic patients.
To best assess peak postprandial glucose levels, the optimal time for blood glucose monitoring is about 1h and 15 min after the start of the meal, albeit with wide interpatient variability. Nevertheless, 80% of post-meal blood glucose peaks were observed at less than 90 min after the start of the meal.
hyperglycemia  diabetes  type  2  a  T1D  T2D  blood  glucose  postprandial  spike  peak  rhythm  meal  SMBG  timing  insulin  dependent  excursion  peer-reviewed  research 
12 weeks ago by Michael.Massing
Effect of carbohydrate distribution on postprandial glucose peaks with the use of continuous glucose monitoring in type 2 diabetes. - PubMed - NCBI
We investigated the effect of carbohydrate distribution on postprandial glucose peaks with continuous blood glucose monitoring (CGMS), when consuming a moderate carbohydrate diet in energy balance in subjects with type 2 diabetes.
Twenty-three subjects with type 2 diabetes were randomly assigned to each of four 3-d interventions in a crossover design with a 4-d washout period. Identical foods were provided for each treatment with a ratio of total carbohydrate to protein to fat of 40%:34%:26% but differing in carbohydrate content at each meal: even distribution (CARB-E; approximately 70 g carbohydrate), breakfast (CARB-B), lunch (CARB-L), and dinner(CARB-D), each providing approximately 125 g carbohydrate in the loaded meal in a 9-MJ diet. Glucose concentrations were continuously measured with CGMS. Outcomes were assessed by postprandial peak glucose (G(max)), time spent > 12 mmol/L (T > 12), and total area under the glucose curve (AUC(20)).
Daily G(max) differed between treatments (P = 0.003) with CARB-L (14.2 +/- 1.0 mmol/L), CARB-E (14.5 +/- 0.9 mmol/L), and CARB-D (14.6 +/- 0.8 mmol/L) being similar but lower than CARB-B (16.5 +/- 0.8 mmol/L). Meal G(max) was weakly related to carbohydrate amount and glycemic load (r = 0.40-0.44). T > 12 differed between treatments (P = 0.014), and a treatment x fasting blood glucose (FBG) interaction (P = 0.003) was observed with CARB-L (184 +/- 74 min) < CARB-B (190 +/- 49 min) < CARB-D (234 +/- 87 min) < CARB-E (262 +/- 91 min). Total AUC(20) was not significantly different between treatments. After adjustment for FBG, treatment became significant (P = 0.006); CARB-L (10 049 +/- 718 mmol/L x 20 h) < CARB-E (10 493 +/- 706 mmol/L x 20 h) < CARB-B (10 603 +/- 642 mmol/L x 20 h) < CARB-D (10 717 +/- 638 mmol/L x 20 h).
CARB-E did not optimize blood glucose control as assessed by postprandial peaks, whereas CARB-L provided the most favorable postprandial profile.
hyperglycemia  diabetes  type  2  T2D  blood  glucose  postprandial  spike  peak  rhythm  meal  excursion  peer-reviewed  research 
12 weeks ago 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  from twitter
may 2017 by Michael.Massing
New Diabetes Products for 2017: Glucometers and CGMs - Diabetes Self-Management
I think it's the Contour Next One that has integrated whole food/diet logging. (Not affiliated with blahblah.) #dcde
diabetes  technology  SMBG  blood  glucose  monitoring  glucometer  food  logging  dietary  management  dcde  meter 
april 2017 by Michael.Massing
Salacia reticulata (Kothala himbutu) revisited; a missed opportunity to treat diabetes and obesity?
The evidence available from animal and human studies point towards effective reduction of plasma glucose and weight in SR treated subjects. Alpha glucosidase inhibition is the most likely mechanism for the reduction of postprandial glucose. Reduction of fasting glucose, improvement in glucose handling following glucose loading and weight is most likely explained by decreased insulin resistance mediated through increasing adiponectin, suppression of lipogenesis and increased lipolysis.

