https://doi.org/10.1007/s12020-021-02831-w

https://pubmed.ncbi.nlm.nih.gov/34342804

Abstract

PURPOSE

To investigate and identify first-trimester fasting plasma glucose (FPG) is related to gestational diabetes mellitus (GDM) and other adverse pregnancy outcomes in Shenzhen population.

METHODS

We used data of 48,444 pregnant women that had been retrospectively collected between 2017 and 2019. Logistic regression analysis was used to evaluated the associations between first-trimester FPG and GDM and adverse pregnancy outcomes, and used to construct a nomogram model for predicting the risk of GDM. The performance of the nomogram was evaluated by using ROC and calibration curves. Decision curve analysis (DCA) was used to determine the clinical usefulness of the first-trimester FPG by quantifying the net benefits at different threshold probabilities.

RESULTS

The mean first-trimester FPG was 4.62 ± 0.42 mmol/L. A total of 6998 (14.4%) pregnancies developed GDM.489(1.01%) pregnancies developed polyhydramnios, the prevalence rates of gestational hypertensive disorder (GHD), cesarean section, primary cesarean section, preterm delivery before 37 weeks (PD) and dystocia was 1130 (2.33%), 20,426 (42.16%), 7237 (14.94%), 2386 (4.93%), and 1865 (3.85%), respectively. 4233 (8.74%) of the newborns were LGA, and the number of macrosomia was 2272 (4.69%), LBW was 1701 (3.51%) and 5084 (10.49%) newborns had admission to the ICU, which all showed significances between GDM and non-GDM groups (all P < 0.05). The univariate analysis showed that first-trimester FPG was strongly associated with risks of outcomes including GDM, cesarean section, macrosomia, GHD, primary cesarean section, and LGA (all OR > 1, all P < 0.05), furthermore, the risks of GDM, primary cesarean section, and LGA was increasing with first-trimester FPG as early as it was at 4.19-4.63 mmol/L. The multivariable analysis showed that the risks of GDM (ORs for FPG 4.19-4.63, 4.63-5.11 and 5.11-7.0 mmol/L were 1.137, 1.592, and 4.031, respectively, all P < 0.05) increased as early as first-trimester FPG was at 4.19-4.63 mmol/L, and first-trimester FPG which was also associated with the risks of cesarean section, macrosomia and LGA (OR for FPG 5.11-7.0 mmol/L of cesarean section: 1.128, OR for FPG 5.11-7.0 mmol/L of macrosomia: 1.561, OR for FPG 4.63-5.11 and 5.11-7.0 mmol/L of

https://doi.org/10.1016/j.diabres.2021.108832

https://pubmed.ncbi.nlm.nih.gov/33895195

Abstract

AIMS

To examine third trimester fasting venous plasma glucose (FVPG) according to the distribution of a Danish population of pregnant women and identify potential local FVPG thresholds for GDM diagnosis related to risks of adverse pregnancy outcomes.

METHODS

In the observational Odense Child Cohort (OCC) study, 1,516 women had FVPG measured at 27-28 weeks' gestation and were considered normal by Danish criteria and remained untreated. Maternal FVPG from OCC were standardized according to the local FVPG mean and standard deviation calibrated to data from the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study. Associations between maternal FVPG and clinical and anthropometric outcomes were analysed. Potential FVPG cut points were identified.

RESULTS

Unadjusted areas under the ROC curve for FVPG to discriminate for large for gestational age (LGA) and hypertensive disorders of pregnancy were 0.61 (95% CI 0.56, 0.67) and 0.57 (95% CI 0.52, 0.63), respectively. The Youden FVPG cut point for LGA was 5.5 mmol/L and 5.0 mmol/L for hypertensive disorders of pregnancy.

CONCLUSIONS

This study identified a potential locally appropriate third trimester FVPG cut point between 5.5-5.7 mmol/L based on LGA risk in pregnancy. This cut point should be validated prospectively in other Danish cohorts.

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Open Access: False

Authors: Richard Christian Jensen - Dorte Møller Jensen - Kristen S. Gibbons - Dorte Glintborg - Tina Kold Jensen - H. David McIntyre - Marianne Andersen -

Additional links: None found

https://doi.org/

https://pubmed.ncbi.nlm.nih.gov/33886461

Abstract

OBJECTIVES

The association between serum uric acid (SUA) and fasting plasma glucose (FPG) has not been fully outlined, in particular in hyperuricaemic population. This study aimed to address this issue, along with the exploration of the role of insulin resistance that was assessed by triglyceride-and-glucose (TyG) index.

