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Hypoglycemic unawareness support

Hypoglycemic unawareness support

Decreased Gold Antioxidant defense system baseline 5. Increased neurogenic and Post-race recovery foods symptom scores Hypogpycemic did Hypoglycemuc differ between Post-race recovery foods and BGAT groups before or after 4 months of intensive diabetes therapy. Hypoglycemia is a common side effect of various diabetes medications, such as insulin and sulfonylureas [ 811 ].

Hypoglycemic unawareness support -

So there's an incredibly important role and we rely on agencies to fund our research. So the JDRF focuses on Type I Diabetes based research.

Everyone has their own interest, personal connections to family members who may have this disease, and I guess we're talking about diabetes, and it's very important for them to feel that they're doing something that is leading towards you know better treatments or a cure, and every agency has their own agenda so to speak that allows them to put money where they think it needs to go.

Interviewer: Your most recent grant from JDRF is supporting your research investigating complications associated with diabetes. So it stems from this paradoxical observation that diabetes causes high blood sugar levels but one of the major problems of diabetes is hypoglycemia, or low blood sugar, how does that happen?

Fisher: Because we're treating diabetes better and better and getting more and more aggressive and trying to get blood sugar down to normal or even below normal levels the incidence of hypoglycemia, that's low blood sugar, has now eclipsed that of high blood sugars in terms of hospital admissions.

People are coming in now because we're treating them more and more aggressively. These low blood sugar reactions can be mild, I mean they happen every day, or every other day for people who have tightly controlled blood sugars.

The problem is as it happens more and more they run the risk of having neurological problems. Again, what happens is your ability to defend against this low blood sugar becomes impaired over time your brain runs almost exclusively on blood sugar so as your blood sugar drops your brain starts having problems functioning, sadly.

You get, it can be as mild as a confused, a little disoriented, but it can cause people to pass out if your blood sugar gets low enough. It can cause people to have seizures if your blood sugars get low enough and a recent study we published shows that low blood sugar actually is fatal.

If your blood sugar is low enough for long enough people die. Interviewer: Wow. Now normally people know when they're becoming hypoglycemic, right? There are different warning signs that the body give you? Fisher: Right so you can imagine as your blood sugar gets low and your brain stops functioning it's a flight or fight stress response.

Your brain activates your adrenaline, your epinephrine, your norepinephrine, other hormones in your body help bring your blood sugar back up. What I'm studying in our laboratory is hypoglycemia unawareness.

What happens is your body doesn't get these traditional warning signs, you don't get hungry. For example, you don't go, "Gee my blood sugar is low," and go get something to eat, go grab a glass of orange juice, etcetera Nocturnal, that is night time; low blood sugar is particularly dangerous.

People with diabetes and hypoglycemia unawareness don't wake up in the middle of the night. This leads to the unfortunate "dead in bed" syndrome, which is as horrible as it sounds. Interviewer: Well obviously it's a very serious problem and your approach is to study it in an animal model. Fisher: Right, that's the novel part about our research, is we've now created an animal model to investigate hypoglycemia unawareness.

So the trick for many, many years is how do you get an animal model to respond hypoglycemia unawareness? In humans it's easy you say, "Do you recognize that your blood sugar is low? You can't ask a rat if they're, how they're feeling.

So what we've done is we've modeled this by saying, "What is going to help somebody if their blood sugar is low? So what we're doing is we're measuring how much food our rat takes when his blood sugar is low, and in our model now what we've done is we make the rats who are currently hypoglycemic, similar to patients that take insulin every day, and if their blood sugar gets you know low one day or the next day they're at high risk for hypoglycemia unawareness the next day and that's what happens in our rats.

Interviewer: So the rats who get food are aware, at least subconsciously aware of their hypoglycemic condition. The rats that don't eat are hypoglycemic unaware. Fisher: Right, and so what the JDRF has, the goal of their research is to say, "Well what we can do to make people more aware?