Meticulously planned studies both animal and human, addressing the unresolved issues as well as studies that involve larger number of human subjects specifically addressing long-term outcomes and safety of SR treatment needs to be performed in the future.
Salacia  reticulata  diabetes  glucose  blood  insulin  postprandial  plasma  HbA1c  serum  lipids  peer-reviewed  research  in  vivo  vitro  clinical  human  body  fat  management  review  overview 
april 2017 by Michael.Massing
Anti-diabetic and Anti-hyperlipidemic Effects and Safety of Salacia reticulata and Related Species. - PubMed - NCBI
Extracts of Salacia reticulata Wight (Hypocrataceae) roots, stems, and leaves have been used in Asia for hundreds of years for the folkloric treatment of diabetes and other health problems. Constituents that have been identified as exhibiting anti-diabetic effects include salacinol, kotalanol, ponkorinol, salaprinol, and their corresponding de-0-sulfonated compounds. Mangiferin, kotalagenin 16-acetate and various proanthocyanidin oligomers have also been isolated. Studies indicate that Salacia extracts modulate multiple targets that influence carbohydrate and lipid metabolism including α-glucosidase, aldose reductase, pancreatic lipase, peroxisomal proliferator-activated receptor-α, glucose transporter-4 mediated glucose uptake, and angiotensin II type 1 receptor. Furthermore, Salacia extracts exhibit free radical scavenging, antioxidant and hepatoprotectant activities. In human studies, Salacia extracts have been shown to decrease plasma glucose and insulin levels, decrease HbA1c, and modulate serum lipid levels with no adverse effects being reported. Similar results have been demonstrated in rat and mouse models as well as in vitro systems. Safety of S. reticulata and other Salacia species as S. oblonga and S. chinensis in rats and mice indicate that extracts are exceedingly safe. No clinical studies have examined the effects of Salacia extracts on human weight loss, although weight loss and decreases in weight gain have been demonstrated in animal models. Because of the large number of pharmacologically active compounds, it is difficult to establish standards for extracts.
Salacia  reticulata  diabetes  glucose  blood  insulin  postprandial  plasma  HbA1c  serum  lipids  peer-reviewed  research  in  vivo  vitro  clinical  human  body  fat  management 
april 2017 by Michael.Massing
Low Carb Diet for Diabetes
Richard K. Bernstein, MD, is a well-known advocate of carbohydrate restriction. Diagnosed with Type 1 diabetes in 1946 at age 12, he developed a very-low-carbohydrate diet in the early 1970s after years of struggling with large blood glucose fluctuations, vision problems, early kidney disease, and pain from neuropathy (nerve damage). He found that by consuming 30 grams of carbohydrate per day — 6 grams for breakfast and 12 grams each for lunch and dinner — and consequently needing only small amounts of insulin to “cover” such small amounts of carbohydrate, his blood glucose could kept in the normal range.

Dr. Bernstein has continued to follow this regimen for the past 40 years and prescribes it to the patients he treats with both Type 1 and Type 2 diabetes at his practice in New York City. In his book Dr. Bernstein’s Diabetes Solution, he writes, “If the kinds of foods you’re eating give you consistently unpredictable blood glucose levels, then it will be impossible to normalize blood sugars.” To prevent such unpredictability, Dr. Bernstein recommends that dietary carbohydrate come only from nonstarchy vegetables, nuts, and other slow-digesting carbohydrate sources.

Steven Parker, MD, is the author of Conquer Diabetes and Prediabetes: The Low-Carb Mediterranean Diet and owner of the Diabetic Mediterranean Diet website (http://diabeticmediterraneandiet.com). Both the book and website provide low-carbohydrate and ketogenic versions of the traditional Mediterranean diet. Parker’s low-carbohydrate version contains 60–100 grams of carbohydrate per day, and his ketogenic version 20–40 grams. The ketogenic version is so named because while some people develop higher blood ketone levels with a “regular” low-carbohydrate diet, many people need to keep their carbohydrate intake under 50 grams per day to see higher ketone levels.