METHODS

A total of 16,297 participants without known diabetes from the SENSIBLE and SENSIBLE-Addition studies were included in the present analysis. Hyperuricaemia was defined as SUA ≥6 mg/dL. Generalised addictive model was applied to establish the relationship of SUA with FPG, and mediation analysis was performed to assess how insulin resistance affected the relationship.

RESULTS

SUA showed an inverted U-shaped association with FPG, with the turning point of FPG at 6.1 mmol/L and 7.5 mmol/L in normouricaemic and hyperuricaemic participants, respectively. However, the significant relationship between SUA and FPG disappeared in hyperuricaemic participants (form B=3.3, 95% CI: 0.6-5.9, p=0.016 to B= -0.2, 95% CI: -3.1-2.7, p=0.894), and attenuated in normouricaemic participants (from B=9.8, 95% CI: 8.0-11.7, p<0.001 to B=7.3, 95% CI: 5.3-9.2, p<0.001) after controlling for TyG index. In the ascending segment, the relationship between SUA and FPG was partially mediated by TyG index in normouricaemic participants, but fully in hyperuricaemic participants.

CONCLUSIONS

SUA had an inverted U-shaped relationship with FPG, and their positive relationship was fully mediated by insulin resistance in participants with hyperuricaemia but not those without.

https://doi.org/10.1016/j.atherosclerosis.2020.12.024

https://pubmed.ncbi.nlm.nih.gov/33465660

Abstract

BACKGROUND AND AIMS

Using a nationwide epidemiological database, we aimed to clarify the association of fasting plasma glucose (FPG) with subsequent cardiovascular disease (CVD) risk among young adults.

METHODS AND RESULTS

Medical records of 1,180,062 young adults (20-49 years old) without a prior history of CVD and who were not taking antidiabetic medications were extracted from the Japan Medical Data Center. We categorized the study population into four groups: normal, FPG level<100 mg/dL (1,007,747 individuals), normal-high, FPG level of 100-109 mg/dL (126,602 individuals), impaired fasting glucose (IFG), FPG level of 110-125 mg/dL (32,451 individuals), and diabetes mellitus (DM), FPG level ≥126 mg/dL (13,262 individuals). The mean age was 39.7 ± 6.9 years, and 57.0% of the study population were men. Mean follow-up period was 1201 ± 905 days on average. Multivariable Cox regression analysis showed that IFG (hazard ratio [HR], 1.38) and DM (HR, 2.09) increased the risk of myocardial infarction. Normal-high (HR, 1.11), IFG (HR, 1.18), and DM (HR, 1.59) groups had an elevated angina pectoris risk. DM (HR, 1.31) increased the risk of stroke compared to normal FPG levels. Normal-high levels (HR, 1.10), IFG (HR, 1.22) and DM (HR, 1.58) elevated the risk of heart failure. DM (HR, 1.69) increased the risk of atrial fibrillation.

CONCLUSIONS

Our analysis of a nationwide epidemiological database demonstrated a close association of the FPG category with subsequent CVD risk. Our results exemplify the importance of optimal FPG maintenance for the primary prevention of CVD in young adults.

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Open Access: False

Authors: Hidehiro Kaneko - Hidetaka Itoh - Hiroyuki Kiriyama - Tatsuya Kamon - Katsuhito Fujiu - Kojiro Morita - Nobuaki Michihata - Taisuke Jo - Norifumi Takeda - Hiroyuki Morita - Hideo Yasunaga - Issei Komuro -

Additional links: None found

Chang MC, Hwang JM, Jeon JH, Kwak SG, Park D, Moon JS. Fasting Plasma Glucose Level Independently Predicts the Mortality of Patients with Coronavirus Disease 2019 Infection: A Multicenter, Retrospective Cohort Study [published online ahead of print, 2020 Aug 26]. Endocrinol Metab (Seoul). 2020;10.3803/EnM.2020.719. doi:10.3803/EnM.2020.719

https://doi.org/10.3803/enm.2020.719

Abstract

Background: Coronavirus disease 2019 (COVID-19) has become a global pandemic, which prompts a consensus for the necessity to seek risk factors for this critical disease. Risk factors affecting mortality of the disease remain elusive. Diabetes and hyperglycemia are known to negatively affect a host's antiviral immunity. We evaluated the relationship between a history of diabetes, fasting plasma glucose (FPG) levels and mortality among severely ill patients with COVID-19.

