HbA1C and Prolactin

I had some lab work done – still waiting for some of it, but here’s what I have so far:

HbA1C Feb 2015 Dec 2015 May 2017
6.7 6.4 5.9

In February 2015 I had a routine HbA1C test done – essentially a summary of my blood sugar over the previous 3 months.  With a result of 6.7, that test earned me a diagnosis of Type 2 diabetes, and the doctor prescribed me Metformin.  I took it for like a week, didn’t like the side effects, and stopped taking it, determined to control my blood sugar with diet instead.  And I did for a while there, with low carb.  However, as soon as I stopped low-carbing my blood sugar shot back up again (and I had to stop low-carbing because I started feeling like crap eating that way long term).  Over the last 4 months I’ve been eating high carb, low fat.   My blood sugar has been well-controlled on this plan, and my fasting blood glucose is routinely in the 80s now.  Here’s a graph of my fasting blood sugar since January:

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For a minute there I thought the steroid I was taking for Lichen Sclerosus was helping my blood sugar somehow, but it was already trending down before I started that.

Anyway, good news – my A1C is below the diabetic range now (which is generally considered a A1C of 6.5 or higher), and I’m firmly in the PRE diabetic range.  I expect that to be a thing of the past too, the next time I test.

So isn’t this interesting?  It’s almost as if carbohydrates don’t actually cause diabetes.  Poor carbs…always getting blamed for everything these days.

Here’s what I’ve learned about myself – I can eat high carb/low fat and my blood sugar will be well-controlled.  I can low carb/high fat and my blood sugar will be well controlled.  What I CAN’T do is eat high carb/high fat.  When I do that my blood sugar trends up and suddenly I’m diabetic again.

Ray Peat talks about the Randle Cycle, and I’ve referenced it in this blog before.  Here it is again:

The antagonism between fat and sugar that Randle described can involve the suppression of sugar oxidation when the concentration of fats in the bloodstream is increased by eating fatty food, or by releasing fats from the tissues by lipolysis, but it can also involve the suppression of fat oxidation by inhibiting the release of fatty acids from the tissues, when a sufficient amount of sugar is eaten.

Readers Digest version: Sugar and fat compete.  Choose one and go with it.

I choose sugar.

So…is my improvement in blood glucose due to eating low fat?  or is it due to improving my gut microbiome with Culturelle Probiotics?  I changed both variables in January….so it’s hard to say.

Last thing – I tested my prolactin, to evaluate whether or not that may have increased since starting Verapamil for high blood pressure, and if so, whether that may be contributing to autoimmunity, as I described here.

Prolactin in March 2014 – 5.4 (range 4.8-23.3)

Prolactin in May 2017 – 5.9 (range 4.8-23.3)

So not much change there.  Can’t really blame prolactin for tipping me over into autoimmunity.

Tomorrow:  A snapshot of exactly what I’m eating these days.

Weight Loss and Autoimmune Update

I got down to 187 about a week ago…a 25 pound loss from my top weight of 212 in January.  Then I started having a lot of cravings. One thing I’ve learned about myself is that I have a strong backbone when it comes to sticking with a diet or plan that is working for me.  I can refuse my favorite foods every single day for months and months at a time, knowing they’re not currently aligned with my commitment to myself to be healthy.  Maybe that sounds extreme – but to me, it’s focused.  SO…..when I have cravings and can’t stop thinking about food and I’m not hungry, I know it’s not a character issue.  I know something biological is causing it.

In the last week I’ve been having cravings for high-fat food.  When I started my weight loss journey I was eating 2 eggs every day and low-fat cottage cheese in the afternoons.  Since I got diagnosed with Lichen Sclerosus I’ve been trying to follow something closer to the Autoimmune Protocol by removing eggs and dairy from my diet.  This has left me with very very little dietary fat – probably around 10-15g a day.  I guess that’s just too damn low and my body is needing more.  I notice my hair, which I used to have to wash daily due to oiliness, now takes much longer to get oily, and I can now go 2-3 days without washing it.  Anyway, the food cravings have been a bit of a problem so in the last few days I’ve been adding eggs back in (which went fine) and I’ll be adding the cottage cheese back in – I could be missing the nutrients in those foods too.