Dr. Parker does not treat people with diabetes on an outpatient basis, but he discusses low-carbohydrate eating plans with the patients he encounters in his job as a hospitalist in Scottsdale, Arizona. He believes carbohydrate restriction can play a valuable role in blood glucose control. And although he recognizes the effectiveness of Dr. Bernstein’s plan, Dr. Parker recommends 60&ndahs;80 grams of net carbohydrate per day for long-term management because he feels it is more acceptable and easier to maintain. (Parker defines net carbohydrate as total carbohydrate minus grams of fiber.)

Helen Hilts, MD, has been prescribing a low-carbohydrate diet to her patients with diabetes for several years. She is the medical director of the DiabeVita medical practice in Scottsdale, Arizona. After being diagnosed with Type 2 diabetes nine years ago, she began following a very-low-carbohydrate diet based on her own research as well as a mentorship with Dr. Bernstein.

“I have a few hundred patients who have followed a very-low-carbohydrate diet for at least two years,” she says. “I recommend no more than 30–45 grams of carbs a day, and those only come in low-carbohydrate vegetables, Greek yogurt, nuts, small portions of berries or tomatoes, etc. No roots, fruits, grains, or liquid milk.” Dr. Hilts follows the same eating plan and maintains an A1C under 5% without medication.

“I see more doctors and diabetes educators reluctantly accepting very-low-carb as viable because they have seen such good results in their patients,” she says, noting that cardiologists seem to accept carbohydrate restriction faster than endocrinologists. “They understand carbohydrates’ effects on insulin resistance, hyperinsulinemia, lipids, and the metabolic syndrome.”

