EXTENDED-RELEASE NIACIN & GLUCOSE LEVELS

[mcs]

Anyone notice impact on fasting and post-prandial glucose levels and a1c from taking high-dose ER niacin to manage lipids? I was on 1.5g per day and increased to 2g per day and now I'm noticing glucose levels about 10 points higher. Wondering if this will subside over time. I know some are taking metformin to bring it back down.

 

[Deleted member 43589]

I will post this just as a sake of a warning. I too was taking high doses of Niacin to lower Lipoprotein(a). I told my cardiologist and he asked me to please stop taking niacin. Of course I was shocked and ask why and he said because it increases the risk of heart attack. Needless to say it kind of burst my bubble but I quit taking it and unfortunately have 3 bottles sitting in the cabinet.

Here is a very good article

Niacin Too Dangerous for Routine Cholesterol Therapy

Mainstay drug now linked to death risk, dangerous side effects and no benefits

news.northwestern.edu

Jane Armitage, F.R.C.P., F.F.P.H., professor of clinical trials and epidemiology, University of Oxford, England; Donald Lloyd-Jones, M.D., chief, preventive medicine, Northwestern University Feinberg School of Medicine and Northwestern Memorial Hospital, Chicago; July 17, 2014, New England Journal of Medicine

Schandelmaier S, Briel M, Saccilotto R, et al. Niacin for primary and secondary prevention of cardiovascular events. Cochrane Database Syst Rev. 2017;6(6):CD009744. Published 2017 Jun 14. doi:10.1002/14651858.CD009744.pub2

Abstract​

Background​

Nicotinic acid (niacin) is known to decrease LDL‐cholesterol, and triglycerides, and increase HDL‐cholesterol levels. The evidence of benefits with niacin monotherapy or add‐on to statin‐based therapy is controversial.

Objectives​

To assess the effectiveness of niacin therapy versus placebo, administered as monotherapy or add‐on to statin‐based therapy in people with or at risk of cardiovascular disease (CVD) in terms of mortality, CVD events, and side effects.

Search methods​

Two reviewers independently and in duplicate screened records and potentially eligible full texts identified through electronic searches of CENTRAL, MEDLINE, Embase, Web of Science, two trial registries, and reference lists of relevant articles (latest search in August 2016).

Selection criteria​

We included all randomised controlled trials (RCTs) that either compared niacin monotherapy to placebo/usual care or niacin in combination with other component versus other component alone. We considered RCTs that administered niacin for at least six months, reported a clinical outcome, and included adults with or without established CVD.

Data collection and analysis​

Two reviewers used pre‐piloted forms to independently and in duplicate extract trials characteristics, risk of bias items, and outcomes data. Disagreements were resolved by consensus or third party arbitration. We conducted random‐effects meta‐analyses, sensitivity analyses based on risk of bias and different assumptions for missing data, and used meta‐regression analyses to investigate potential relationships between treatment effects and duration of treatment, proportion of participants with established coronary heart disease and proportion of participants receiving background statin therapy. We used GRADE to assess the quality of evidence.

Main results​

We included 23 RCTs that were published between 1968 and 2015 and included 39,195 participants in total. The mean age ranged from 33 to 71 years. The median duration of treatment was 11.5 months, and the median dose of niacin was 2 g/day. The proportion of participants with prior myocardial infarction ranged from 0% (4 trials) to 100% (2 trials, median proportion 48%); the proportion of participants taking statin ranged from 0% (4 trials) to 100% (12 trials, median proportion 100%).
Using available cases, niacin did not reduce overall mortality (risk ratio (RR) 1.05, 95% confidence interval (CI) 0.97 to 1.12; participants = 35,543; studies = 12; I2 = 0%; high‐quality evidence), cardiovascular mortality (RR 1.02, 95% CI 0.93 to 1.12; participants = 32,966; studies = 5; I2 = 0%; moderate‐quality evidence), non‐cardiovascular mortality (RR 1.12, 95% CI 0.98 to 1.28; participants = 32,966; studies = 5; I2 = 0%; high‐quality evidence), the number of fatal or non‐fatal myocardial infarctions (RR 0.93, 95% CI 0.87 to 1.00; participants = 34,829; studies = 9; I2 = 0%; moderate‐quality evidence), nor the number of fatal or non‐fatal strokes (RR 0.95, 95% CI 0.74 to 1.22; participants = 33,661; studies = 7; I2 = 42%; low‐quality evidence). Participants randomised to niacin were more likely to discontinue treatment due to side effects than participants randomised to control group (RR 2.17, 95% CI 1.70 to 2.77; participants = 33,539; studies = 17; I2 = 77%; moderate‐quality evidence). The results were robust to sensitivity analyses using different assumptions for missing data.

