Low Carb, High Fat/High Protein Bolus

Hello Everyone;

I was diagnosed with T1 in November and am still in my “honeymoon phase” but I am trying to prepare in everyway I can. I am currently on 6 U of Lantus after coming down from my 338 mg/dl high at diagnosis. My average BG is 92 for the moment.

I started doing low carb (30-40 carbs per day) but the literature is rather mixed on bolus suggestions for this kind of macro intake.

I am fully aware that this is a rehash of the topic but I was wondering if anyone would care to share personal experiences with dosing a bolus (I will likely go the pump route as things progress).

If anyone would care to send PM’s with data so I can review them. I do not want to put anyone on the spot about it so I apologize if this is overstepping any lines.

I am trying blunt the learning curve and I appreciate the wealth of knowledge I have already been able to get from you folks.

PS, I am currently using a Dexcom G6 and with either be Looping via aftermarket apps or may go with a pseudo artificial pancrea set up commericially.

Thanks again.

hi, I have been using insulin for almost 47 years but i have had to go through this process maybe 6 times. Still after the first time everything builds incrementally.

So using the dexcom will be a big help. be sure and keep track of carb consumption as well. I suggest tracking total as well as net carb. your CDE will use that information to make inferences about how to go forward. There is no exact science to this. they will likely start a program. ask you wait one week or two then report, agree on adjustments and repeat.

It will be at least a little rocky. but that is OK, stick with it and eventually you will get there. I wish you good luck my friend.

Are you familiar with insulin to carb ratios (I:C), insulin sensitivity factors (ISF and sometimes called correction factors (CF), duration of insulin action, and insulin on board (IOB)?

Sorry to throw all of this terminology at a relatively new insulin user, but being conversant with these terms and the underlying meaning of them is important for someone who must now run their glucose metabolism on manual.

Medical professionals like doctors and CDEs can help but the reality of living with diabetes is that they are not available to you 24/7. Therefore, I believe that learning as much as you can to support good decision making on your part is the best road forward. Doctors can help with less time sensitive info but they’re rarely available at 2:00 a.m. in the middle of a three day holiday weekend when metabolic crises inevitably happen.

Doctors are indispensable for longer-term health decisions but they can’t be there every time you need moment-to-moment advice; that’s your job!

I’m using a do-it-yourself open-source automated insulin dosing system now (pump, CGM, app running on iPhone), but before that I also dosed insulin using an insulin to carb ratio to calculate an immediate bolus. Since I eat a low carb, high-fat diet, I also used my pump to deliver an extended bolus for 50% of protein grams and 10% of fat grams counted as “equivalent carbs.”

My description makes it look more complicated than it is. The key is to understand the terms well, carefully experiment, keep good records and set safe alarm levels on a CGM.

The honeymoon phase is challenging, since you won’t know how much insulin your pancreas is contributing.

However, since you use Dexcom, I think you could easily respond to that and dose as needed. 92 average now says you’re doing great. Your cgm readings/trends will be your guide.
Check out the book Sugar Surfing for using cgm data/trends to guide your food choices/quantity, and insulin dosing.

As LADA, your pancreas insulin contribution may vary or be a gradual decline. Some think that lower carb meals and less pancreas insulin will extend the time for pancreas insulin. Others think it gets easier once pancreas stops its erratic contributions, choosing higher carb at first to wear it out!!

1 Like

Hello Terry;
I am familiar with I:C, ISF and approximate length of different actions of various insulin types. I understand IOB and how it pertains to insulin stacking and such. The issue I have right now is that this is all in the abstract because I am on a single injection of Lantus a day so I get the general idea but not the practice. I feel like I want to get myself practice with dry runs. I already weigh my food and cook a bunch so that helps. I also bought wet erase markers to write the data on top of my pyrex lids so that when I get it out I can just quickly pull the data. Afterwards you just wash the numbers right of the lid with water. Trying to streamline things anywhere I can.

I took a Nutrition and A&P class so I am glad I have a solid understanding of gluconeogenesis from carbs, protein and fats. I am doing everything I can to be as prepared as reasonably possible and am very grateful that places like this exist and people are willing to share experiences. We stand on the shoulders of giants.

Hopefully going forward I will be able to ask more informed questions.

Thank you


What have you learned from your G6? How does your Blood Glucose (BG) vary after meals?

Typical climb is about 15-20 mg/dl over about an hour to an hour and a half. I an pretty closely following the 6,12,12 protocol at the moment so I suspect that has something to do with the control. Between meals it is really steady so I think my current basal amount is pretty well tuned (for now). If so some reason I see a slightly more agressive climb I take a quick walk for decrease the curve. I am only on Lantus currently so that is the only way I have of mitigating the climb.

Below is my clarity report for the last 2 weeks. Had a few mild low due to lantus being to high and some over treatments (showing the highs),
Any input would be appreciated.

clarity_2021-01-10_154045.pdf (642.8 KB)

I’m impressed by your Clarity Overlay Report. Your time in range 70-120/130 looks very high (I’m guessing 95%+) while your lows are few and just as important, your glucose variability looks low.

I prefer the 14-day AGP report. I find that it provides me a clearer look at what time of the day I need to take action, lists all the important statistics and does it all in a single page format.

It looks like your Bernstein-style of carb limits serves you well. Keep up the good work! I’d be happy to comment if you post your 14-day AGP report.

What is the 6,12,12 protocol?