After being diagnosed with Type 1 diabetes in 1998, Keith Runyan, MD, had a difficult time controlling his blood glucose levels on the low-fat diet he was advised to follow. While preparing for his first Ironman triathlon in 2011, he began researching dietary strategies to keep his blood glucose stable for long periods. By February 2012, he had devised the very-low-carbohydrate, high-fat, whole-foods–based diet that he continues following today. Dr. Runyan says that he no longer has large blood glucose fluctuations and that hypoglycemia is now a very rare occurrence for him. In addition, he reports having better energy levels during endurance exercise, as well as overall. He recommends this way of eating for the patients with diabetes, obesity, and kidney disease seen in his St. Petersburg, Florida, medical office.
low  carb  carbohydrate  diet  type  1  2  diabetes  T1D  T2D  mellitus  mealplanning  restriction  science  history  guidelines 
march 2017 by Michael.Massing
Dietary chromium supplementation for targeted treatment of diabetes patients with comorbid depression and binge eating. - PubMed - NCBI
Dietary chromium supplementation for the treatment of diabetes remains controversial. The prevailing view that chromium supplementation for glucose regulation is unjustified has been based upon prior studies showing mixed, modest-sized effects in patients with type 2 diabetes (T2DM). Based on chromium's potential to improve insulin, dopamine, and serotonin function, we hypothesize that chromium has a greater glucoregulatory effect in individuals who have concurrent disturbances in dopamine and serotonin function--that is, complex patients with comorbid diabetes, depression, and binge eating. We propose, as suggested by the collective data to date, the need to go beyond the "one size fits all" approach to chromium supplementation and put forth a series of experiments designed to link physiological and neurobehavioral processes in the chromium response phenotype.
chromium  picolinate  comorbidity  depression  T2D  type  2  diabetes  individual  response  variability  treatment  intervention  psychotropic  appetite  carbohydrate  craving  peer-reviewed  research  Plexus  opinion  overview 
march 2017 by Michael.Massing
Post-Transplant Diabetes Mellitus: Causes, Treatment, and Impact on Outcomes. - PubMed - NCBI
Post-transplant diabetes mellitus (PTDM) is a frequent consequence of solid organ transplantation. PTDM has been associated with greater mortality and increased infections in different transplant groups using different diagnostic criteria. An international consensus panel recommended a consistent set of guidelines in 2003 based on American Diabetes Association glucose criteria but did not exclude the immediate post-transplant hospitalization when many patients receive large doses of corticosteroids. Greater glucose monitoring during all hospitalizations has revealed significant glucose intolerance in the majority of recipients immediately after transplant. As a result, the international consensus panel reviewed its earlier guidelines and recommended delaying screening and diagnosis of PTDM until the recipient is on stable doses of immunosuppression after discharge from initial transplant hospitalization. The group cautioned that whereas hemoglobin A1C has been adopted as a diagnostic criterion by many, it is not reliable as the sole diabetes screening method during the first year after transplant. Risk factors for PTDM include many of the immunosuppressant medications themselves as well as those for type 2 diabetes. The provider managing diabetes and associated dyslipidemia and hypertension after transplant must be careful of the greater risk for drug-drug interactions and infections with immunosuppressant medications. Treatment goals and therapies must consider the greater risk for fluctuating and reduced kidney function, which can cause hypoglycemia. Research is actively focused on strategies to prevent PTDM, but until strategies are found, it is imperative that immunosuppression regimens are chosen based on their evidence to prolong graft survival, not to avoid PTDM.
post-transplant  new-onset  after  renal  transplantation  posttransplantation  diabetes  mellitus  NODAT 
march 2017 by Michael.Massing
Dietary supplementation of n-3 PUFA reduces weight gain and improves postprandial lipaemia and the associated inflammatory response in the obese JC... - PubMed - NCBI
JCR:LA-cp rats (14 weeks of age) were fed either a control, isocaloric, lipid balanced diet (15% w/w total fat, 1.0% cholesterol, P:S ratio 0.4), a lipid balanced diet with 5% n-3 PUFA [fish oil derived eicosapentaenoic acid (EPA)/docosahexaenoic acid (DHA)] or a lipid balanced diet with 10% n-3 PUFA for 3 weeks. Fasting plasma lipid, cytokine levels, postprandial chylomicron (apoB48) metabolism and the postprandial inflammatory response [haptoglobin and lipopolysaccharide binding protein (LBP)] were assessed following a standardized 'oral fat challenge'.
