Tomorrow it is going to be 5 weeks/1 month into this nutrition change to a low carb diet. Time for some conclusions.
Perimeters: Before this change, we ate pretty healthy for todays standards. That means no heavily refined fast food or prepared meals. Approximately 50% Carbohydrates, 25 % Fats, 25% Protein of 2,000 calories daily.
We changed to a 5% Net Carbs (deduct the fiber), 70% Fat, 25% Protein
No to little carbs equals insulin reduction. This is pretty obvious since you re not consuming any food that requires insulin to be broken down into energy. Do not try this if you are having trouble with hypo’s to begin with and a difficult time to control those. If you are having trouble bringing hyperglycemic results down and do not want to use more insulin, this might be a good approach.
For me the insulin reduction was: basal -25%, bolus -65%.
If you are well in control, let’s say below a 7.0 A1C, you still will see some improvements. I would guess with higher A1C’s the improvements will become more dramatic.
Weight loss: I lost almost 7 pounds in 4 weeks. This is a pretty good amount in my eyes but definitely not the “Magic Pill” over any other diet as a lot of “Keto-diets” will promise you. Even though I was consistently below the recommended Net-Carbs of 24 grams and constantly below the recommended calorie level of 1,942 cal with an average of 1,564 cal, I never entered that “magic” state of Ketosis, constantly reading “zero”. I technically should have been in that starving mode but I was not as far as I can tell. My wife reached ketosis frequently, mostly in the afternoons, between 0.9 -1.7 on a breathalyzer. She dropped some weight but percentage wise not as much as me, even with being in Ketosis.
This leads to my last observation and a brand-new question and my conclusion to that question. It might challenge the bio-chemists and hopefully we might get some understanding which I can not readily find to that question. We T-1’s can obviously synthesize large amounts of ketones with uncontrolled high blood sugar levels which will lead to ketoacedosis.
Can T-1 diabetics synthesize ketones with controlled blood sugar levels?
The Synthesis and Utilization of Ketone bodies
“Ketone body synthesis occurs normally under all conditions. However, the formation of ketone bodies increases dramatically during starvation. This seems to be due to a combination of factors. Prolonged low levels of insulin result in both increased fatty acid release from adipose tissue, and increased amounts of the enzymes required to synthesize and utilize ketone bodies. In addition, in the liver, increased demand for gluconeogenesis results in depletion of oxaloacetate, and therefore in decreased capacity for the TCA cycle. This causes a rise in the levels of acetyl-CoA, the substrate for ketone body production.”
A non-diabetic will meet the requirements for ketone body synthesis with automatically having low levels of insulin resulting in higher amounts of fatty acid and enzymes required to synthesize and utilize ketone bodies when being on a low carb diet.
What does this mean for a Type-1 diabetic on an insulin pump? How do you achieve “prolonged low levels of insulin” without raising your glucose levels and going into ketoacedosis instead of ketosis? This would only be possible in a “starvation-diet” with zero carbs and no insulin administration. But with that situation ”no level of insulin” since you are not administering artificially insulin is different to “low levels of insulin” your body would produce in that starvation-mode?
Or do you go on a fine balancing act of lowering your insulin as much as you can without going above a certain glucose level? But that is what we are doing already, otherwise we would go hypo.
Conclusion: A type-1 diabetic on an insulin pump will never be able to meet the requirement of “low levels of insulin” unless he stops treatment. Stopping treatment will lead to high glucose levels even with a very low carb diet. This will lead to ketoacedosis. It appears that another trigger for the liver to synthesize ketones is missing with the absence of Islets of Langerhans, or at least the beta cells in those islets. I am thinking that all the differences between reactions of T-1’s to anything could depend on the individuals extent of the damage to those Islets “about which little known”.