Authors' conclusions​

Moderate‐ to high‐quality evidence suggests that niacin does not reduce mortality, cardiovascular mortality, non‐cardiovascular mortality, the number of fatal or non‐fatal myocardial infarctions, nor the number of fatal or non‐fatal strokes but is associated with side effects. Benefits from niacin therapy in the prevention of cardiovascular disease events are unlikely.

More

Don't Take Niacin for Heart Health, Docs Warn

Niacin, or vitamin B3, is too dangerous and should not be used routinely by people looking to control their cholesterol levels or prevent heart disease, doctors say.

www.livescience.com

 

[mcs]

I will post this just as a sake of a warning. I too was taking high doses of Niacin to lower Lipoprotein(a). I told my cardiologist and he asked me to please stop taking niacin. Of course I was shocked and ask why and he said because it increases the risk of heart attack. Needless to say it kind of burst my bubble but I quit taking it and unfortunately have 3 bottles sitting in the cabinet.

Here is a very good article

Niacin Too Dangerous for Routine Cholesterol Therapy

Mainstay drug now linked to death risk, dangerous side effects and no benefits

news.northwestern.edu

Jane Armitage, F.R.C.P., F.F.P.H., professor of clinical trials and epidemiology, University of Oxford, England; Donald Lloyd-Jones, M.D., chief, preventive medicine, Northwestern University Feinberg School of Medicine and Northwestern Memorial Hospital, Chicago; July 17, 2014, New England Journal of Medicine

Schandelmaier S, Briel M, Saccilotto R, et al. Niacin for primary and secondary prevention of cardiovascular events. Cochrane Database Syst Rev. 2017;6(6):CD009744. Published 2017 Jun 14. doi:10.1002/14651858.CD009744.pub2

Abstract​

Background​

Nicotinic acid (niacin) is known to decrease LDL‐cholesterol, and triglycerides, and increase HDL‐cholesterol levels. The evidence of benefits with niacin monotherapy or add‐on to statin‐based therapy is controversial.

Objectives​

To assess the effectiveness of niacin therapy versus placebo, administered as monotherapy or add‐on to statin‐based therapy in people with or at risk of cardiovascular disease (CVD) in terms of mortality, CVD events, and side effects.

Search methods​

Two reviewers independently and in duplicate screened records and potentially eligible full texts identified through electronic searches of CENTRAL, MEDLINE, Embase, Web of Science, two trial registries, and reference lists of relevant articles (latest search in August 2016).

Selection criteria​

We included all randomised controlled trials (RCTs) that either compared niacin monotherapy to placebo/usual care or niacin in combination with other component versus other component alone. We considered RCTs that administered niacin for at least six months, reported a clinical outcome, and included adults with or without established CVD.

Data collection and analysis​

Two reviewers used pre‐piloted forms to independently and in duplicate extract trials characteristics, risk of bias items, and outcomes data. Disagreements were resolved by consensus or third party arbitration. We conducted random‐effects meta‐analyses, sensitivity analyses based on risk of bias and different assumptions for missing data, and used meta‐regression analyses to investigate potential relationships between treatment effects and duration of treatment, proportion of participants with established coronary heart disease and proportion of participants receiving background statin therapy. We used GRADE to assess the quality of evidence.