n-3 PUFA treatment resulted in a significant improvement (i.e. decrease) in the postprandial response for triglyceride (45%) (p < 0.05), apoB48 (45%) (p < 0.03) and LBP (33%) (p < 0.05) compared to controls (measured as area under the clearance curve). In contrast, we observed a significant elevation in postprandial haptoglobin (165%) (p < 0.001) in obese rats supplemented with 10% n-3 PUFA. Treatment with 5% n-3 PUFA in the JCR:LA-cp obese animals resulted in a complementary decrease in total body weight gain (6%) (p < 0.001) and an increase (i.e. improvement) in adiponectin (33%) (p < 0.05) compared to controls, without a concomitant reduction in food intake.
Acute dietary n-3 PUFA dietary supplementation can improve fasting as well as postprandial lipid metabolism and components of the associated inflammatory response in the JCR:LA-cp rat. Further, moderate dose n-3 PUFA supplementation may reduce corresponding body weight during conditions of hypercholesterolaemia and/or modulate inflammation associated with obesity and the metabolic syndrome
fish  oil  omega-3  fatty  acids  EPA  DHA  peer-reviewed  research  overview  risk  benefit  diabetes  triglycerides  dyslipidemia  animal  in  vivo 
march 2017 by Michael.Massing
Effects of eicosapentaenoic acid (EPA) treatment on insulin sensitivity in an animal model of diabetes: improvement of the inflammatory status. - PubMed - NCBI
The major goal of this study was to analyze the effects of fatty acid supplementation on both insulin sensitivity and inflammatory status in an animal model of type 2 diabetes. Diabetic rats (Goto-Kakizaki model) were treated with eicosapentaenoic acid (EPA) or linoleic acid at 0.5 g/kg body weigh (bw) dose. In vivo incorporation of (14)C-triolein into adipose tissue was improved by the ω-3 administration. In vitro incubations of adipose tissue slices from EPA-treated rats showed an increase in (14)C-palmitate incorporation into the lipid fraction. These observations were linked with a decreased rate of fatty acid oxidation. EPA treatment resulted in a decreased fatty acid oxidation in incubated strips from extensor digitorum longus (EDL) muscles. The changes in lipid utilization were associated with a decrease in insulin plasma concentration, suggesting an improvement in insulin sensitivity. These changes in lipid metabolism were associated with an activation of AMP-activated protein kinase (AMPK) in white adipose tissue. In addition, EPA treatment resulted in a decreased content of peroxisome proliferator-activated receptor-α (PPARα) and PPARδ and in increased GLUT4 expression in skeletal muscle. Moreover, EPA increased 2-deoxy-D-[(14)C]glucose (2-DOG) uptake in C2C12 myotubes, suggesting an improvement in glucose metabolism. Concerning the inflammatory status, EPA treatment resulted in a decreased gene expression for both tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) both in skeletal muscle and adipose tissue. The data suggest that EPA treatment to diabetic rats clearly improves lipid metabolism although the evidences on insulin sensitization are less clear.
omega-3  fatty  acids  EPA  DHA  peer-reviewed  research  inflammation  benefit  diabetes  triglycerides  dyslipidemia  insulin  sensitivity  in  vivo  animal 
march 2017 by Michael.Massing
Role of ω3 long-chain polyunsaturated fatty acids in reducing cardio-metabolic risk factors. - PubMed - NCBI
Fish oil, rich in eicosapentaenoic (EPA, 20:5ω3) and docosahexaenoic (DHA, 22:6ω3) acids, has been found to cause a modest reduction in blood pressure at a dose level of >3g/d both in untreated and treated hypertensives. Whilst a multitude of mechanisms may contribute to the blood pressure lowering action of ω3 LC-PUFA, improved vascular endothelial cell function appears to play a central role. Recent studies which evaluated the potential benefits of fish oil in type-2 diabetes have helped to alleviate concerns raised in some previous studies which used relatively large dose (5-8 g/d) and reported a worsening of glycemic control. Several meta-analyses have confirmed that the most consistent action of ω3 LC-PUFA in insulin resistance and type-2 diabetes is the reduction in triglycerides. In some studies, fish oil has been found to cause a small rise in LDL-cholesterol, but a change in the LDL particle size, from the smaller more atherogenic form to the larger, less damaging particle size, have also been noted. ω3 LC-PUFA are effective modulators of the inflammation that accompanies several cardio-metabolic abnormalities. Taking into consideration the pleiotropic nature of their actions, it can be concluded that dietary supplementation with ω3 LC-PUFA will lead to improvements in cardio-metabolic health parameters. These fatty acids pose only minor side effects and more importantly, do not interact adversely with the common drug therapies used in the management and treatment of hypertension, dyslipidemia, type-2 diabetes, and obesity/metabolic syndrome, but in some instances work synergistically, thereby providing additional cardiovascular benefits.
fish  oil  omega-3  fatty  acids  EPA  DHA  peer-reviewed  research  overview  risk  benefit  diabetes  triglycerides  dyslipidemia 
march 2017 by Michael.Massing
Minnesota House passes dismemberment and death sentence for diabetics.
SaveACA  DSMA  Diabetes  DOC  from twitter_favs
january 2017 by Michael.Massing
FDA lets Lilly cite Jardiance heart data, shares jump | Reuters
At the time of approval [of Lilly's SGLT2 inhibitor Jardiance] the FDA asked that a separate trial be conducted to show the drug did not increase the risk of cardiovascular problems.