So for the moment, my weight is back up to 190 – on the upswing because I have been eating things not supportive of my weight loss goals.

Had a doctor’s appointment with my functional med doc a few days ago. He didn’t want to test for Lyme, given the poor reliability of testing (regardless of lab, he says) and the extreme nature of treatment if I do get a positive.  He said that unless I was really feeling terrible it wouldn’t be worth it.  I can’t disagree with that.  He also said that lots of things cause autoimmunity – not just Lyme, and that Lyme isn’t even the most likely culprit.

When I got home from that appointment I saw this article in my Facebook feed: Trigger for Autoimmune Disease Identified, which references this study that was published a couple of months ago.  The basic idea is this:

B cells expressing the transcription factor T-bet promote the rapid appearance of autoantibodies and germinal centers in spontaneous murine models of systemic lupus erythematosus (SLE). Conditional deletion of T-bet from B cells impaired the formation of germinal centers and mitigated the development of kidney damage and rapid mortality in SLE mice.

So the B cells – I guess this is a kind of white blood cell – may or may not be expressing transcription factor T-bet.  The mice that were expressing T-bet and who were genetically susceptible to autoimmunity, had a high rate of autoimmunity.  The susceptible mice who had T-bet deleted from their B cells stayed healthy.

So what causes T-bet expression?

Check this out (h/t to Ruth in my Ray Peat Facebook group): “Prolactin (PRL) exposure stimulates expression of T-bet, an immunoregulatory transcription factor for Th1 development, and alters secreted cytokine profile in peripheral blood mononuclear cells (PBMC)”.

Prolactin = bad.  Just like Ray Peat sez!

Before I go on…a bit of background about prolactin from Self Hacked:

Prolactin is a peptide hormone made by the pituitary gland and various other parts of the body. It is also referred to as the luteotropic hormone (luteotropin) and PRL. Prolactin is encoded by the PRL gene (R).

Primarily, prolactin is responsible for the stimulation of milk production in women (lactogenesis) (R).

When a woman is pregnant, prolactin levels increase by up to 10-20 times the  normal amount.  The levels return to normal within a few weeks after the mother stops breastfeeding.

Despite what its name suggests, prolactin does much more than only promote lactation. It is found in men as well and is influential in over 300 separate processes.  It is recognized as a multipurpose hormone with one of the widest ranges of physiological actions of any hormone (R).

Here are more studies that discuss prolactin’s negative effects on the immune systems (specifically B cells):

Prolactin Alters the Mechanisms of B Cell Tolerance Induction

Prolactin Levels Correlate with Abnormal B Cell Maturation in MRL and MRL/lpr Mouse Models of Systemic Lupus Erythematosus-Like Disease

Prolactin modulates the naive B cell repertoire

Prolactin Rescues Immature B-Cells from Apoptosis Induced by B-Cell Receptor Cross-Linking

What’s interesting to me is that this hormonal connection between Prolactin and autoimmunity may help explain why far more women than men have autoimmune conditions.

So then I googled “What causes high prolactin?”  I know I could burrow through articles at raypeat.com and find this answer but I’m short on time these days.  The Pituitary Society seemed as good a source as any….oh hey look!  The medication I take for hypertension actually INCREASES prolactin!  Awesome…so Verapamil increases histamine release (and thus sustains my hot flashes) and also increases prolactin, perhaps causing and/or sustaining my autoimmune condition.

AWESOME!!!!

Ok, I seriously have to get my blood pressure down.  Immediately.  I need to get off this big pharma rollercoaster.

Fortunately, I have a baseline prolactin level from testing I did 2 years ago, long before starting this medication.  I’m going to get it tested again today to compare.