We're giving many different kinds of drugs that act in the central nervous system to these rats, these rats that we've made hypoglycemia unaware, and then we're seeing which drug is really going to make them say, "Oh geez I feel horrible I've got to go eat," and any drug that can help them decide to go eat is a drug which is enhancing hypoglycemia awareness.

There was no difference between structured education programs in flexible insulin therapy and programs with a psychological approach when compared head to head, and this may be because in teaching users the basics of insulin pharmacodynamics and how to adjust their insulin regimens around their lifestyles to achieve glucose targets that exclude hypoglycemia, hypoglycemia exposure is lessened.

There is perhaps a need to seek the common factors in successful programs to distill the essential elements of any new programs. Meanwhile, DAFNE-HART had a much higher baseline level of SH than any of the other studies and was the only study that took people who were IAH despite prior education.

Although a small nonrandomized study, it demonstrated that a psychobehavioral therapeutic approach can have a sustained effect on SH and nonsevere hypoglycemic episodes in people whose IAH seems resistant to other interventions Thus, in unselected populations with T1D, structured education in flexible insulin usage reduces SH and may reduce the proportion of people with IAH and SH.

In those with IAH, further education or BGAT reduces SH, with the greatest reductions seen in programs with a behavioral component. CSII can reduce SH with greater reductions in those with greater SH at baseline 52 , although there was evidence that in an unselected population, CSII and improved control may cause some deterioration of awareness In observational studies, CGM showed a reduction in SH, even in those who remained in IAH despite education and CSII A RCT of LGS compared with CSII in young people with IAH showed improved awareness and reduced SH with LGS-enabled SAP Most studies with technology, such as CSII or CGM, were done in patients who had received prior education.

Thus, in people with IAH despite prior education, CSII, CGM, and, in particular, sensor-augmented pump therapy with LGS provide additional benefits. The HypoCOMPaSS study 63 is in keeping with earlier studies by Cranston et al. HypoCOMPaSS clearly illustrates the value of a holistic approach to the management of people with IAH, using structured education as a core foundation combined with optimized MDI and the use of CSII in selected individuals, to provide far greater advantages than one intervention alone.

We thus propose a stepped-care algorithm that may guide the health care professional in choosing the appropriate intervention when faced with a person with IAH Fig.

We would argue that step one—provision of structured education in flexible insulin therapy—should be available to any person with T1D but that additional resources for individuals with higher care needs may be focused in centers where the more intensive interventions combining psychoeducational and technological interventions are available, to which people with IAH and SH posteducation can be referred.

Proposed algorithm for the selection of interventions in patients with IAH and SH. The gray shading indicates recommendation based on expert opinion, with as yet no completed evidence.

For future research, we would recommend that outcome measures such as SH rates and HA scores should be reported in a standardized manner to allow future systematic reviews and meta-analyses. Because incidence and prevalence of SH rates are not normally distributed, the median IQR SH rate may be more appropriate than the mean SD commonly used.

Measures of assessment of HA should also be standardized using Gold or Clarke scores because these have been shown to correlate well with clinical and clamp findings and each other. The proportion of patients with baseline IAH and then improved awareness should be reported as well as Gold or Clarke scores and their change.

Future research may be needed to compare structured education, possibly using psychotherapeutic techniques, and optimized MDI using insulin analogs, with comparisons against new diabetes technologies such as LGS-enabled SAP.

Psychotherapeutic techniques may provide additional benefit, in particular in improving HA status, and large RCTs using this approach should be conducted. Use of technology in diabetes, either better warning systems through CGM or through improved insulin delivery via CSII, can reduce SH rates and improve HA without worsening glycemic control, but without restoring counterregulatory hormone responses.

A stepped approach is recommended in the management of people with IAH. The authors thank the authors of the original cited studies who were contacted for sharing the information required from their studies. received fellowship funding as part of the Health Manpower Development Plan award from Khoo Teck Puat Hospital, Alexandra Health Pte, Ltd.

received PhD funding as part of a Diabetes UK project grant. None of the funding or supportive agencies were involved in the design or conduct of the study; collection, management, analysis, or interpretation of the data; or preparation, review, or approval of the manuscript.

