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I gave up on Sema myself. My first run of it for a few months had excellent results with minimal sides. I attempted to run it three more times later that year and this year. Each time had very reduced appetite suppression and greatly increased sides. I split the dose in half (I ramped up very slowly to even 1mg a week over the course of three months), and I swear by splitting it, while reducing the sides, it also reduced the overall benefit, however small for me now. Weird compound.
But right now, I'm not having issues with cravings anymore since I got rid of all the artificial sweeteners I was consuming. Maybe I'll try Tirz, Reta, or whatever new ones come along in the future if I have the problem come back. Hopefully by then Tirz or Reta will have come down in price, too.
But right now, I'm not having issues with cravings anymore since I got rid of all the artificial sweeteners I was consuming. Maybe I'll try Tirz, Reta, or whatever new ones come along in the future if I have the problem come back. Hopefully by then Tirz or Reta will have come down in price, too.
MR. BMJ
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ORIGINAL ARTICLE| JUNE 22 2024
Diabetes Care dc240491
doi.org
Article history
PubMed:
38907683
OBJECTIVE
To determine whether semaglutide slows progression of glycemia in people with cardiovascular disease and overweight or obesity but without diabetes.
RESEARCH DESIGN AND METHODS
In a multicenter, double-blind trial, participants aged ≥45 years, with BMI ≥27 kg/m2, and with preexisting cardiovascular disease but without diabetes (HbA1c <6.5%) were randomized to receive subcutaneous semaglutide (2.4 mg weekly) or placebo. Major glycemic outcomes were HbA1c and proportions achieving biochemical normoglycemia (HbA1c <5.7%) and progressing to biochemical diabetes (HbA1c ≥6.5%).
RESULTS
Of 17,604 participants, 8,803 were assigned to semaglutide and 8,801 to placebo. Mean ± SD intervention exposure was 152 ± 56 weeks and follow-up 176 ± 40 weeks. In both treatment arms mean nadir HbA1c for participants was at 20 weeks. Thereafter, HbA1c increased similarly in both arms, with a mean difference of −0.32 percentage points (95% CI −0.33 to −0.30; −3.49 mmol/mol [−3.66 to −3.32]) and with the difference favoring semaglutide throughout the study (P < 0.0001). Body weight plateaued at 65 weeks and was 8.9% lower with semaglutide. At week 156, a greater proportion treated with semaglutide were normoglycemic (69.5% vs. 35.8%; P < 0.0001) and a smaller proportion had biochemical diabetes by week 156 (1.5% vs. 6.9%; P < 0.0001). The number needed to treat was 18.5 to prevent a case of diabetes. Both regression and progression were dependent on glycemia at baseline, with the magnitude of weight reduction important in mediating 24.5% of progression and 27.1% of regression.
CONCLUSIONS
In people with preexisting cardiovascular disease and overweight or obesity but without diabetes, long-term semaglutide increases regression to biochemical normoglycemia and reduces progression to biochemical diabetes but does not slow glycemic progression over time.
****************************************************************
Does Wegovy (higher dose than Ozempic semaglutide) slow progression of high blood sugar in people with obesity and heart disease obesity but without type 2 diabetes?
*Select Trial showed reduced risk of heart attack, stroke and death from heart disease.
*Blood sugar was studied by looking at HbA1c (achieving normal average blood sugars per HbA1c <5.7% and progressing to diagnostic criteria for diabetes HbA1c ≥6.5%.
*17,604 participants randomized to semaglutide and placebo and both had lowest HbA1c at 20 weeks. Thereafter, HbA1c increased similarly in both arms, but −0.32 percentage points favoring semaglutide throughout the study.
1. Body weight plateaued at 65 weeks and was 9% lower with semaglutide.
2. At week 156, a greater proportion treated with semaglutide had “normal” blood sugars (69.5% vs. 35.8%; P < 0.0001) and a smaller proportion had criteria for type 2 diabetes by week 156 (1.5% vs. 6.9%; P < 0.0001).
3. The number needed to treat was 18.5 to prevent a case of diabetes.
4. Magnitude of weight reduction important in mediating 24.5% of progression and 27.1% of regression.
Effect of Semaglutide on Regression and Progression of Glycemia in People With Overweight or Obesity but Without Diabetes in the SELECT Trial
Diabetes Care dc240491
Effect of Semaglutide on Regression and Progression of Glycemia in People With Overweight or Obesity but Without Diabetes in the SELECT Trial
OBJECTIVE. To determine whether semaglutide slows progression of glycemia in people with cardiovascular disease and overweight or obesity but without diabe
doi.org
PubMed:
38907683
OBJECTIVE
To determine whether semaglutide slows progression of glycemia in people with cardiovascular disease and overweight or obesity but without diabetes.
RESEARCH DESIGN AND METHODS
In a multicenter, double-blind trial, participants aged ≥45 years, with BMI ≥27 kg/m2, and with preexisting cardiovascular disease but without diabetes (HbA1c <6.5%) were randomized to receive subcutaneous semaglutide (2.4 mg weekly) or placebo. Major glycemic outcomes were HbA1c and proportions achieving biochemical normoglycemia (HbA1c <5.7%) and progressing to biochemical diabetes (HbA1c ≥6.5%).
RESULTS
Of 17,604 participants, 8,803 were assigned to semaglutide and 8,801 to placebo. Mean ± SD intervention exposure was 152 ± 56 weeks and follow-up 176 ± 40 weeks. In both treatment arms mean nadir HbA1c for participants was at 20 weeks. Thereafter, HbA1c increased similarly in both arms, with a mean difference of −0.32 percentage points (95% CI −0.33 to −0.30; −3.49 mmol/mol [−3.66 to −3.32]) and with the difference favoring semaglutide throughout the study (P < 0.0001). Body weight plateaued at 65 weeks and was 8.9% lower with semaglutide. At week 156, a greater proportion treated with semaglutide were normoglycemic (69.5% vs. 35.8%; P < 0.0001) and a smaller proportion had biochemical diabetes by week 156 (1.5% vs. 6.9%; P < 0.0001). The number needed to treat was 18.5 to prevent a case of diabetes. Both regression and progression were dependent on glycemia at baseline, with the magnitude of weight reduction important in mediating 24.5% of progression and 27.1% of regression.
CONCLUSIONS
In people with preexisting cardiovascular disease and overweight or obesity but without diabetes, long-term semaglutide increases regression to biochemical normoglycemia and reduces progression to biochemical diabetes but does not slow glycemic progression over time.
****************************************************************
Does Wegovy (higher dose than Ozempic semaglutide) slow progression of high blood sugar in people with obesity and heart disease obesity but without type 2 diabetes?
*Select Trial showed reduced risk of heart attack, stroke and death from heart disease.
*Blood sugar was studied by looking at HbA1c (achieving normal average blood sugars per HbA1c <5.7% and progressing to diagnostic criteria for diabetes HbA1c ≥6.5%.
*17,604 participants randomized to semaglutide and placebo and both had lowest HbA1c at 20 weeks. Thereafter, HbA1c increased similarly in both arms, but −0.32 percentage points favoring semaglutide throughout the study.
1. Body weight plateaued at 65 weeks and was 9% lower with semaglutide.
2. At week 156, a greater proportion treated with semaglutide had “normal” blood sugars (69.5% vs. 35.8%; P < 0.0001) and a smaller proportion had criteria for type 2 diabetes by week 156 (1.5% vs. 6.9%; P < 0.0001).
3. The number needed to treat was 18.5 to prevent a case of diabetes.
4. Magnitude of weight reduction important in mediating 24.5% of progression and 27.1% of regression.