Main results​

We included 23 RCTs that were published between 1968 and 2015 and included 39,195 participants in total. The mean age ranged from 33 to 71 years. The median duration of treatment was 11.5 months, and the median dose of niacin was 2 g/day. The proportion of participants with prior myocardial infarction ranged from 0% (4 trials) to 100% (2 trials, median proportion 48%); the proportion of participants taking statin ranged from 0% (4 trials) to 100% (12 trials, median proportion 100%).
Using available cases, niacin did not reduce overall mortality (risk ratio (RR) 1.05, 95% confidence interval (CI) 0.97 to 1.12; participants = 35,543; studies = 12; I2 = 0%; high‐quality evidence), cardiovascular mortality (RR 1.02, 95% CI 0.93 to 1.12; participants = 32,966; studies = 5; I2 = 0%; moderate‐quality evidence), non‐cardiovascular mortality (RR 1.12, 95% CI 0.98 to 1.28; participants = 32,966; studies = 5; I2 = 0%; high‐quality evidence), the number of fatal or non‐fatal myocardial infarctions (RR 0.93, 95% CI 0.87 to 1.00; participants = 34,829; studies = 9; I2 = 0%; moderate‐quality evidence), nor the number of fatal or non‐fatal strokes (RR 0.95, 95% CI 0.74 to 1.22; participants = 33,661; studies = 7; I2 = 42%; low‐quality evidence). Participants randomised to niacin were more likely to discontinue treatment due to side effects than participants randomised to control group (RR 2.17, 95% CI 1.70 to 2.77; participants = 33,539; studies = 17; I2 = 77%; moderate‐quality evidence). The results were robust to sensitivity analyses using different assumptions for missing data.

Authors' conclusions​

Moderate‐ to high‐quality evidence suggests that niacin does not reduce mortality, cardiovascular mortality, non‐cardiovascular mortality, the number of fatal or non‐fatal myocardial infarctions, nor the number of fatal or non‐fatal strokes but is associated with side effects. Benefits from niacin therapy in the prevention of cardiovascular disease events are unlikely.

More

Don't Take Niacin for Heart Health, Docs Warn

Niacin, or vitamin B3, is too dangerous and should not be used routinely by people looking to control their cholesterol levels or prevent heart disease, doctors say.

www.livescience.com

I don't know what specifically your cardiologist is basing that advice on. I had seen this older article before. It isn't even a case of 'correlation doesn't = causation'. All it really says is that niacin is supposedly ineffective in preventing mortality and says nothing about it causing any disease and to date, I haven't seen any papers on it increasing CV events of any kind. I've only seen papers that emphasize a decrease in those events.
Here's a more recent update on niacin.

Niacin is still being used quite successfully today to reduce small dense LDL-C, Lp(a) and trigs by notable docs like Ford Brewer and Tara Dall. I believe it has worked in my case to reduce LDL-P and trigs and am hoping it will, over time, reduce small LDL, Lp(a) and boost my HDL as well. The only issues I'm concerned over are increases in liver enzymes and glucose. So far, so good on the liver enzymes. That leaves me with the glucose, hence, my post.

 

[Deleted member 43589]

I read all of the older research too. From what I see the newer research show other wise. So unfortunately I am going defer to my cardiologist who is more of an expert that I can be in this field. I am not going to second guess when it concerns having a heal attack. But anyway my cardiologist works for DeBakey Cardiology Associates at Methodist Hospital here in Houston, Texas. He has a very impressive background:

Khurram Nasir, MD​

Dr. Nasir received his MD from Pakistan, followed by a MPH at John Hopkins University. Dr. Nasir completed his internal medicine residency at Boston Medical Center and a cardiology fellowship at Yale University. He also received postdoctoral research training at the division of cardiology at John's Hopkins Hospital, and was the recipient of NIH - T-32 fellowship in cardiac imaging at Massachusetts General Hospital. He recently earned a Master’s degree in health economics and Policy Management from the London School of Economics & Political Science.