Methods: This was a retrospective cohort study that assessed 106 adult inpatients (aged ≥18 years) from two tertiary hospitals in Daegu, South Korea. The participants were transferred to tertiary hospitals because their medical condition required immediate intensive care. The demographic and laboratory data were compared between COVID-19 patients who survived and those who did not.

Results: Compared with the survivor group, age, and the proportions of diabetes, chronic lung disease and FPG were significantly higher in the deceased group. In the Cox proportional hazards regression model for survival analysis, FPG level and age were identified as significant predictors of mortality (P<0.05). The threshold values for predicting high mortality were age >68 years and FPG of 168 mg/dL, respectively. ***Among those without diabetes, high FPG remained a significant predictor of mortality (P<0.04)***.

Conclusion: High FPG levels significantly predicted mortality in COVID-19, regardless of a known history of diabetes. These results suggest intensive monitoring should be provided to COVID-19 patients who have a high FPG level.

I want a clean place where I can get this, can someone please suggest some places? I’m doing it for the army as my dad had it and I thought if I have it, I should know it as it could be a reason to get me out.

https://doi.org/10.1080/07420528.2020.1842754

https://pubmed.ncbi.nlm.nih.gov/33307847

Abstract

The purpose of this study was to investigate the influence of lunar phases on fasting plasma glucose, heart rate, and blood pressure in type 2 diabetic patients. The present cross-sectional study was carried out during four phases, i.e., full moon (FM), first quarter (FQ), new moon (NM), and third quarter (TQ), of the lunar month. The study was conducted on 42 randomly selected patients (22 males and 20 females) from the Diabetes Clinic of Calcutta Medical College. Fasting plasma glucose (FPG) of each subject was determined and heart rate (HR) and blood pressure (BP) were measured at rest and during static exercise conditions, i.e., performance of a standard handgrip dynamometer test. The FPG level during the NM and FM was significantly higher (p < .001) than during the TQ and FQ for both males and females, respectively. The mean HR during static exercise during the NM and FM for both males and females was significantly higher than that during the FQ (p < .05) and TQ (p < .01). It appears from the present study that lunar phases may affect fasting plasma glucose level and cardiovascular functions of aged type 2 diabetic patients both at rest and during exercise.

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Open Access: False

Authors: Sutanu Dutta Chowdhury - Subhasish Pramanik - Koena Bhattacharjee - Lakshmi Kanta Mondal -

Additional links: None found

Full study: Effects of berberine on glucose-lipid metabolism, inflammatory factors and insulin resistance in patients with metabolic syndrome (2019)

Berberine is an hypoglycemic agent that works by disrupting cellular energy (ATP) production (Complex I inhibitor). The ATP deficit induced by Berberine causes has to be compensated for - cells compensate by pulling in more glucose from the bloodstream to fill that purpose. The eventual lowering of blood glucose results in improvement in glucose metabolism. This same mechanism of action is shared by Metformin.

This study had tested the effects of Berberine on patients with metabolic syndrome (all participants had type 2 diabetes, dyslipidemia & hypertension) - 40 were treated with Berberine, the 40 others received placebo. Berberine was given at a dose of 120mg, 3 times daily.

Following 1 month of daily treatment, significant decreases were seen in fasting glucose, postprandial (post-meal) glucose, plasma triglycerides, total cholesterol, and systemic inflammation markers (lower plasma IL-6 and TNF-α concentrations) in the Berberine treatment group.

A past study has shown similar effects of Berberine. However, Metformin, which is equally as effective as Berberine in improving glucose metabolism, failed to decrease triglycerides and total cholesterol in that study, whereas Berberine significantly decreased them.

Chevli PA, Ahmad MI, Hari K, Anees MA, Soliman EZ. Impact of low fasting plasma glucose on mortality in the general population. Diab Vasc Dis Res. 2020;17(3):1479164120930599. doi:10.1177/1479164120930599

https://doi.org/10.1177/1479164120930599

Abstract

Background: While the association between hypoglycaemia and poor outcomes in diabetes is well established, it is unclear whether such an association is generalizable to those without diabetes.

Methods: A total of 8497 participants free of cardiovascular disease and diabetes from the Third National Health and Nutrition Examination Survey were included. We examined the relationship between baseline low (<80 mg/dL) and high (⩾126 mg/dL) fasting plasma glucose compared to normal levels (80-99 mg/dL).