The views expressed are those of the author s and not necessarily those of the funding agencies. Duality of Interest. has received travel support from Roche and Lilly UK. No other potential conflicts of interest relevant to this article were reported.

Author Contributions. undertook the literature search and reviewed the abstracts and full articles. wrote the manuscript.

performed and supervised the statistical analysis. conceived the idea for the review. All authors designed the study, contributed to the discussion, and critically reviewed the final manuscript.

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Sign In. Skip Nav Destination Close navigation menu Article navigation. Volume 38, Issue 8. Previous Article Next Article. Research Design and Methods. Article Information. Article Navigation. Systematic Review July 14 Interventions That Restore Awareness of Hypoglycemia in Adults With Type 1 Diabetes: A Systematic Review and Meta-analysis Ester Yeoh ; Ester Yeoh.

Corresponding author: Ester Yeoh, esteryeoh nhs. This Site. Google Scholar. Pratik Choudhary ; Pratik Choudhary. Munachiso Nwokolo ; Munachiso Nwokolo. Salma Ayis ; Salma Ayis.

Stephanie A. Amiel Stephanie A. Diabetes Care ;38 8 — Article history Received:. Get Permissions. toolbar search Search Dropdown Menu. toolbar search search input Search input auto suggest. Figure 1. View large Download slide.

Table 1 Summary of the 43 studies that were included in the final systematic review. First author, year ref. Intervention, brief description. N ; study duration. Age years ; diabetes duration years. SH rates.

HA score. HbA 1c. Mean SH Gold score from 5. Clarke score from 5. No change in HbA 1c : baseline 7. Jordan, 4 Tayside insulin management course: Structured group education, 1 day of education per week for 4 consecutive weeks.

Decrease in number of patients with HU Median HbA 1c reduction: 8. Hopkins, 21 DAFNE audit: Structured diabetes group education program, 5-day course in flexible insulin therapy.

Improved HbA 1c : 8. Hernandez, 29 Self-awareness education on body cues associated with various levels of glycemia. Eight 3-h, biweekly sessions, follow-up study of Hernandez, Improved detection of symptom cues of euglycemia and hypoglycemia.

Kubiak, 31 IG with hypoglycemia-specific education program 6 lessons, 45 min vs. Using modified Gold score: visual analog scale Improved HbA 1c in both groups; no difference between IG: 6. Broers, 22 Dutch adaptation of BGAT-III 6 weekly 1.

individual setting. Psychoeducational intervention, follow-up study to Broers, Improved recognition of hypoglycemia in both groups No change in HbA 1c : 7.

Hernandez, 30 Refer to Hernandez, No increase in ability to detect hypoglycemia but subjects could identify normal BG more accurately. No change in HbA 1c : 8.

Broers, 23 Refer to Broers, Accuracy index of BG perception increased from 8. Improved autonomic and neuroglycopenic symptom scores during hypoglycemic clamp. No change in epinephrine and norepinephrine responses. Increased HbA 1c : 6.

Cox, 24 BGAT-II psychoeducational group program, follow-up study of Cox, Booster intervention did not affect these benefits. No change in HbA 1c : Dagogo-Jack, 33 Avoidance of hypoglycemia, 3-year follow-up study of Dagogo-Jack, No report on SH. Improvement in neurogenic and neuroglycopenic symptoms score at 1 year postreversal from preintervention.

Slight increase in HbA 1c : 7. Fritsche, 25 5-day inpatient diabetes education program DTTP , 25 min lessons on flexible insulin therapy, carbohydrate counting, correction and prevention of hypo- and hyperglycemia.

those with no history of SH. Improved accuracy index of BG estimation in patients with SH but no improvement in the group without SH. Decreased HbA 1c : 8. Fanelli, 35 Avoidance of hypoglycemia for 6 months in patients with T1D 8 without diabetic autonomic neuropathy [DAN], 13 with DAN and 15 subjects without T1D.