Dr. Nasir serves as Associate Editor for Circulation: Quality of Care and Outcomes, an editorial board member for Circulation as well as on the board of directors for the American Society of Preventive Cardiology (ASPC). He was honored with the John's Hopkins Distinguished Alumnus Award in 2013, which acknowledges alumni who have typified John's Hopkins tradition of excellence and brought credit to the University by their personal accomplishments, professional achievements, or humanitarian service.

Dr. Nasir has over 500 peer-reviewed articles that are published in top journals such as Lancet, New England Journal of Medicine, JAMA, Archives of Internal Medicine, Circulation, Journal of American College of Cardiology and European Heart Journal. Dr. Nasir has lectured extensively throughout the world on coronary atherosclerosis, cardiac imaging, and prevention.

 

[mcs]

I read all of the older research too. From what I see the newer research show other wise. So unfortunately I am going defer to my cardiologist who is more of an expert that I can be in this field. I am not going to second guess when it concerns having a heal attack. But anyway my cardiologist works for DeBakey Cardiology Associates at Methodist Hospital here in Houston, Texas. He has a very impressive background:

Khurram Nasir, MD​

Dr. Nasir received his MD from Pakistan, followed by a MPH at John Hopkins University. Dr. Nasir completed his internal medicine residency at Boston Medical Center and a cardiology fellowship at Yale University. He also received postdoctoral research training at the division of cardiology at John's Hopkins Hospital, and was the recipient of NIH - T-32 fellowship in cardiac imaging at Massachusetts General Hospital. He recently earned a Master’s degree in health economics and Policy Management from the London School of Economics & Political Science.

Dr. Nasir serves as Associate Editor for Circulation: Quality of Care and Outcomes, an editorial board member for Circulation as well as on the board of directors for the American Society of Preventive Cardiology (ASPC). He was honored with the John's Hopkins Distinguished Alumnus Award in 2013, which acknowledges alumni who have typified John's Hopkins tradition of excellence and brought credit to the University by their personal accomplishments, professional achievements, or humanitarian service.

Dr. Nasir has over 500 peer-reviewed articles that are published in top journals such as Lancet, New England Journal of Medicine, JAMA, Archives of Internal Medicine, Circulation, Journal of American College of Cardiology and European Heart Journal. Dr. Nasir has lectured extensively throughout the world on coronary atherosclerosis, cardiac imaging, and prevention.

Just curious, so what are you using now to help reduce your Lp(a) and for general lipid management and has it been effective?

 

[mcs]

I read all of the older research too. From what I see the newer research show other wise. So unfortunately I am going defer to my cardiologist who is more of an expert that I can be in this field. I am not going to second guess when it concerns having a heal attack. But anyway my cardiologist works for DeBakey Cardiology Associates at Methodist Hospital here in Houston, Texas. He has a very impressive background:

Khurram Nasir, MD​

Dr. Nasir received his MD from Pakistan, followed by a MPH at John Hopkins University. Dr. Nasir completed his internal medicine residency at Boston Medical Center and a cardiology fellowship at Yale University. He also received postdoctoral research training at the division of cardiology at John's Hopkins Hospital, and was the recipient of NIH - T-32 fellowship in cardiac imaging at Massachusetts General Hospital. He recently earned a Master’s degree in health economics and Policy Management from the London School of Economics & Political Science.

Dr. Nasir serves as Associate Editor for Circulation: Quality of Care and Outcomes, an editorial board member for Circulation as well as on the board of directors for the American Society of Preventive Cardiology (ASPC). He was honored with the John's Hopkins Distinguished Alumnus Award in 2013, which acknowledges alumni who have typified John's Hopkins tradition of excellence and brought credit to the University by their personal accomplishments, professional achievements, or humanitarian service.

Dr. Nasir has over 500 peer-reviewed articles that are published in top journals such as Lancet, New England Journal of Medicine, JAMA, Archives of Internal Medicine, Circulation, Journal of American College of Cardiology and European Heart Journal. Dr. Nasir has lectured extensively throughout the world on coronary atherosclerosis, cardiac imaging, and prevention.

