A list of puns related to "Type 1 Diabetes Mellitus"
Stumbled on this paper from 2018 discussing the issues of keeping a solider in the military after a diagnosis as a T1 diabetic. It expand one horizons on what is possible.
Abstract:
US Army soldiers diagnosed with type 1 diabetes were previously considered unfit for duty. For highly motivated soldiers, current advanced technologies allow the possibility of not only retention on active duty, but military deployment. We present our experience at Fort Bragg, North Carolina, taking care of soldiers newly diagnosed with type 1 diabetes mellitus. Through intensive diabetes education, extensive military and physical training, optimization of diabetes technology, and remote real-time monitoring, soldiers are able to continue to serve their country in the most specialized roles.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6134313/
The first few paragraphs:
When a US Army soldier is diagnosed with type 1 diabetes, it is widely assumed that they will be found unfit for duty and their military career is over.
Previously, the rigors of an unpredictable lifestyle and intense physical requirements precluded continuation on active duty. But for a select group of highly motivated and skilled soldiers, continuation on active duty is possible.
Fort Bragg, North Carolina, is home to some of the most skilled men and women in the military, many having spent years of education and intense operational training to achieve their level of skill, experience, and proven performance. When a soldier is diagnosed with type 1 diabetes, the Army may face a difficult decision.
What should be done for an exceptionally skilled soldier who is also highly motivated to stay on active duty?
How will hypoglycemia and hyperglycemia be managed?
From a tactical viewpoint, the unit commander has the responsibility to ensure not only the safety of the soldier with diabetes, but to ensure the safety of the entire unit. A soldierβs removal from assignment due to a medical complication could significantly affect the unitβs mission.
Army regulations stipulate that any soldier with diabetes requiring medication for glycemic control will be referred to a Medical Evaluation Board (MEB) to determine the soldierβs ability to serve on active duty. Many are found unfit for duty, ending their military careers. We have demonstrated that it is possible to not only retain but to deploy soldiers with type 1 diabetes.1
https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0041-1739666?device=desktop
Glut1 Deficiency Syndrome and Diabetes Mellitus Type 1: Review of the Literature and Presentation of a New Case
A. SchΓΆnlaub, A. HΓΆller, S. Hofer, E. Haberlandt, D. Karall, S. Scholl-BΓΌrgi βΊ Author Affiliations βΊ Further Information Congress Abstract Full Text
Background/Purpose: Glucose transporter type 1 deficiency syndrome (Glut1DS) is a rare metabolic disorder that leads to an encephalopathy due to disturbed glucose transport via the bloodβbrain barrier and consecutive energy deficit of the brain. Symptoms are early-onset epilepsy, complex movement disorders and developmental delay. The ketogenic dietary therapy (KDT) is the first-line therapy and includes classic ketogenic diet and modified Atkins diet (MAD). Ketone bodies are an alternative fuel for the brain. KDT leads to ketosis and ensures energy supply of the brain.
Case Report: We describe a 15-year-old girl with Glut1DS treated effectively with modified Atkins diet who developed diabetes mellitus type 1 (T1DM) with diabetic ketoacidosis. Insulin pump was initiated while staying on MAD. With this treatment regimen no further diabetic ketoacidosis occurred and HbA1c was 7%. She kept ketosis in a range between 1.5 and 2.5 mmol/L Ξ²-hydroxybutyrate without any neurologic symptoms.
In literature, there are three cases of patients with T1DM treated with insulin who are on KDT at the same time because of therapy refractory epilepsy or pyruvate dehydrogenase deficiency, but none with Glut1DS. In all cases, a moderate ketosis was kept and admission of insulin was tried to keep as low as possible.
Conclusion: Treatment of Glut1DS with MAD and T1DM with insulin at the same time is challenging but feasible. It is important to keep ketosis while being aware of ketoacidosis.
Carbohydrate-restricted diets and Type 1 diabetes mellitus: research considerations
Type 1 diabetes mellitus (T1DM) is managed via careful control of blood glucose, exogenous insulin, diet, exercise, and other physiologic factors. Interestingly, the dietary recommendations for T1DM have had very little systematic research. Many clinical observations, as well as emerging research studies, have noted that a carbohydrate-restricted diet can lead to normalization of blood glucoses with reduction in hypoglycemic reactions among motivated individuals.
In this paper, we review observations of carbohydrate restriction and propose a series of studies to test two levels of dietary carbohydrate intake for the management of individuals affected by T1DM. We recommend that the studies start in otherwise healthy adults with hemoglobin A1c > 8%, and then progress to more complicated populations including children, those with secondary complications and/or good glycemic control. Larger, long-term studies would then address growth in children, and diabetic complications including cardiovascular outcomes.
