By: Dr. Mona Morstein

Dr. Mona Morstein-Dawn Phenomenon  The physiological event known as the “Dawn Phenomenon” (DP) is a frustrating effect for nearly every diabetic patient, whether they have T2, T1.5, or T1.  The DP is the main reason fasting glucose levels are usually the last one to get under full control in most diabetic patients, even though the post-prandial numbers are within good limits.  There are several biochemical reasons why the DP occurs and I’ll discuss those and then give a couple of ideas of how to weaken the DP effect.

First, as we know, fasting glucose numbers should be between 75-99, although 85 mg/dl is considered the ideal number.   Post-prandial glucose numbers should be less than 130 mg/dl.  Now, let’s talk about what raises that fasting value.

The four factors involved with Dawn Phenomenon include:

  1. The rise in cortisol from the adrenals in the early morning hours.  This innate elevation in cortisol secretion causes the interference with our sleep hormone melatonin, it helps us wake up.  It also signals the liver to engage in producing sugar from stored starch and protein molecules. In our abdominally overweight T2DM patients, a great deal of cortisol is also made in their abdominal fatty tissue, so that can aggravate the DP situation.
  2. From secretion from the pancreas to liver degradation, insulin only has a half life of seven minutes in the bloodstreamIn the early morning hours this is increased as the liver breaks down more insulin to keep glucose higher and more energize the body cells.
  3. Secretion of Growth Hormone (GH) happens during fasting and at night when we are asleep.  In general, GH causes a reflex production of insulin-like factor one (IGF-1), which is a molecule similar to insulin. However, this type of insulin has receptors on muscle cells, while typical insulin mostly has receptors on fat and liver cells.  When IGF-1 is secreted at night, muscle rejuvenation, healing and growth can occur.  However, if someone’s liver is not healthy due to fatty liver (a problem with overweight and obese T2DM patients), or other reasons, or the blood sugar goes too high at night due to poor diet choice, the other DP phenomenon factors, under-dosed insulin, then enough IGF-1 cannot be produced and the body switches to insulin, which can make the liver insulin resistant.  As #4 explains below, the liver’s insulin resistance definitely increases glucose production and elevated morning numbers.
  4. The liver becoming insulin resistant.  Okay, a few background facts here.  The liver does not have any sensors for glucose—it only measures insulin amounts in the blood.  If the insulin is high, say after a meal, the liver senses that and thus takes in glucose from meals and stores it in its tissues, thus helping to lower the blood sugar.  In between meals, the liver does not sense insulin that much and so breaks down starch and transforms amino acids into sugar molecules, releasing them into the blood stream to prevent hypoglycemia.  (Cortisol is a signaling hormone for that, and so is glucagon, from the alpha cells in the pancreas).   During the night in our abdominally overweight T2DM (or in fact, any abdominally overweight diabetic, including T1 and T1.5; but this is uncommon in T1DM pediatric patients), the adipose tissues release free fatty acids into the bloodstream.  All bloodstream associated with the gut goes directly to the liver via the portal venous system.  In the middle of the night, if the liver receives an overload of free fatty acids, it makes the liver insulin resistant.  This means the liver cannot sense any insulin floating around in the bloodstream; when it cannot sense insulin, it believes it must produce more glucose and this is what the insulin does, potentially significantly raising the glucose levels.   There are other factors for inducing insulin resistance in the liver – glucose or insulin being too high in the bloodstream, or deficiency of certain nutrients.  Losing that gut fat can wipe out this factor entirely.

A good way for trying to get the Dawn Phenomenom under control could include these recommendations:

  1. Lose the abdominal fat!
  2. Do not eat before bed; the longer the fast, the better the control of one’s blood sugar.  If, however, the diabetic patient is having hypoglycemic events in the middle of the night, one must do some investigation as to why, to ensure safe and responsible treatment.  Ideally, the treatment would not include having to eat at bedtime.
  3. Adding in various insulin resistance nutrients:  Perhaps one might take some chromium (Max: 2000 mcg/day) or zinc (balance with copper) at night.  Alpha lipoic acid, and N-acetyl cysteine also decrease insulin resistance and protect the liver, keeping it healthy.
  4. Add in various insulin resistance herbs: Gymnema sylvestre, bitter melon, holy basil, or berberine.  I am especially interested in berberine given recent studies showing its efficacy in safely enabling significant hypoglyemia, equal to Metformin’s treatment effects.

The last thing to remember is patience—be calm if morning glucose numbers are not ideal and realize that they will likely be hardest to consistently control.  With education and understanding of physiology, we can work with our diabetic family members in a supportive and positive way, which is even more important than perfect morning numbers.

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