The study instead unexpectedly showed Jardiance slashed deaths by 32 percent in patients with type 2 diabetes at risk of heart attack and stroke, when added to standard diabetes medications.

It was the first time any diabetes drug was shown to reduce risk of cardiovascular death. Moreover, patients taking Jardiance had a 35 percent lower rate of hospitalization for heart failure. That information can now be included on the drug's label.

[Other SGLT2 inhibitors] include Johnson & Johnson's $1.3 billion-a-year Invokana and AstraZeneca Plc's Farxiga.

[Per @MarkHamel, Victoza has similar data.]
drug  effects  benefit  treatment  diabetes  type  2  T2D  cardiovascular  heart  risk  morbidity  mortality  dcde 
december 2016 by Michael.Massing
1st set of standards for treatment of PWD that include psychosocial aspects: stress, depression, anxiety & ED…
ADA  American  Diabetes  Association  psychosocial  symptoms  stress  depression  anxiety  eating  disorders  erectile  dysfunction  ED  from twitter_favs
november 2016 by Michael.Massing
RT : It can be hard to burst someone's hope, but it's far more dangerous to not point out while manageable is…
diabetes  from twitter
november 2016 by Michael.Massing
Clinical trial for People with Type 2 Diabetes
Use Victoza+metformin for type 2 ? New trial to eliminate daily injections. No placebo. Learn more.
T2D  diabetes  from twitter
october 2016 by Michael.Massing
RT : Tonights topic: Halloween with - Looking forward to your comments! -Clem
DCDE  Diabetes  from twitter
october 2016 by Michael.Massing
Half of All Type 1 Diabetes Develops After 30 Years of Age
MUNICH — Onset of type 1 diabetes is just as likely to occur in people older than 30 years of age as in those younger, new research shows.

The data were presented September 16, 2016, here at the European Association for the Study of Diabetes (EASD) 2016 Annual Meeting by Dr Nicholas JM Thomas, of the Institute of Biomedical and Clinical Science, University of Exeter Medical School, United Kingdom.

Obtained using genetic data from the UK Biobank, the startling results refute the long-held belief that type 1 diabetes is primarily a "juvenile" condition.

Clinically, the findings are particularly relevant for primary care, where people who develop autoimmune-mediated diabetes in adulthood are often misdiagnosed as having type 2 and prescribed metformin instead of insulin.

"I think it's an eye-opener and obviously has implications for how we diagnose and manage people and also the education people receive. We very much focus on childhood and adolescence and perhaps people diagnosed later don't get the same education," Dr Thomas told Medscape Medical News in an interview.

Still, identifying these individuals in primary care is challenging for a number of reasons: The vast majority of older adults with new-onset diabetes have type 2 diabetes, and antibody tests to identify autoimmune-mediated diabetes are too expensive for routine use. Moreover, overweight/obesity is nearly universal in type 2 but also common in type 1 diabetes....

[Dr Thomas] advised that clinicians should at least be aware that adults can develop autoimmune diabetes, as either classic type 1 or the slower-onset phenomenon known as "latent autoimmune diabetes of adulthood (LADA)."
incidence  presentation  diagnosis  misdiagnosis  type  1  LADA  diabetes  adult-onset  demographics  population  study  research  EASD 
october 2016 by Michael.Massing
RT : Panel guest tonight: talking about at work & school. -Clem
DCDE  diabetes  from twitter
august 2016 by Michael.Massing
RT : Panel guest tonight: talking about at work & school. -Clem
DCDE  diabetes  from twitter
august 2016 by Michael.Massing
RT : There are very few things in world that require as much 24/7/365 being on your A-game as . Respect.
dsma  diabetes  from twitter
july 2016 by Michael.Massing
A Nutritional Biochemist Gives You His Top Diabe... | Diabetic Connect
The order of your meal and the composition of your meal influences how fast the carbohydrates in that meal are digested and enter your blood, raising your blood glucose. In both type 2 and type 1 diabetes, slower increases in blood glucose are easier to manage.

There is evidence that eating your salad or low-carbohydrate vegetables first can slow the digestion of carbohydrates afterward and that meals with protein, before or with the carbohydrates, can also slow the release of the glucose in the carbohydrates.