Due to the clinical observations of improvements using carbohydrate-restricted nutrition for T1DM, we recommend that these types of studies addressing the level of dietary carbohydrate be urgently conducted.
https://preview.redd.it/55zze5q0btl71.png?width=2000&format=png&auto=webp&s=ae7c5a215ac6abbe518e113254a23c10461e4951
The current dietary recommendations for T1DM have received very little comparative study to other diets, and strong clinical observation experience suggests that carbohydrate restriction is effective among motivated individuals. There is a strong rationale to lower the dietary carbohydrate for the treatment of a condition defined by elevated blood glucoses. The βlaw of small numbersβ provided a mechanistically obvious solution: restrict both carbohydrate quantity and all rapid acting carbohydrates [7]. Because of concerns about safety and feasibility for those who may not be so motivated, prospective studies are in order.
We have outlined the first of many possible studies to assess the safety and
... keep reading on reddit β‘https://www.hindawi.com/journals/crie/2021/3511281/
Yotsapon Thewjitcharoen,1 Ekgaluck Wanothayaroj,1 Haruethai Jaita,1 Soontaree Nakasatien,1 Siriwan Butadej,1 Ishant Khurana,2 Scott Maxwell,2 Assam El-Osta,2,3,4 Waralee Chatchomchuan,1 Sirinate Krittiyawong,1 and Thep Himathongkam1
Show moreAcademic Editor: Toshihiro Kita
Received20 Jun 2021Accepted25 Aug 2021
Published 02 Sep 2021
Context. The βhoneymoonβ phase among people with type 1 diabetes mellitus (T1DM) refers to the period (mostly less than 1 year) in which beta-cells remain functional and are able to produce insulin to maintain good glycemic control shortly following the development of diabetes. This phenomenon is still not completely understood. Previous studies have shown that the absence of diabetic ketoacidosis (DKA) at initial presentation, short duration of symptoms, older age at presentation, and strenuous exercise could be potential factors that influence the honeymoon phase.
Objective. To describe a usual case of adult-onset T1DM with prolonged honeymoon period for more than 5 years.
Methods. Repeated mixed meal stimulation tests for a period of 6β12 months together with monitoring pancreatic autoantibodies and laboratory data were followed following the onset of diagnosis.
Results. We report a 24-year-old Thai patient with T1DM with sustained remission without antidiabetic medication for more than 5 years while maintaining low-carbohydrate intake and regular exercise. Repeated mixed meal stimulation tests for a period of 6β12 months revealed preserved beta-cell functions. Interestingly, repeated pancreatic autoantibodies at 5 years after diagnosis still showed positive anti-GAD, anti-IA2, and anti-ZnT8.
Conclusion. Restored beta-cell function with complete insulin withdrawal in new-onset T1DM has been reported in very few cases with some common factors as in our patient (low-carbohydrate intake with regular exercise). Delaying autoimmune activity by reducing metabolic load in newly diagnosed T1DM might play a role in maintaining the honeymoon period and could lead to an innovative therapeutic option in new-onset T1DM.
https://preview.redd.it/x7tdx6gyzbm71.png?width=639&format=png&auto=webp&s=1178bc1afa58b00179abe9a6b5ca81622b6f5267
Prolonged Honeymoon Period in a Thai Patie
... keep reading on reddit β‘Good evening everyone I an img and I passed step one with an above average score. I was diagnosed with type 1 DM when I was one year old and I want to get into a residency that will help me find a definitive treatment of type 1 DM. Is there's a pancreas surgery fellowship after surgery residency? Or I have to apply for internal medicine residency and take endocrine fellowship? Thanks in advance Ramdan kareem
So there's been research over the last 5-10 years of the secretion of GABA from beta inslet cells. As type 1 diabetes is the result of autoimmune attack of these cells, further research has found a significant decrease in GABA in type 1s. This alongside the more than 75% of type 1s experiencing a form of mental illness is really interesting. Do you think that sustained GABA medication would be beneficial for type 1 diabetics? As the withdrawal would potentially be their current baseline. I'm not a doctor at all, so I'm just interested in other's opinions.
Type 2 diabetes mellitus is the main risk factor for cardiovascular diseases. It has been reported that the reduction of mitochondrial protein sirtuin protein 3 contributes to the development of type 2 diabetes mellitus by impacting mitochondrial respiration.
Cordycepin is an adenosine derivative and is isolated from the culture filtrate of Cordyceps Militaris. This study explored the protective effect of cordycepin on vascular impairment induced by type 2 diabetes mellitus and its property mechanism.
In this study, a type 2 diabetes mellitus rat model was established. The endothelium-dependent relaxation of the thoracic aorta ring decreased in type 2 diabetes mellitus rats that could be reversed by cordycepin. Next, the mitochondrion impairment in human umbilical vein endothelial was detected by JC-1 staining.