SH did not occur. Improved autonomic and neuroglycopenic symptoms in all groups. Responses remained lower than in subjects without T1D. Increased HbA 1c in all groups but remained within therapeutic target: 6.

Liu, 36 Avoidance of hypoglycemia with less strict glycemic control and higher BG targets, SMBG 4 times daily with modification of insulin doses. Improved symptoms scores for sweating and lack of concentration. Improved GH and epinephrine responses but no changes in glucagon, norepinephrine, and cortisol.

Cox, 26 BGAT-II, refer to Cox, No report of SH. Better accuracy in detecting BG fluctuations and low BG levels. Those with reduced HA had improved detection of low BG.

Not available. Davis, 27 Conventional insulin therapy vs. intensive insulin therapy. intensive insulin therapy was 0.

Reduction in total hypoglycemia symptom scores with intensive insulin therapy, with no reversal on reinstitution of conventional therapy. Lower plasma glucose to stimulate plasma epinephrine secretion during intensive therapy compared with initial conventional therapy without complete reversal on reinstitution of conventional therapy.

HbA 1c in conventional group: 9. Dagogo-Jack, 34 Refer to Dagogo-Jack, Original group of 18 patients 6 HA, 6 HU, 6 healthy volunteers. Increase in total neurogenic and neuroglycopenic symptoms score responses to hypoglycemia.

No significant increases in neuroendocrine responses epinephrine, pancreatic polypeptide, glucagon, GH, and cortisol after intervention. Increase in HbA 1c : 7. Improved symptoms scores after 3 weeks of no hypoglycemia.

Improved glucose threshold for recognition of hypoglycemia in group A from glucose threshold of 2. Improved counterregulatory hormone adrenaline, noradrenaline, GH responses.

No significant change in HbA 1c during intervention period; group A: 6. Fanelli, 38 Intensive insulin therapy physiologic insulin replacement and continuous education with avoidance of hypoglycemia.

no decrease in frequency of hypoglycemia in CG. Baseline 9 patients had at least 1 SH during the year before study to no episodes of SH during study.

Improvement in autonomic symptoms in IG, glucose threshold for autonomic symptoms at baseline from 2. No change in CG. Improved counterregulatory hormones adrenaline, cortisol, GH responses in IG maintained at 1-year follow-up, but not normalized to healthy volunteers.

No changes in CG. Increased HbA 1c in IG but still within target 5. CG: HbA 1c showed no increase over 3 months. Fanelli, 37 Avoidance of hypoglycemia with adjustment of doses of insulin aiming for higher fasting, preprandial, and bedtime BG targets. Baseline 2 patients had at least 1 SH in the year preceding study to no SH during study.

Improved neuroendocrine and symptom responses with no difference in autonomic glycemic thresholds compared with healthy volunteers.

Epinephrine responses increased from baseline but still lower than in healthy volunteers. Increased HbA 1c : 5. DTTP CG. IG: 0. Improvement in HA modified Clarke score in both groups: CG: 1.

IG: 1. Improved HbA 1c in PRIMAS group: 8. no change in CG: 8. Hermanns, 43 HyPOS IG vs. standard education CG , long-term follow-up study of Hermanns, ; CG: 0. Not reported. No difference in glycemic control: CG: 7.

HyPOS: 7. Hermanns, 44 Refer to Hermanns, IG: 3. Improved detection of low BG and treatment of low BG. Increased intensity of hypoglycemia symptoms scores in HyPOS group. HbA 1c improved in CG 7. Schachinger, 45 Randomized to BGAT—III IG vs. physician-guided self-help control intervention CG.

CG: 1. Improved recognition of low, high, and overall BG in BGAT vs. Detection of low BG improved in BGAT: No change in HbA 1c : 6. SMBG CG. No change in HbA 1c : HAATT group 8. Kinsley, 47 BGAT vs. cholesterol awareness CG in patients enrolled into an intensive diabetes treatment program.