You may already know about the glycemic index (the relative ranking of how a carbohydrate affects blood glucose), but this concept can be extended to entire meals. Meals made up of low-glycemic carbohydrates will have a lower impact on blood glucose, but meals with higher glycemic index carbohydrates that are consumed with protein and low-carbohydrate vegetables can also slow the release of carbohydrates and decrease the effect on blood glucose.

So, want to help manage your blood glucose? Tip 3: Pick salad as your first course.
diet  meal  planning  eating  blood  glucose  management  glycemic  index  type  1  2  diabetes  T1D  T2D  sugars 
july 2016 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 
june 2016 by Michael.Massing
New FDA Recommendations for Metformin
Patients who have an eGFR between 30 and 45 mL/min/1.73 m2 can continue to receive metformin or metformin-containing medications as long as there is an appropriate assessment of the risks and benefits of the therapy.

Of course everyone has been concerned about the risk for lactic acidosis with metformin (which is actually relatively rare), particularly in individuals with mild or moderate chronic kidney disease. What is not recommended as part of the new labeling is what some think is appropriate, which is a reduction in the dose of metformin by about 50% in those with an eGFR between 30 and 45 mL/min/1.73 m2.

The new labeling still indicates that metformin should not be used in patients who have an eGFR below 30 mL/min/1.73 m2, but it can be continued in those who start it while their eGFR is above 45 mL/min/1.73 m2. Interestingly enough, the new labeling doesn't recommend starting metformin in patients with an eGFR between 30 and 45 mL/min/1.73 m2. The label indicates that we should only start metformin at an eGFR above 45 mL/min/1.73 m2, continue it with assessment of the risks as it falls below 45 mL/min/1.73 m2, and then stop it altogether if and when the eGFR falls below 30 mL/min/1.73 m2.

There are other cautions about the use of contrast material and so forth that are not new. The good news from this—and I think it was a good move by the FDA—is that the new labeling will now allow access to metformin and metformin-containing medications to many people with diabetes who would benefit from this medication and were not able to receive it in a way that was consistent with the prior black box warning.
metformin  diabetes  treatment  guidelines  risk  benefit  FDA  creatinine  eGFR  prescription  type  2  T2D 
june 2016 by Michael.Massing
Numbers Matter: 1-Hour Post Prandial Glucose Possible Predictor of Prediabetes Risk
A 1-h glucose value > 155 mg/dl predicts mortality even when the 2-h level is < 140 mg/dl.
An elevated 2-hour glucose level indicated increased mortality risk, independent of the 1-hour level.
Patients with a 2-hour glucose level less than 140 mg/dL but an elevated 1-hour glucose had a 28% increased mortality risk

One-hour post-load plasma glucose level during the OGTT predicts mortality: observations from the Israel Study of Glucose Intolerance, Obesity and Hypertension. Diabet Med. 2016 Mar 21. doi: 10.1111/dme.13116. [Epub ahead of print]
diabetes  diagnostic  standards  impaired  fasting  glucose  tolerance  blood  mortality  risk  IGT  threshold  diagnosis  screening  peer-reviewed  research  human  in  vivo 
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 
may 2016 by Michael.Massing
RT : BG control is often the solution to any of our problems. Keep a closer eye on BG, be open to advice.
DCDE  diabetes  from twitter
may 2016 by Michael.Massing
D-is-for-Diabetes: Medicare's Competitive Bidding Program Puts Beneficiaries' Lives at Risk
The Forum built upon the GAO's analysis by examining access to diabetes testing supplies for Medicare beneficiaries living with diabetes and requiring insulin therapy.  Working with some of the nation's leading endocrinologists,* the Forum's study found that the Competitive Bidding Program disrupted beneficiaries' ability to access diabetes testing supplies, and this disruption was associated with an increase in mortality, higher hospitalization rates and inpatient costs.

"Self-monitoring blood glucose supplies are a critical component of diabetes care among insulin-treated individuals and the value of safe, effective testing supplies cannot be underestimated," said Jaime Davidson, M.D., clinical professor of Medicine at the University of Texas Southwestern Medical Center, and an author of the study. "We are particularly concerned about the disruption we detected in our analysis given the predominant use of rapid- and short-acting insulin by Medicare beneficiaries, who are at significantly greater risk for hypoglycemia than younger individuals with insulin-treated diabetes."