Perhaps your doc is basing his opinion on this study which I hadn't seen before:

Niacin Increases Atherogenic Proteins in High-Density Lipoprotein of Statin-Treated Subjects​

 

[Deleted member 43589]

Just curious, so what are you using now to help reduce your Lp(a) and for general lipid management and has it been effective?

Just for the record, the niacin was absolutely not effective with me, never saw any changes up or down but the doctor put me on ezetimibe, 10 mg tablet. I tried a statin but had muscle soreness that was unbearable. I can't see that ezetimibe is doing much either, I have asked to be put on PCSK9,which is sold under the brand name at Repatha. He wants to see these numbers lower (LDL, HDL higher) but I don't see the problem. He said he is not concerned with Lipo (a) because it is mostly genetic, but my large particles are very high.

My blood work showed
CHOLESTEROL, TOTAL 154 Reference Range: <200 mg/dL
HDL CHOLESTEROL 47 Reference Range: > OR = 47 mg/dL
TRIGLYCERIDES 68 Reference Range: <150 mg/dL
LDL-CHOLESTEROL 94 mg/dL Reference range: <100
CHOL/HDLC RATIO 3.4 optimal <=3.5
NON-HDL CHOLESTEROL 112 optimal <130
LDL PARTICLE NUMBER 1031 optimal <1138
LDL SMALL 131 optimal <142
LDL MEDIUM 184 optimal <215
HDL LARGE 4492 high <5353
LDL PATTERN A optimal A
LDL PEAK SIZE 223.6 optimal >222.9
APOLIPOPROTEIN B 76 optimal <90
LIPOPROTEIN (a) 84 optimal <75

 

[mcs]

Just for the record, the niacin was absolutely not effective with me, never saw any changes up or down but the doctor put me on ezetimibe, 10 mg tablet. I tried a statin but had muscle soreness that was unbearable. I can't see that ezetimibe is doing much either, I have asked to be put on PCSK9,which is sold under the brand name at Repatha. He wants to see these numbers lower (LDL, HDL higher) but I don't see the problem. He said he is not concerned with Lipo (a) because it is mostly genetic, but my large particles are very high.

My blood work showed
CHOLESTEROL, TOTAL 154 Reference Range: <200 mg/dL
HDL CHOLESTEROL 47 Reference Range: > OR = 47 mg/dL
TRIGLYCERIDES 68 Reference Range: <150 mg/dL
LDL-CHOLESTEROL 94 mg/dL Reference range: <100
CHOL/HDLC RATIO 3.4 optimal <=3.5
NON-HDL CHOLESTEROL 112 optimal <130
LDL PARTICLE NUMBER 1031 optimal <1138
LDL SMALL 131 optimal <142
LDL MEDIUM 184 optimal <215
HDL LARGE 4492 high <5353
LDL PATTERN A optimal A
LDL PEAK SIZE 223.6 optimal >222.9
APOLIPOPROTEIN B 76 optimal <90
LIPOPROTEIN (a) 84 optimal <75

What were your numbers before the ezetimibe? How long on it before these labs? Did it have any effect on your trigs, LDL-P and small LDL? Or no effect? How are you able to get a prescription for a PCSK9 inhibitor when it is specifically prescribed for FH? My HDL is low as well. My total and LDL levels are about the same as yours however, I still have elevated LDL-P and small LDL and Pattern B. How is your glucose/insulin control? I would assume pretty good. Lastly, how are your thyroid levels (TSH, free T3/T4, rT3)?

 

[Deleted member 43589]

What were your numbers before the ezetimibe? How long on it before these labs? Did it have any effect on your trig s, LDL-P and small LDL? Or no effect? How are you able to get a prescription for a PCSK9 inhibitor when it is specifically prescribed for FH? My HDL is low as well. My total and LDL levels are about the same as yours however, I still have elevated LDL-P and small LDL and Pattern B. How is your glucose/insulin control? I would assume pretty good. Lastly, how are your thyroid levels (TSH, free T3/T4, rT3)?