The in vitro studies reveal that cordycepin plays a beneficial role in advanced glycation end products-induced endothelial mitochondrion impairment. Moreover, according to the cordycepin molecular docking analysis, cordycepin can bind to sirtuin protein 3. Cordycepin increased the expression and activation of sirtuin protein 3 in a dose-dependent manner. sirtuin protein 3 interruption blocked the protective effect of cordycepin on mitochondrion in human umbilical vein endothelial.
Cordycepin can conclusively protect vascular function impaired by type 2 diabetes mellitus, and the mechanism may potentially be involved in the sirtuin protein 3 signal pathway.
From :
- https://www.dl.begellhouse.com/references/708ae68d64b17c52,forthcoming,41927.html
https://doi.org/10.3390/ijms222212310
https://pubmed.ncbi.nlm.nih.gov/34830192
Recently, type 2 diabetes mellitus (T2DM) has been reported to be strongly associated with Alzheimer's disease (AD). This is partly due to insulin resistance in the brain. Insulin signaling and the number of insulin receptors may decline in the brain of T2DM patients, resulting in impaired synaptic formation, neuronal plasticity, and mitochondrial metabolism. In AD patients, hypometabolism of glucose in the brain is observed before the onset of symptoms. Amyloid-Ξ² accumulation, a main pathology of AD, also relates to impaired insulin action and glucose metabolism, although ketone metabolism is not affected. Therefore, the shift from glucose metabolism to ketone metabolism may be a reasonable pathway for neuronal protection. To promote ketone metabolism, medium-chain triglyceride (MCT) oil and a ketogenic diet could be introduced as an alternative source of energy in the brain of AD patients.
------------------------------------------ Info ------------------------------------------
Open Access: True
Authors: Junpei Takeishi - Yasuko Tatewaki - Taizen Nakase - Yumi Takano - Naoki Tomita - Shuzo Yamamoto - Tatsushi Mutoh - Yasuyuki Taki -
Additional links:
https://www.ncbi.nlm.nih.gov/pubmed/31185481
Dallak M1, Al-Ani B1, Abdel Kader DH2, Eid RA3, Haidara MA4,5.
We sought to determine whether insulin can protect against type 1 diabetes mellitus (T1DM)-induced cardiac ultrastructural alterations in an animal model of the disease. This has not been investigated before.
Rats were either injected once with 65 mg/kg streptozotocin (STZ) before being sacrificed after 8 weeks or were treated with a daily injection of insulin 2 days by STZ and continued until being sacrificed.
Harvested tissues obtained from left ventricles in the untreated T1DM rats showed substantial damage to the cardiomyocyte ultrastructure as demonstrated by disintegrated myofibrils and their sarcomeres, damaged mitochondria and lipid droplets, which was substantially protected by insulin. Insulin also significantly inhibited T1DM-induced hyperglycemia (p < 0.001), dyslipidemia (p < 0.0001), malondialdehyde (MDA; p < 0.0001), tumor necrosis factor-alpha (TNF-Ξ±; p < 0.001) and interleukin-6 (p < 0.001). We further demonstrated a significant (p β€ 0.001) correlation between either sarcomere or mitochondrial injury scoring and the serum levels of glucose, dyslipidemia, and biomarkers of oxidative stress (OxS) and inflammation.
These results indicate that insulin effectively suppresses left ventricular cardiomyocyte ultrastructural damage, which substantially slows down the progression of diabetic cardiomyopathy for 8 weeks in a rat model of T1DM, possibly due to the glycemic control and inhibition of dyslipidemia, OxS and inflammation
https://doi.org/10.1097/MED.0000000000000669
https://pubmed.ncbi.nlm.nih.gov/34392261
PURPOSE OF STUDY
Type 1 diabetes mellitus (T1DM) is managed via careful control of blood glucose, exogenous insulin, diet, exercise, and other physiologic factors. Interestingly, the dietary recommendations for T1DM have had very little systematic research. Many clinical observations, as well as emerging research studies, have noted that a carbohydrate-restricted diet can lead to normalization of blood glucoses with reduction in hypoglycemic reactions among motivated individuals.
RECENT FINDINGS
In this paper, we review observations of carbohydrate restriction and propose a series of studies to test two levels of dietary carbohydrate intake for the management of individuals affected by T1DM. We recommend that the studies start in otherwise healthy adults with hemoglobin A1c > 8%, and then progress to more complicated populations including children, those with secondary complications and/or good glycemic control. Larger, long-term studies would then address growth in children, and diabetic complications including cardiovascular outcomes.
SUMMARY
Due to the clinical observations of improvements using carbohydrate-restricted nutrition for T1DM, we recommend that these types of studies addressing the level of dietary carbohydrate be urgently conducted.
------------------------------------------ Info ------------------------------------------
Open Access: False
Authors: David T. Dikeman - Eric C. Westman -
Additional links: None found
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