"We are troubled that CMS failed to detect these 'unintended' consequences and, instead, reported that the program was a success," said Gary A. Puckrein, Ph.D., president and CEO of the National Minority Quality Forum and a study author. "Based on our findings and employing the safety monitoring protocols commonly used to protect human subjects, we believe policymakers should immediately suspend the program until CMS can demonstrate its ability to effectively monitor the effects of the program, correct the structural flaws causing this problem and ensure that the lives of America's greatest generation are no longer at risk." 

The ahead of print article "Impact of CMS Competitive Bidding Program on Medicare Beneficiary Safety and Access to Diabetes Testing Supplies: A Retrospective, Longitudinal Analysis" can be found online: Impact of CMS Competitive Bidding Program on Medicare Beneficiary Safety and Access to Diabetes Testing Supplies: A Retrospective, Longitudinal Analysis . The full article will also be published here: http://dx.doi.org/10.2337/dc15-1264.
watchdog  diabetes  insulin-dependent  SMBG  supplies  cost  benefit  mortality  hospitalization  competitive  bidding  Medicare  in  vivo  situ  human  peer-reviewed  research  health  disparities  healthcare 
may 2016 by Michael.Massing
Impact of CMS Competitive Bidding Program on Medicare Beneficiary Safety and Access to Diabetes Testing Supplies: A Retrospective, Longitudinal Analysis | Diabetes Care
RESEARCH DESIGN AND METHODS The study population consisted of insulin users: 43,939 beneficiaries in the nine test markets (TEST) and 485,688 beneficiaries in the nontest markets (NONTEST). TEST and NONTEST were subdivided: those with full self-monitoring of blood glucose (SMBG) supply acquisition (full SMBG) according to prescription and those with partial/no acquisition (partial/no SMBG). Propensity score–matched analysis was performed to reduce selection bias. Outcomes were impact of partial/no SMBG acquisition on mortality, inpatient admissions, and inpatient costs.

RESULTS Survival was negatively associated with partial/no SMBG acquisition in both cohorts (P < 0.0001). Coterminous with CBP (2010–2011), there was a 23.0% (P < 0.0001) increase in partial/no SMBG acquisition in TEST vs. 1.7% (P = 0.0002) in NONTEST. Propensity score–matched analysis showed beneficiary migration from full to partial/no SMBG acquisition in 2011 (1,163 TEST vs. 605 NONTEST) was associated with more deaths within the TEST cohort (102 vs. 60), with higher inpatient hospital admissions and associated costs.

CONCLUSIONS SMBG supply acquisition was disrupted in the TEST population, leading to increased migration to partial/no SMBG acquisition with associated increases in mortality, inpatient admissions, and costs. Based on our findings, more effective monitoring protocols are needed to protect beneficiary safety.

Received June 12, 2015.
Accepted January 9, 2016.
© 2016 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.

Impact of CMS Competitive Bidding Program on Medicare Beneficiary Safety and Access to Diabetes Testing Supplies: A Retrospective, Longitudinal Analysis
Gary A. Puckrein, Gail Nunlee-Bland, Farhad Zangeneh, Jaime A. Davidson, Robert A. Vigersky, Liou Xu, Christopher G. Parkin, David G. Marrero
Diabetes Care 2016 Mar; http://dx.doi.org/10.2337/dc15-1264
diabetes  insulin-dependent  SMBG  supplies  cost  benefit  mortality  hospitalization  competitive  bidding  Medicare  in  vivo  situ  human  peer-reviewed  research 
may 2016 by Michael.Massing
8 things I wish people understood about having Type 1 diabetes - Vox
RT @picardonhealth: "8 things I wish people understood about having Type I #diabetes" via @vo
type  1  diabetes  T1D 
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 
may 2016 by Michael.Massing
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