The same numbers before and after. Since they are wanting my lipids down and I am unable to take a statin and not responding to ezetimibe, I requested to be put on the PCSK9. I have jumped through all the required insurance hoops to qualify for this. My glucose fasted is in the low 80's and non-fasted was 89. Thyroid levels are normal.

 

[mcs]

The same numbers before and after. Since they are wanting my lipids down and I am unable to take a statin and not responding to ezetimibe, I requested to be put on the PCSK9. I have jumped through all the required insurance hoops to qualify for this. My glucose fasted is in the low 80's and non-fasted was 89. Thyroid levels are normal.

Along with all the other drawbacks, statins could actually increase Lp(a).

From what you've stated + your labs, I don't see any reason why you would need to be on any lipid management, especially when you're fortunate enough to have thyroid & glucose levels optimized without any intervention. Suppressing your LDL any further is actually detrimental and will cause a loss of hormone production. I don't see how in the world you would be able to get PSCK9 inhibitor when you don't have any markers out of whack enough to warrant it. Maybe higher dose of fish oil and some dietary adjustment (i.e. lower carb, eliminate all grains) for such a small adjustment in your case. Otherwise, whatever you or your doc are trying to do with meds would be overkill - and as far as Lp(a), the meds you take or plan to take to reduce it, may not have any effect at all (the only meds that I have shown to be effective in reducing it are anti-sense meds). Just my two cents.

 

[Deleted member 43589]

I totally agree with you, which was why I insisted on doing the particle test. In any case, I have an appointment with another cardiologist on the 23rd. My wife used this guy when she had cardiac issues with long covid. He was very good. Already taking the fish oil Nattokinase and even K2. My doctor also suggested I start a keto diet......NO WAY.

 

[mcs]

I totally agree with you, which was why I insisted on doing the particle test. In any case, I have an appointment with another cardiologist on the 23rd. My wife used this guy when she had cardiac issues with long covid. He was very good. Already taking the fish oil Nattokinase and even K2.

I don't care how many credentials a cardiologist may have behind their name. If they are completely pro-pharmaceutical and don't consider the whole picture and outside factors such as hypothyroidism, insulin resistance, diet, lifestyle, and are against non-drug remedies like fish oil, niacin, etc. with nothing to back up their claims, then they are very suspect in my book. Good you are getting another opinion. Speaking of which, I have come to the realization that most cardiologists are no the best docs to go for for a lipid management and preventive cardiology. I will therefore be seeking out one in particular, Dr. Tara Dall, MD. She is a well respected lipidologist that actually trains other physicians and knows way more than probably 99% of the cardiologists out there when it comes to dyslipidemia and all the factors that surround it.

 

[Deleted member 43589]

The biggest issue with my doctor is despite the great credentials I have only seen him two times in 2 years and one was a video conference. The rest of the time i see his nurse practitioner. I have no idea anymore if she acts on his advice or is now my "doctor." Tomorrow I have to travel downtown to do an EGK and it will most likely be my last time there and she is the one doing it all. My wife has use a Dr. Phillip Berman who is very good and he personally sees all of this patients. Not so happy knowing my cardiac health is in the hands of a nurse.

 

[Geezer40]

Anyone notice impact on fasting and post-prandial glucose levels and a1c from taking high-dose ER niacin to manage lipids? I was on 1.5g per day and increased to 2g per day and now I'm noticing glucose levels about 10 points higher. Wondering if this will subside over time. I know some are taking metformin to bring it back down.

Well, after 15 years on 2gm ER niacin, I'm still trying to figure out which bedtime snack works best. I'm generally on a moderate carbohydrate diet (about 120 gm per day) and I suspect that if my bedtime snack does not have enough carbs I will get high fasting glucose (about 120 mg/dl). This is the highest reading of the day. I will usually have 2hr postprandial readings in the mid-high 90s and at worst 105 or so. The other night I had a higher carb snack than usual and had AM fasting glucose of 98. I believe the way nighttime ER niacin works is by forcing the use of carbs at night, so this might make sense.

