Dawn Effect v Isulin Reistance

(Ian) #1

Does anyone know if the degree and duration of the dawn effect (i.e. the increase in blood sugar in response to cortisol) is related to the degree of insulin resistance (IR)?

My understanding is that the body releases cortisol and some other hormones approximately 8 hours after we go to sleep, so that blood glucose levels increase slightly to help us prepare for waking and becoming active. It is also my understanding that this normal process happens to everyone, even metabolically healthy individuals. However, the glucose release appears to be higher and is sustained for a longer period of time in people with IR, because cellar uptake and depletion of glucose is impaired (this is my presumption and I would appreciate any links to science that confirms this).

If my understanding is correct, do you think it would be possible to monitor and assess improvements in IR using the dawn effect as a surrogate for improving metabolic function?, Specifically, based on how much the magnitude and/or duration of your dawn effect declines over time, in response to a period of low carb consumption?

I have not been able to find out what is a typical magnitude and/or duration for the dawn effect glucose spike for metabolically health individuals. It would be useful to know what is a normal BG spike and how long does it take for this spike to return to baseline. Considering, I am essentially OMAD, it should be relatively straightforward to track the time it takes for BG to get back to baseline without introducing an interfering event.

(Katie the Quiche Scoffing Stick Ninja ) #2

Your dawn effect does not ‘decline’ as far as I am aware. Your fasting blood glucose can drop though, I am led to believe.

Just before waking around 4am, the body secretes higher levels of growth hormone, cortisol, glucagon, and adrenaline. Together these are called the counterregulatory hormones - they counter the blood sugar lowering effects of insulin, meaning that they raise blood sugar. It’s a hormonal surge to prepare your body for the day ahead. Glucagon tells the liver to start ushing some glucose. Adrenaline gives the body some energy. Growth hormone is involved in cell repair and the synthesis of new protein. Coritsol, the stress hormone, increases as a general activator. All of these hormones peak in the early morning hours and then fall to low levels during the day. Insulin also increases in the morning to make sure the blood glucose does not go too high. The same phenonemum is seen during fasting, insulin levels drop, but the hormones are still causing stored sugar to be released into the bloodstream, raising blood sugar levels.

(joseph) #3

Dr. Annette Bosworth, Dr. Boz on her you tube channel has good info on this. She treats T1D and T2D patients and uses this frequently to see how much the liver empties out glucose.

(Bunny) #4

Maybe this is what your looking for?

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Cortisol? I do wonder if cortisol has anything to do with anything and everything being correlated to it[1], to me it seems more like a tyrosine deficiency taking place within the medulla of the adrenal cortex inside the adrenal gland itself and iodine balance problem in the thyroid? (i.e. obesity, diabetes, metabolic dysregulation, cancer etc.)

Footnotes:

[1] Adrenal fatigue does not exist: a systematic review ”…To our knowledge, this is the first systematic review made by endocrinologists to examine a possible correlation between the HPA axis and a purported “adrenal fatigue” and other conditions associated with fatigue, exhaustion or burnout. So far, there is no proof or demonstration of the existence of “AF”. While a significant number of the reported studies showed differences between the healthy and fatigued groups, important methodological issues and confounding factors were apparent. Two concluding remarks emerge from this systematic review: (1) the results of previous studies were contradictory using all the methods for assessing fatigue and the HPA axis, and (2) the most appropriate methods to assess the HPA axis were not used to evaluate fatigue. Therefore, “AF” requires further investigation by those who claim for its existence. …” …More

[2] “…Tyrosine is a nonessential amino acid and can be formed by the hydroxylation of phenylalanine in the liver when the intake of tyrosine in the diet is low. …” …More

[3] Large neutral amino acids block phenylalanine transport into brain tissue in patients with phenylketonuria

[4] An Overview of Phenylalanine and Tyrosine Kinetics in Humans