No data on SH. Increased neurogenic and neuroglycopenic symptom scores but did not differ between CG and BGAT groups before or after 4 months of intensive diabetes therapy.

Increased epinephrine response in BGAT group to hypoglycemia. Improved HbA 1c in both groups: 9. Cox, 48 Long-term follow-up of BGAT patients with a proportion of patients receiving BGAT booster training. SH not reported. BGAT patients had better estimation of BG levels than control subjects. Improved HbA 1c over time: BGAT: Improved Clarke score, baseline 5.

At baseline, 19 subjects were HU according to Clarke test, and at 24 months, 3 of 20 were HU. Leinung, 56 Retrospective study on CGM use on HbA 1c and SH rates.

Improved HbA 1c : 7. Ryan, 54 CGM use in patients with SH. Hübinger, 53 Patients started on CSII with changes in HA. Improved HbA 1c in HU group: 8.

CSII with or without RT-CGM in SH 2 × 2 factorial design. All patients received structured diabetes and hypoglycemia education, weekly telephone contact, and monthly clinic visits.

Overall study population decreased Gold score: 5. CSII only in patients with HU. Mean SH in LGS: 1. Improvement in Clarke score in both groups: CSII: 6. No difference in epinephrine response to hypoglycemia between groups.

HbA 1c was similar in both groups at baseline and did not change at end of study. CSII: 7. Leelarathna, 59 HypoCOMPaSS clamp study refer to Little, Decreased Gold scores: baseline 5.

Glucose threshold at which subjects felt hypoglycemic improved: 2. Improved autonomic and neuroglycopenic symptoms scores.

Improved metanephrine response. Kovatchev, 62 SMBG with HHC device providing feedback, randomized to different sequences: or 1: routine SMBG, 2: added estimated HbA 1c , hypoglycemia risk and glucose variability, 3: estimates of symptoms potentially related to hypoglycemia.

Not reported on follow-up. Thomas, 60 Randomized to optimized MDI preprandial insulin lispro and pre-evening meal glargine , CSII, or education. Incidence of SH was 0. No change in HbA 1c in education group: 8.

improved HbA 1c in analog group: 8. improved HbA 1c in CSII: 8. Kanc, 61 Randomized crossover study to 2 groups: A bedtime NPH vs. B nighttime CSII. SH outcome not reported.

Autonomic symptoms appeared earlier at higher BG levels in CSII than in NPH group: 3. No differences between CSII and NPH for hypoglycemic thresholds for neuroglycopenic symptoms. No differences in end HbA 1c between CSII and NPH: 7. human soluble insulin SI with NPH. No significant differences in total symptom scores or counterregulatory hormone responses during hypoglycemia clamp.

HbA 1c not different between SI 6. Fanelli, 66 Randomized crossover trial, 2 different insulin regimens: A split regimen of 4 daily insulin injections 3 bolus plus bedtime NPH vs. B mixed regimen of 3 daily insulin injection 3 bolus plus mixed regular insulin and NPH at dinner.

No SH in either group. Autonomic symptom scores increased earlier with split regimen than with mixed regimen BG threshold: 3. Similar neuroglycopenic symptoms threshold in both groups. Better HbA 1c with split vs. mixed insulin regimen 7.

Ferguson, 65 Randomized crossover trial: insulin lispro vs. regular human insulin in patients with HU and history of frequent SH. Initial Gold score 4. No differences in HbA 1c : 9. human regular insulin before meals and NPH at bedtime. SH occurred in 1 patient in each group.

HM therapy associated with slightly lower total epinephrine response, and autonomic symptom response occurred at a lower BG level during experimental hypoglycemia. No differences in HbA 1c : 7.

Chalon, 68 Propranolol: 20 mg twice a day for first 2 weeks, followed by 30 mg twice a day for the next 2 weeks vs. propranolol More sweating in propranolol group during biochemical hypoglycemia compared with placebo.

