Just read this on Facebook, I'm sure it will make more sense to you than me but it's very interesting re blood glucose readings
My Fasting Challenge
[Long post, but interesting, I hope, especially with those who are highly insulin resistant and struggle to bring down blood sugars even while fasting.]
NOTE: I am under the care of a weight-loss doctor who uses low-carb/keto diet and fasting protocols to treat her patients. She is a licensed Internal Medicine specialist, and is fully aware of my efforts and trusts me to monitor my blood sugars closely and self-dose insulin conservatively.
After a binge on movie-theater popcorn on the evening of Friday, Feb 7, I decided to restart my commitment to using prolonged fasting to reverse this disease. [I was diagnosed with T2DM in 2002, and started injected insulin in 2016].
**My Background in Fasting/Keto**
I am no newbie to fasting. I have often done OMAD (one meal a day), ADF (alternate day fasting), and other intermittent fasting protocols (I define intermittent fasting as any fasts lasting 16 to 48 hours between eating windows). And when I am on these protocols,I tend to stay pretty strictly keto during my eating windows. However, my compliance is spotty on the fasting, and I find that if I eat *anything* it can start a cascade into compulsive overeating. I have also done a few extended fasts in the past-- several 3.5 days fasts and my longest fast of 115 hours (5 hours short of 5 days).
**The Perplexing Question**
In my experience of all this, a mystery has developed about my body: My waking blood sugars have always been high, due to strong Dawn Phenomenon in me, but contrary to all expectations of Type 2 diabetics, my blood sugars don't come down quickly when fasting. On an extended fast, it's not uncommon to start my fast with a waking BG of 285, and have it gently slide down to 245, 230, 205, on each subsequent morning, and still be at 190 after 4 full days of fasting. Where does the sugar come from? My understanding of metabolism is that the liver and muscles store only about 1300 calories of glycogen. Surely, I'd have burned through all my existing blood sugar and those glycogen reserves in 4 days, right???!!! When I've asked about this in forums, I've been told flat-out by some people that I must be lying about my fasting-- that I must be cheating on the fast-- because there's no way I could have a BG of 200 after 4 days of fasting.
**Mystery Solved?**
So last Monday, after 2 days of fasting and the same pattern emerging, I dove back into the research, and I found out about CRTC2, a "transcription co-factor" which is found in the cytoplasm of liver cells. These molecules bond with something called CREB, allowing the CREB to enter the cell nuclei to trigger glyco-and gluco-neogenesis, processes which convert proteins and lipids into carbohydrates.
Believe me, my eyes also get crossed when I read the gritty details of the science, but long-story a bit shorter: CRTC2 is believed to be a part of the body's means of preventing hypoglycemia when we fast. It served the evolutionary purpose of preventing our ancestors from collapsing when they couldn't find food for a few days, tapping any fat reserves in their bodies for energy while they continue their hunting/gathering efforts.
CRTC2 is only *supposed* to get triggered when blood sugar is low, but rodent studies have shown that the "on switch" for this co-factor can get stuck in the ON position in diabetic mice. What this means is that, when these hyperglycemic mice are fasted, their blood sugars remain high for quite some time. Sound familiar? It's because, even though they aren't eating carbs, their livers are in overdrive converting fats and proteins into carbs.This is the best explanation for my experience in fasting to date.
Although CRTC2 is technically a good thing, having it switched ON when I don't need it is frustrating and presents a challenge: it constantly pushes my blood sugar over 200, requiring me to use insulin to bring it back down to a safer range (Dr. Fung, a nephrologist, says kidney damage begins at about 170+). However, insulin itself is the cause of insulin resistance-- so taking insulin sets me back in my attempts to reverse it.