Results: Over a median follow-up of 14 years, 2101 deaths occurred, of which 570 were due to cardiovascular disease. In a model adjusted for sociodemographic and cardiovascular disease risk factors, individuals with low fasting plasma glucose were at increased risk of cardiovascular disease and all-cause mortality [hazard ratio = 1.79 (95% confidence interval = 1.04-3.08) and hazard ratio = 1.35 (95% confidence interval = 1.02-1.78), respectively], compared to those with normal fasting plasma glucose. These associations were stronger among men than women for both cardiovascular disease mortality and all-cause mortality.

Conclusion: Low fasting plasma glucose in individuals without diabetes is a risk factor for cardiovascular disease and all-cause mortality, especially in men.

https://journals.sagepub.com/doi/pdf/10.1177/1479164120930599

https://preview.redd.it/m1zfh0iq3te51.png?width=1018&format=png&auto=webp&s=daff9d2f3afb756153b86649d3569e18a9ce1be5

Ye N, Yang L, Wang G, et al. Admission fasting plasma glucose is associated with in-hospital outcomes in patients with acute coronary syndrome and diabetes: findings from the improving Care for Cardiovascular Disease in China - Acute Coronary Syndrome (CCC-ACS) project. BMC Cardiovasc Disord. 2020;20(1):380. Published 2020 Aug 20. doi:10.1186/s12872-020-01662-3

https://doi.org/10.1186/s12872-020-01662-3

Abstract

Background: The discrepancy between glycosylated hemoglobin (HbA1c) and fasting plasma glucose (FPG) in clinical practice may be related to factors such as acute stress, renal dysfunction, and anemia, and its relationship with in-hospital outcomes is uncertain. The aim of this study was to investigate the association between the type of discrepancy between HbA1c and FPG and in-hospital outcomes in patients with acute coronary syndrome (ACS) and diabetes.

Methods: The Improving Care for Cardiovascular Disease in China - Acute Coronary Syndrome (CCC-ACS) project is a national, hospital-based quality improvement project with an ongoing database. Patients with ACS, diabetes and complete HbA1c and FPG values at admission were included. The consistent group included patients with HbA1c < 6.5% and FPG < 7.0 mmol/L or HbA1c ≥ 6.5% and FPG ≥ 7.0 mmol/L. The discrepancy group included patients with HbA1c ≥ 6.5% and FPG < 7.0 mmol/L (increased HbA1c group) or HbA1c < 6.5% and FPG ≥ 7.0 mmol/L (increased FBG group).

Results: A total of 7762 patients were included in this study. The numbers of patients in the consistent and discrepancy groups were 5490 and 2272 respectively. In the discrepancy group, increased HbA1c accounted for 77.5% of discrepancies, and increased FPG accounted for 22.5% of discrepancies. After adjusting for confounders, patients in the increased FPG group had a 1.6-fold increased risk of heart failure (OR, 1.62; 95% CI, 1.08-2.44), a 1.6-fold increased risk of composite cardiovascular death and heart failure (OR, 1.63; 95% CI, 1.09-2.43), and a 1.6-fold increased risk of composite major adverse cardiovascular and cerebrovascular events (MACCEs) and heart failure (OR, 1.56; 95% CI, 1.08-2.24) compared to patients in the increased HbA1c group.

Conclusions: Patients with an increased FPG but normal HbA1c had a higher risk of in-hospital adverse outcomes than those with increased HbA1c but normal FPG. This result may indicate that when HbA1c and FPG are inconsist

I have talked to my doctor.

A month ago my a1c was 5.2 and I was struggling to keep my glucose up during exercise, so my doctor reduced my metformin from 2000/day to 500. My fasting glucose has risen about 15-20 points and even when I exercise, it doesn't really go below 100. I realize these are still safe numbers, and he says "well your a1c is gonna go up" but...two things:

1. I've had to be wayyy more careful with carbs, because I feel real gross over 135/140 (and try to stay below that anyway). It's ok but..ugh.
2. Shouldn't I be aiming for fasting/morning/post exercise glucose levels that are <100? If the point is to have non-diabetic/prediabetic numbers? I'm glad to not be crashing to 70 when I exercise, for sure, but is there maybe something in the middle?

Thoughts? Experiences?

I also realize that I prefer really tight control, and that's not everyone's reality, but it works for me.

Hey, guys, what does it mean when only my fasting glucose is elevated ? 108-118 mg/dL after waking up . It’s been like this for nearly four years . I have tested after high carb meals thousands of times and levels are normal . A1C is also normal . Why is only my fasting high and how worried should I be when my after meals are normal and my A1C is typically 5.2-5.4? I do have belly fat to lose and plan on getting lean .

