An inability to oxidise glucose through aerobic glycolysis, being stuck in anaerobic glycolysis, which produces lactic acid, which then is converted back to glucose by the liver through gluconeogeneis, which in turn exacerbates the stress response due to cortisol spike. If people are eating virtually no glucose through LCHF, or Keto, then how are they maintaining BG levels of 5 and above? It's because the liver can still convert protein and fat, and lactic acid, into glucose. It's endogenous production of glucose through the liver that is the main driver of high glucose in diabetics [see quotes below]
---> This article is long but incredibly insightful: https://academic.oup.com/edrv/article/25/5/807/2355272
"b. Gluconeogenesis.
A
gradual and progressive increase in endogenous glucose production contributes to hyperglycemia in persons with type 2 diabetes. In the fasted state, gluconeogenesis is increased in diabetic compared with control persons and is incompletely suppressed by insulin in the postprandial state (194). Thus, increased hepatic glucose production contributes to hyperglycemia in both the fasting and postprandial states."
"Increased
endogenous glucose production is a consistent feature of type 2 diabetes"
"Elevated plasma lactate levels have been demonstrated to be an independent risk factor for the development of type 2 diabetes"
"This hyperlactinemia may lead to insulin resistance by increased gluconeogenesis in liver and decreased glucose uptake in muscle (213)"
The secondary output of fermenting-metabolism (anaerobic glycolysis) is the lower output of ATP, hence why many people will complain about low energy/tiredness/poor sleep. The poor sleep is exacerbated by a lack of glycogen storage (or perhaps, glycogen release/use - need to do more reading on this) in the liver/muscles, meaning BG swings massively in the night, and is kept high not by use of glycogen, but by stress hormones converting protein and lipids into glucose when we sleep. This is the real cause of dawn phenomenon, and why people will complain of 4am (cortisol) wakenings.
-----
There are many, many, many ways to improve overall metabolic function and glucose oxidation. I could probably list 20/30, but would need to look more into it. Off the top of my head: Thyroid, potassium, sodium, magnesium, calcium, vitamin d, succinic acid. Away from supplements, things like regular smaller meals, reduced stress etc. I definitely don't have the final answer,
I just think people on here should spend some time understanding that many, many, many pathways affect fasting blood glucose, not just the amount of Carbs you consume and insulin. I don't think this is a controversial statement: is it?
I'm just doing quick searches for publications on some of these, if I had 3/4 hours i could get 20 or more for each of these to show you i'm not just making this up, this is based on years of reading scientific literature.
THYROID:
https://www.ncbi.nlm.nih.gov/pubmed/2935391
"The oxidative metabolism of glucose is accelerated in most brain areas by treatment with high doses of T3, as is shown by the increase in HK activity, approaching normality on reducing the dose. This decrease can also by observed in the PFK activity through the effect of assayed doses of thyroxine. "
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3175696/ --> this one particularly good in the whole article, could have taken many quotes from it
"Thyroid hormones exert both insulin agonistic and antagonistic actions in different organs. However, this occurs in a fine balance necessary for normal glucose metabolism. Deficit or excess of thyroid hormones can break this equilibrium leading to alterations of carbohydrate metabolism.
"
MAGNESIUM:
"Intracellular Mg plays a key role in regulating insulin action, insulin-mediated-glucose-uptake and vascular tone. Reduced intracellular Mg concentrations result in a defective tyrosine-kinase activity, postreceptorial impairment in insulin action and worsening of insulin resistance in diabetic patients. "
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4549665/
http://diabetes.diabetesjournals.org/content/65/1/3
"Over the past decades, hypomagnesemia (serum Mg2+ <0.7 mmol/L) has been strongly associated with type 2 diabetes mellitus (T2DM). Patients with hypomagnesemia show a more rapid disease progression and have an increased risk for diabetes complications."
CALCIUM/VIT D:
[calcium is a very complex system, because if you don't get enough calcium, your body breaks it down from bone, so weirdly calcium cerum levels may be elevated in people who don't get much calcium, but this is from a stress response. So the correlation between serum calcium and diebetes is not as clear)
https://www.nutritionexpress.com/article+index/health+concerns/diabetes/showarticle.aspx?id=1138
"Women who consumed the most calcium were 27 percent less likely to develop type 2 diabetes than women who consumed the least. Also, men and women who consumed the most magnesium were 20 percent less likely to develop type 2 diabetes than men and women who consumed the least."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2085234/
"Vitamin D and calcium insufficiency may negatively influence glycemia while combined supplementation with both nutrients may be beneficial in optimizing glucose metabolism."
http://care.diabetesjournals.org/content/30/4/980
"we found that daily supplementation with 500 mg calcium citrate and 700 IU vitamin D3 for 3 years prevented increases in plasma glucose and insulin resistance in the subgroup of participants with IFG (impaired fasting glucose, FPG 5.6–6.9 mmol/l) at baseline "
SUCCINIC ACID
http://www.diabetesincontrol.com/breakthrough-in-understanding-development-of-type-1-diabetes/
https://www.ncbi.nlm.nih.gov/pubmed/12096444
"[succinic acid] improves glycemic control, pallestesia and quality of life. "
NIACINAMIDE/NICOTINAMIDE
"Nicotinamide improves glucose metabolism "
" NAM 100 treatment affected glucose control significantly, as shown by lower levels of accumulative area under the curve during oral glucose tolerance test, serum fasting glucose, serum fasting insulin, and homeostasis model assessment of insulin resistance, and higher levels of serum adiponectin. "
POTASSIUM
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3197792/
"In both analyses, investigators found a statistically significant inverse association between serum potassium and risk of incident diabetes, with lower potassium levels predicting increased risk. "
"Lower levels of potassium have been found to be associated with a higher risk of diabetes in some studies."
SODIUM:
Mixed results, but should be looked into, eg affect of sodium restriction on aldosterone
https://academic.oup.com/jcem/article/83/5/1552/2865396
"Dietary sodium restriction may result in a decrease in peripheral insulin sensitivity in normotensive patients with NIDDM"
"Activation of the renin-angiotensin system (RAS), which occurs during
sodium restriction, might therefore be expected to result in
decreased insulin sensitivity. "
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4731857/
Based on the amount of sodium intake, the insulin resistance increased with extremely low sodium diets (less than 40 mmol/day of sodium (≒ 0.92 g/day of sodium, 2.34 g/day of NaCl),
https://www.medscape.com/viewarticle/901683
"increased levels of aldosterone are independently associated with a greater risk of type 2 diabetes"
"Overall, a 100% increase in aldosterone was associated with a 2.6-mg/dL higher fasting plasma glucose, in addition to increased abnormalities in measures of glucose homeostasis"