**My Protocol for Insulin Use While Fasting**
Following Dr. Fung's protocol for insulin-using T2 diabetics, I take just enough Humalog to target a 130-170 mg/dL range 2 hours after a bolus (when it's at its peak action), and I have to carefully estimate the effectiveness of the insulin. I track each bolus and the followup meter reading in a spreadsheet, and have it calculate a ratio of mg/dL reduction divided by the number of units in the bolus. That first morning when I woke up with a 315 BG, I took 100 units. Two hours later, I was at 221, meaning I saw a ratio of 0.9 mg/dL to 1 unit of insulin. I followed that up with another 75 unit bolus and only got down to 186 for a 0.7:1 ratio. That's RESISTANT! Later that day, I took an additional bolus of 25 units which ended up at a 2.6:1 ratio (I'm usually more sensitive in the afternoons), so at least there was some progress!
The next morning, I had a BG of 245, and I took 50 units (I have a lot of experience with sensitivity increasing rapidly during fasting, so I wanted to be conservative). My 2 hour reading was 198, so I still had a 0.9:1 sensitivity. I took an additional 30 units, which ended up putting me in the target range at a sensitivity of 2.8:1
Monday (the day I did that research) through Wednesday produced the following results: Mon: AM BG 232, Bolus 15, sensitivity 4.6:1 Tue: AM BG 230, Bolus 15, sensitivity 2.2:1 Wed: AM BG 199, no bolus.
I chose not to take insulin on Wednesday, believing from experience that the AM BG would soon slide down on its own, and I was right.
I broke my fast Wednesday evening and continued eating largely keto through Saturday night. My numbers through today: Sun: AM BG 283, Bolus 15, sensitivity 5.5:1 Mon: AM BG 211, Bolus 10, sensitivity (not calculated, because I missed doing my 2 hour follow-up reading). Tue: AM BG 205, Bolus 5, sensitivity 2.0:1
**Re-Considered Assumptions**
Okay, so, here's the thing-- what I'm reading as "sensitivity" based on the ratio of blood glucose reduction to units in the bolus could be based on the faulty assumption that the liver isn't producing carbs. The latter reading could be elevated by the gluconeogensis. I'm okay with that. It's obvious that these extended fasts are improving my insulin sensitivity. I have also been losing weight. After 11 days of fasting, I'm down 10.6 lbs. I know that some of that is water-weight only, but estimating my metabolic rate and calories consumed, I believe I've lost an actual 5.8 lbs.
The coolest part is that the CRTC2 being stuck in the ON position means I'll be able to lose weight faster, because my liver is in "gluconeogenesis overdrive" converting fat in the body into sugars. Yes, it's a nuisance for blood sugar control, but it's also a blessing for weight loss. In particular, the liver prefers to access intraorgan fats first, especially the liver itself. Reducing my liver fat will reduce my inflammation levels in my system. Reducing pancreatic fat helps to re-enable the beta-cells to produce their own insulin. That's what's at the heart of reversing Type 2 diabetes. (Note: I used to do "fat fasting" where I'd consume up to a few hundred calories a day of pure fats while 'fasting.' Now I understand this is just slowing down my liver's breakdown of existing fat stores.)
**Interventions Suggested by Research**
Additional research has shown that weight loss is the #1 way to fix the CTRC2 switch. Of course, this is difficult while taking insulin.
Other than that, eating a diet high in fermentable oligosaccharides and glycans also helps. This is where I may vary from my keto routine. I'm willing to get some carbs in my diet (when I'm eating) if they are in the form of high-fiber foods. I've never understood before why oatmeal seems to help some diabetics, given it's a high-ish carb food, but apparently the fermentable soluble fiber in oatmeal is the reason. The research also indicates dark, leafy greens to be very effective.
Also, it's important to get sufficient protein, even while fasting, so bone-broth is a recommended fasting-aid for people with a CTRC2 problem. I can theoretically consume up to 80g/day of protein without it affecting my blood sugar. Bone broth is mostly collagen protein, and isn't as insulinogenic as things like whey protein isolate.
Finally, the research indicates that exercise is far more important for diabetics with CTRC2 issues than for others. In fact, it may be the most effective intervention of all.
***DISCLAIMER: The above is based on my personal experiences and understanding of the research and is not intended to be medical advise to anyone. Those who are interested in doing something similar should do their own research and discuss it with their doctor.
Never give up on a dream just because of the time it will take to accomplish it. The time will pass anyway.