 

[mcs]

Well, after 15 years on 2gm ER niacin, I'm still trying to figure out which bedtime snack works best. I'm generally on a moderate carbohydrate diet (about 120 gm per day) and I suspect that if my bedtime snack does not have enough carbs I will get high fasting glucose (about 120 mg/dl). This is the highest reading of the day. I will usually have 2hr postprandial readings in the mid-high 90s and at worst 105 or so. The other night I had a higher carb snack than usual and had AM fasting glucose of 98. I believe the way nighttime ER niacin works is by forcing the use of carbs at night, so this might make sense.

That seems to be a paradoxical to what one would think: that fasting would keep the fasting glucose levels lower and a bedtime snack would make them higher. Can't figure that one out. I am just the opposite. If I snack, my readings will always be higher, especially with any form of carbs or even protein (gluconeogenesis). I haven't notice whether the niacin make that worse or better.

 

[Geezer40]

That seems to be a paradoxical to what one would think: that fasting would keep the fasting glucose levels lower and a bedtime snack would make them higher. Can't figure that one out. I am just the opposite. If I snack, my readings will always be higher, especially with any form of carbs or even protein (gluconeogenesis). I haven't notice whether the niacin make that worse or better.

If Chris Masterjohn is correct on this (

), high dose niacin surpasses the release of free fatty acids in the few hours after taking it, so the body has to rely on carbs for fuel and becomes "very good at it". I think he's referring to IR niacin, so it seems that for ER niacin this would be true for the entire night. So my hypothesis is that if not enough carbs are available during that period (all night) you get a reactive release of glucose which may overcompensate and lead to excess blood glucose in the early morning hours (I'm not medically or bio science-trained, so this is based on my readings of the dawn phenomenon or Somogyi effect). I'll also venture a guess that it's a U-shaped curve: Too little carbohydrate leads to the reactive flood of glucose, too much and your nighttime metabolism can't cope. Since I'm restricting (but not eliminating) daytime carbs and I exercise daily, I might not be getting enough without the bedtime snack to get through the night.

 

[mcs]

If Chris Masterjohn is correct on this (

), high dose niacin surpasses the release of free fatty acids in the few hours after taking it, so the body has to rely on carbs for fuel and becomes "very good at it". I think he's referring to IR niacin, so it seems that for ER niacin this would be true for the entire night. So my hypothesis is that if not enough carbs are available during that period (all night) you get a reactive release of glucose which may overcompensate and lead to excess blood glucose in the early morning hours (I'm not medically or bio science-trained, so this is based on my readings of the dawn phenomenon or Somogyi effect). I'll also venture a guess that it's a U-shaped curve: Too little carbohydrate leads to the reactive flood of glucose, too much and your nighttime metabolism can't cope. Since I'm restricting (but not eliminating) daytime carbs and I exercise daily, I might not be getting enough without the bedtime snack to get through the night.

Interesting mechanism. In my case, despite my low carb diet (<100g), I think my insulin sensitivity has gradually degraded with age as is normal. I take glucose disposal agents like cinammon, banaba leaf, berberine, etc. but have not noticed much difference. I'm looking into metformin and semaglutide.

 

[Geezer40]

I suspect that's the case for me as well (increased insulin resistance) and will probably discuss metformin with my doc soon.

 

[nodoctor]

I've got a separate thread on here but had good experience with metformin, and now on semaglutide with pretty good results as well. Experimenting with frag 176-191 but more for fat loss. Going vegan also probably helped a ton, but my a1c went from over 6 (not awful I guess) to I think 5 or so. No negative interactions with TRT that I can tell.

 

[Geezer40]

I've got a separate thread on here but had good experience with metformin, and now on semaglutide with pretty good results as well. Experimenting with frag 176-191 but more for fat loss. Going vegan also probably helped a ton, but my a1c went from over 6 (not awful I guess) to I think 5 or so. No negative interactions with TRT that I can tell.

frag 176-191?