Have been fasting for three days. First day the glucose reading was 88, second day it dropped to 82 and today it is 73. Is this a cause for concern ?Planning to fast for a week. At what point does glucose level stop dropping? Thanks

I went to sleep kind of late last night and woke up around 8am. At that point my blood sugar was 131. But I didn't eat anything until.around 9am when I had coffee and by the time I drank coffee, my sugar was down to 106. So is 106 my fasting sugar, or 132? My last meal was over at 730pm the night before.

Hello, I'm a 24 male, 6'5, 317 pounds. I have suspected insulin resistance. My doctor never diagnosed me, however:

I have high triglycerides (peaking at 190 in August 2021) I have impaired fasting glucose at the lab in the morning (104 mg/dl) (now 100 mg/dl) I had a borderline a1c in August 2021 (5.6) (now 5.2) I have high blood pressure

My fasting glucose over time:

2017: 100mg/dl 2018: 102mg/dl 2019: 99mg/dl Aug21: 104mg/dl Dec21: 100mg/dl

My highest weight was 363 in early May 2021. After that, I started slowly cutting back and losing weight. In the middle of July I started dieting pretty heavily with intermittent fasting and watching what I eat. In August when I had my first tests, I was 344. I've continued to lose weight but I decided to buy a glucose meter and start checking my reaction to foods and this is what I found:

My number are consistently below 120, even after eating.

I ate 139 grams of carbs in the form of some Korean beef pasta, here were the results:

15 minutes: 106 mg/dL 1 hour: 108 mg/dl 2 hours: 94 mg/dl 3 hours: 112 mg/dl 4 hours: 108 mg/dl

The highest my blood sugar ever read was after chugging 50g of carbs in the form of a Gatorade. About 15-20 minutes later my bg was 124, an hour later it was down to 112.

I took my fasting glucose in the morning, and it was 84, which is odd since at the lab it's always been around 100-102

Based on my at home glucometer, I respond decently to carbs. I can't get out of my head that I have some kind of hidden prediabetes or diabetes. I'm also concerned that since I had lost weight at the time of my August test that I would have been considered prediabetic in May, which started the progressive disease of diabetes.

I can't stop thinking about this and testing myself. I keep thinking I'm missing something. Obviously either way I'm going to continue to lose weight and increase my fitness level, but I feel like I can't get my insulin sensitivity back ever and I'll eventually end up diabetic. I've also read about people with isolated ifg like me don't really see improvements with weight loss and diet changes. I feel as though I'm doomed and my pancreas is permanently damaged.

Question for you all: I just received my blood work back (yay) and I’m kinda freaked out about my A1C (I also have health anxiety, so that doesn’t help things).

My A1C: 5.4 (up from 5.1 in 2019) Estimated Average Glucose: 108 Fasting Glucose: 85

I don’t have an appt. scheduled until about April (long story), so until I actually hear from her I’m hoping someone more knowledgeable than me could shed light here.

33 M, USA

My morning fasting glucose is always slightly elevated, but all of my other readings that would help indicate possible prediabetes are always normal.

If I were insulin resistant wouldn’t my glucose be abnormal after meals? It’s not.

If I were insulin resistant wouldn’t my HBA1C be elevated? It’s not.

If I were insulin resistant wouldn’t my fasting insulin level be high? It’s not.

I’m 33, lift 5 days per week, count calories and macros and eat very healthy. I weigh 170-175 and have 12-15% bf.

21f, 5’4, 125 lbs, half japanese half white, lorazepam 1 mg per day, propranolol 20 mg with each meal (40-60 mg daily), never drank, smoked or done drugs, panic disorder, agoraphobia, gad, bpd, mdd, no physical health conditions

my diet has been admittedly not great, and i’ve lived a pretty sedentary lifestyle. i drink quite a bit of soda per day, maybe 2 cans or 1 can and 1 large fountain drink. other than that, i don’t eat much sugar and typically go for savory foods. cheeseburgers, pizza, and salty mexican food but i cut my meals in half so i don’t take in too many calories daily. i didn’t think it was too big of a deal, given my age and my peers eating similar diets. until i started getting recurrent yeast infections and looked up a possible cause.

i ordered a blood glucose meter. fasting was 103 the first day i checked and 111 the second day. i was shocked. i have a family history of type II, my maternal grandmother has it, along with my paternal grandfather and my dad had prediabetes (he hasn’t gone to the doctor in a while, but last he checked it reversed without any significant lifestyle changes). but despite my not great diet, they ate far worse. i’m talking a dozen donuts and a 2-liter bottle of mountain dew for breakfast. i always thought type II was completely lifestyle, but looking into it more there are genetic risks. and boy do i have genetic risks.