View Large. Figure 2. Figure 3. Hypoglycaemia: the limiting factor in the glycaemic management of Type I and Type II diabetes. Search ADS. Reduced neuroendocrine and symptomatic responses to subsequent hypoglycemia after 1 episode of hypoglycemia in nondiabetic humans.

Prevalence of impaired awareness of hypoglycaemia in adults with Type 1 diabetes. The Tayside insulin management course: an effective education programme in type 1 diabetes.

Impaired hypoglycaemia awareness and employment in people with Type 1 diabetes. The decision not to drive during hypoglycemia in patients with type 1 and type 2 diabetes according to hypoglycemia awareness.

Severe hypoglycaemia in adult patients with type 1 diabetes: influence of risk markers and selection. Restoration of hypoglycaemia awareness in patients with long-duration insulin-dependent diabetes.

Centre for Reviews and Dissemination. Systematic Reviews. CRD's Guidance for Undertaking Reviews in Health Care. York, U. American Diabetes Association. Reduced awareness of hypoglycemia in adults with IDDM. A prospective study of hypoglycemic frequency and associated symptoms.

Frequency of severe hypoglycemia in patients with type I diabetes with impaired awareness of hypoglycemia. Workgroup on Hypoglycemia, American Diabetes Association. Defining and reporting hypoglycemia in diabetes: a report from the American Diabetes Association Workgroup on Hypoglycemia.

Blood glucose estimation and symptoms during hyperglycemia and hypoglycemia in patients with insulin-dependent diabetes mellitus.

Preferred reporting items for systematic reviews and meta-analyses: the PRISMA statement. Meta-analysis of observational studies in epidemiology: a proposal for reporting.

Meta-analysis Of Observational Studies in Epidemiology MOOSE group. AHRQ series paper 5: grading the strength of a body of evidence when comparing medical interventions—Agency for Healthcare Research and Quality and the effective health-care program. Improved biomedical and psychological outcomes 1 year after structured education in flexible insulin therapy for people with type 1 diabetes: the U.

DAFNE experience. Blood glucose awareness training in Dutch type 1 diabetes patients: one-year follow-up. Blood Glucose Awareness Training in Dutch Type 1 diabetes patients. Short-term evaluation of individual and group training.

Diabetes teaching program improves glycemic control and preserves perception of hypoglycemia. Recovery of epinephrine response but not hypoglycemic symptom threshold after intensive therapy in type 1 diabetes. de Zoysa. A psychoeducational program to restore hypoglycemia awareness: the DAFNE-HART pilot study.

Evaluation of a self-awareness intervention for adults with type 1 diabetes and hypoglycemia unawareness. Hernandez CA, Hume MR, Rodger NW: Six-month evaluation of a diabetes self-awareness intervention.

Outcomes Manage ;—; quiz — Evaluation of a self-management-based patient education program for the treatment and prevention of hypoglycemia-related problems in type 1 diabetes.

Avoidance of hypoglycemia restores hypoglycemia awareness by increasing beta-adrenergic sensitivity in type 1 diabetes.

Reversal of hypoglycemia unawareness, but not defective glucose counterregulation, in IDDM. Long-term intensive therapy of IDDM patients with clinically overt autonomic neuropathy: effects on hypoglycemia awareness and counterregulation.

Improved counter-regulatory hormonal and symptomatic responses to hypoglycemia in patients with insulin-dependent diabetes mellitus after 3 months of less strict glycemic control.

Throughout the day, depending Understanding your metabolic rate multiple factors, blood glucose also called blood Hypoglycemic unawareness support levels will L-carnitine benefits or supprot. This is Hypogglycemic. But if Hypogljcemic goes unawaeness the healthy Hypoglyycemic and is not Hypoglycemic unawareness support, it can get dangerous. Low blood glucose is when your blood glucose levels have fallen low enough that you need to take action to bring them back to your target range. However, talk to your diabetes care team about your own blood glucose targets, and what level is too low for you. Each person's reaction to low blood glucose is different. Learn your own signs and symptoms of when your blood glucose is low.

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