Dr. Bernstein suggests 6 carbs in the morning and 12 and 12 in the afternoon and evening meals, equaling 30 carbs a day.

1 Like

Hopefully this is more concise.

Here’s the pertinent part of @ar87’s 14-day AGP report.

This report from a diagnosed T1D amazes me. The five lines (10th thru 90th percentile) are closely packed together. In my years of following my AGP, I’ve never seen this level of control. I think that you likely were diagnosed relatively early in your diabetes onset.

Are you aware of TrialNet? They are interested in cases like yours as they are looking for ways to extend the honeymoon period and work toward finding a way to block progression to full blown T1D. If it were me, I’d contact them as this level of glucose control is rare in the T1D world. Every day you spend with this glycemia will benefit your long-term health.

Your adoption of a vey low carb diet has reduced the demand on your failing beta cells to well within their ability to well control your glucose levels. Have you had your antibody levels checked? Do you know that your immune system is misfiring? There is another form of diabetes called maturity onset diabetes of the young or MODY and it is not autoimmune-mediated.

If you indeed live with LADA, a form of T1D, it will progress and your pancreas will produce less and less insulin over time. Your aggressive use of carb limits may help you the lengthen your honeymoon, maybe even for a few years.

1 Like

I have recently inquired wit TrialNet and and waiting to see what they say. I have looked at other small studies including a 2014 study using a beta blocker to slow progression but my endo would not prescribe the medication. I am hoping that with some dilligence, possibly being part of a trial and maybe some medication that I can lengthen my current honeymoon period. My longer delay will hopefully give more time for further improved technologies and therapies to progress. That is the hope.

Regarding my exact diagnosis I am not sure if it is MODY, I will inquire with my endo regarding additional testing to that end.

I appreciate the input. Gonna keep pushing forward.

It would be relatively easy for your doctor to order a few antibody tests. For reasons I fail to understand, many doctors are reluctant to do this. Check out @Melitta’s informative post on these tests.

Testing for MODY involves genetic analysis, is very expensive, and is not often covered by insurance. Therefore, I think doing the antibody tests and if you came up positive then you could conclude that you have autoimmune diabetes, the LADA form of T1D.

Well my C-Peptide is lower than nominal 0.51 vs .8-3.85 and my GAD65 Antibodies are through the roof (>250) so I suspect T1D is the culprit. Early stages though.

Ok, with your GAD65 antibody that high, you’re definitely a T1D. MODY does not apply. My C-peptide is < 0.1, the lower threshold of the lab. The longer your C-peptide stays “elevated,” the better off you’ll be. I think you’re doing everything possible and you’ll just have to accept that the immune system will do what it does while you pay close attention to your levels.

You could also research the trials of using arthritic immunosuppressive medications. In the hope of extending function.

I googled this as an example

Hi ar87, I am HNF1-alpha (genetic type) and not type 1 (or type 2). I will give you my theoretical insight, and I think that this could be more important than anything else for your future.
I have not really spent much time reading about the so-called “honeymooon” period, but to me being within this interval implies some retention and/or (normally temporary) recovery of insulin granulation. Granules are the storage form of insulin within the beta cells, and are absolutely critical/required for acute insulin prandial response (to meals).
There is a lot of evidence, including many clinical cases, that a T1D can retain a substantial population of beta cells indefinitely if the case is properly intervened at an early enough stage. Diagnosis almost always occurs with first loss of insulin granulation (for all forms of diabetes), at which point acute insulin response is lost and severe prandial glycemic instability (first) occurs. This happens initially with loss of ~80% of beta-cell (aggregate/total-population) function (i.e. 20% remaining).
The main (if not only) exception is with earlier diagnosis by HbA1c and other symptoms not generally recognized by MDs, or by the early-developing diabetic himself/herself if sufficiently knowledgeable to do so (e.g. self-administered OGTT).
Assuming you have been diagnosed in the usual way recently you still have ~20% (maybe a bit higher for now) beta-cell function. That is a LOT – HUGE in comparison to what more mature T1Ds have which is < 5%. And that is plenty more than the low level (maybe 5% at most) which induces the so-called “insulin-dependent” state, at which point one becomes susceptible to ketoacidosis due to loss of the negative feedback of islet/blood ketones upon glucagon secretion via islet insulin increment (and hence ketosis or hepatic generation of ketones). That is, increasing blood ketones act directly upon the beta cells to increase insulin secretion and indirectly decrease glucagon secretion, thus avoiding the glucagon-runaway condition of DKA. And alpha-cell function inevitably degenerates after a few years of overt T1DM as part of the same hormonal deficiency picture.
It would be my strong advice to read Richard Bernstein’s writing on this subject ASAP. And he is hardly the only clinician to have observed cases of avoidance of insulin dependence and retention of substantial (though partial) beta-cell function in T1DM cases with early intervention.
To oversimply somewhat, the intervention required is the utmost of carb restriction (for life) and carefully calibrated/monitored/adjusted insulin therapy (again, for as long as necessary). BOTH shoud be immediately practiced. In some successful cases of intervention it is possible to eliminate insulin therapy altogether, but in the other cases it is very light/mild insulin therapy that is required for the long term to supplement the retained endogenous capacity – much smaller amounts of insulin than required by a mature T1D. Good luck.

1 Like

I’ve read Bernstein’s book and general comments on the matter. Do you have other studies or resources for reference?