i had a blood test done in june 2021, my blood glucose was 93. i’ve always ran a bit on the high side of normal. 98 when i was 18 and 99 at 17. but my doctor never mentioned it.

so i guess what i’m asking is, is it likely someone my age and weight would have prediabetes? would my blood sugar go up from normal to definitely prediabetes in less than 7 months? if i make lifestyle changes in every other area, can i get away with the 1-2 sodas a day?

i’m going to see a doctor, but being the hypochondriac i am i’ll freak out about it beforehand. anything will help. thank you!

edit: 2 hour post eating blood sugar was 131.

The horrible night I had last night has prompted this post. I've been intermittent fasting for about four nights. This is about the fourth time I've tried over the course of three years. I always lose some weight. The first time I tried it, I lost ten pounds. However, I always have to quit because of the awful insomnia. It wasn't so bad the first time I did it years ago but the last three times have been terrible. It's maddening when I hear other people doing so well on IF.

Last night was particularly bad. Usually, I will stop eating around 7 p.m. and then have breakfast around 11 a.m. I took half of a glimepiride before my evening meal at 5 p.m. because I ate bread. I always take half. I think it's something like 5 mg. Got really super sleepy around 9:30 p.m. Went to bed, closed my eyes, and nothing. I tossed and turned for hours. Then, I started having strange sensations like phantom smells, weird pin pricking on skin, strange visual lights when I closed my eyes, and just feeling unwell. I may have slept for 2 to 3 hours here and there. I got up at 7 a.m. because I thought maybe I was dehydrated and also may need some electrolytes. Drank a bunch of water, waited in my chair for a while, then went back to bed. I slept until almost 11 a.m. Took my blood sugar upon waking at it was 137. I'm perturbed because all this hard work should lower my bs not make it higher!

Also, the day before, I noticed my bs was not right. I would hardly eat any carbs and it would shoot up to 187.

So, this whole intermittent fasting thing has messed up my sleep, my blood sugar, and my mood. When I go online, all I read about are people with diabetes having such great numbers and effects from intermittent fasting. I've always eaten something around 9 p.m. (carbs, not the best idea), so tonight I will try just protein. I need to lose weight dammit but I don't want to suffer insomnia and high blood sugar to do it. Any ideas? Thanks!

I've been suspecting insulin issues due to my overactive bladder . I did the fasting insulin and ogtt test . I calculated my HOMA ir online using the fasting insulin and glucose levels . I did this at an independent lab because no docs are listening to me except my Dermatologist who said I may have PCOS . Should I be worried about these results ?

I'm really confused, can someone shed some light here?

My OBGYN prescribed metformin after diagnosing PCOS in late September, 2 x 500mg/day.

After the diagnosis, I read up on PCOS and insulin resistance and a lot of things made so much sense. Some of my lifelong symptoms, steady weight gain over the past few years, belly fat, constant appetite, menstrual cycle shortening, migraine phase of second half of the cycle getting longer and longer, hair increasing on legs, acne, high testosterone, low HDL, inflammation, infertility - well, you know how it goes.

I started taking the metformin and also started a low carb diet. I'm lucky to have few side effects from metformin.

I'm a stickler for hard data, so I tracked my fasting blood glucose daily, and checked after meals sometimes to see the impact of different foods. I am losing weight at a comfortable pace.

Guys, this is where things go weird: my fasting blood glucose started to rise 1 month into metformin, to where it was suddenly steadily over the healthy range (>100), despite the diet. I have never had that. My insulin, blood glucose and Hba1c levels have always been normal. Suddenly I started having insulin resistance/pre-diabetes symptoms I *never* had before: constant thirst, frequent urination.

This worried me and I started to read more about insulin resistance and treatment options. As an experiment, I stopped metformin but continued the low carb diet. Within 2 days, my blood glucose started dropping and is now in an extremely healthy range (80-87, better than it has ever been) and looks like it is staying there without the metformin (2 weeks now). What the actual fuck?

I have googled far and wide to see if anyone else had issues with metformin making blood glucose go up instead of down, and the reverse after withdrawal - no luck, by all accounts it should be the other way around.

Does anyone know what is going on here? [I know I should speak to my doctor but I don't plan on going back to that one for other reasons, and my GP doesn't really understand PCOS - it might take me some time to find the right specialist]