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Why My HbA1c is 5.1 (and how I plan to move my blood sugar numbers lower)

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In the Gene Food scoring system, my diet type is Mediterranean, a diet that is more liberal with complex carbohydrates. In the nutrition world, people that have greater ability to clear and use glucose (rather than having it linger in the blood) from the carbohydrate they eat are said to be more “insulin sensitive.” This means that when the pancreas pumps out insulin in response to glucose entering the bloodstream, that insulin does a good job of getting the carbs into cells where they can be used as fuel. Other diet types, like California Coastal for example, have less wiggle room with carbs and are therefore placed on a diet that puts greater emphasis on preventing large spikes in blood sugar.

This is a post about my blood sugar numbers, including HbA1c (a metric that measures average blood sugar levels over the past 3 months), why they’re relatively low and strategies we can all use to keep our blood sugar in check. Anything below 5.7 is considered a normal HbA1c levels by most labs.

At the end of this post, Aaron gives a full genetic breakdown, explaining why I am genetically unlikely to develop type 2 diabetes (“T2D”).

What are “good” blood sugar numbers?

The big 4 blood sugar tests are:

  1. Oral glucose tolerance – what your blood sugar looks like immediately after a meal (possibly more important than HbA1c but hard to measure without a continuous blood glucose monitor)
  2. Fasting glucose
  3. Fasting insulin
  4. HbA1c

When I say my HbA1c numbers are “low,” I mean they are basically in range (anything at or above 5.7 is trouble), well outside the scope of the type 2 diabetes (“T2D”), insulin resistance world. I do not mean that I am hypoglycemic, which is a condition associated with blood sugar that is dangerously low. To the contrary, part of today’s discussion centers around people who trend hyperglycemic, meaning their blood sugar numbers are chronically elevated which places them at greater risk of developing metabolic syndrome and T2D. I also include below a chart mapping my latest insulin data.

My Result
Unit of Measurement
Insulin Resistance Score (SJC)
< 33
> 66
Insulin, Intact, LC/MS/MS (5)(SJC)
≤ 16
> 16
C-peptide, LC/MS/MS (6) (SJC)
≤ 2.16
> 2.16

As a foundational principle, let’s just come right out and say that high blood sugar is a bad thing. Some believe that elevated HbA1c and insulin resistance increase the risk for cancer and dementia, and there are studies to back them up. Don’t listen to the nutrition gurus out there who tell you all blood sugar issues are driven by animal products. They do play a role, but just as the Keto world tends to downplay the potential risks associated with dietary fat, the Vegan world downplays the dangers of sugar. Especially if you’re at a genetic disadvantage in clearing and using glucose, elevated blood sugar is a very real problem and one of the primary drivers of the chronic disease epidemic. And no matter what you may have heard from the Vegan podcast and film world, you can be diabetic as a vegetarian.1 Perhaps not as likely, but still possible. 

So, bottom line: absent hard N=1 data, take Keto advice on fats with a grain of salt, and same for the Vegans on sugar. The goal is to understand what is driving spikes in your blood sugar (not someone else’s) and plan accordingly. If you haven’t had HbA1c and related markers tested lately, EverlyWell offers at home blood sugar test kits.

Glucose – the universal fuel source

Blood sugar basically means blood glucose.

When we eat carbohydrates, the body breaks down the food into glucose, a simple sugar every cell in the body can use for energy. Insulin is the hormone the body then uses to get glucose into cells, or into the “bank” as glycogen where it is stored for later use. That’s right, since glucose is vital to life, we evolved to store it for a rainy day. The glucose storage bank comes in layers, with the first storage option being the liver and muscle tissue. Glucose stored in the liver or in the muscles is banked as glycogen, which is essentially a large strand of glucose molecules bound together. When we lift weights, or go for a run, the body draws down stored glycogen in the muscles and we become more “insulin sensitive.”

In an ideal world, every one of us would be perfectly insulin sensitive and use most all of the glucose we consume.

However, in today’s high sugar world, not all of us do such a great job of effectively using the glucose we eat. In some cases, especially in people who are at a genetic disadvantage in clearing and using glucose, excess glucose is stored as fat, or it remains elevated in the blood which leads to a cycle of inflammation.2 The idea here is that the body can only store so much glucose as glycogen. When the liver and muscles are “full” of stored glycogen, a process known as “de novo lipogenesis” allows the body to convert the excess glucose to triglyceride fat and store it in fat tissue.3 The first layer glucose storage organs have limits on glycogen, but there is no limit to the fat that a person will store.

This is why people who have elevated blood sugar tend also to have high triglycerides, and why I included my historical triglyceride data alongside the more traditional diabetes metrics below.

What is HbA1c?

HbA1c, or hemoglobin A1c, tests measure your average blood sugar level over the past 2-3 months. Hemoglobin is a protein found in red blood cells. Glucose in the blood “glycates,” or binds to these hemoglobin proteins. So, the more glucose in the blood, the more red blood cells bind to the blood sugar, which then gives us the ability to measure blood sugar levels over time. The 2-3 months of blood sugar data we get from HbA1c tests correlates to the average life cycle of a red blood cell, which is about 3 months.

Startups like EverlyWell allow consumers to measure their blood glucose and HbA1c levels from the comfort of their own home.

HbA1c tests are most often used to gauge the risk of developing diabetes, but HbA1c numbers have also been linked to neurological health by neurologists like Dr. David Perlmutter of Grain Brain fame. Dr. Perlmutter has published blogs analyzing data tending to show that the size of our brains actually shrink as HbA1c levels climb. And here’s the rub: HbA1c levels thought to be “normal,” even some of the results from my old labs I share below, register in a range associated with some degree of cognitive decline.4

Dr. Perlmutter’s work has motivated me to move my HbA1c number down below where it currently sits at between 5.1 – 5.4. My target is a sub 5.0 HbA1c.

Why does elevated blood sugar cause inflammation?

Metabolically, this is an insanely complex issue, but I have come to understand it as follows: the body wants us to use glucose, it’s central to life and universally recognized at the cellular level as fuel.

However, like everything else in the body, it has its place, and that place is inside the cell. The immune system knows this and goes on alert when glucose hangs around in the blood for too long. When blood glucose levels stay high over long periods of time, the immune system is triggered, almost as if to say, “hey, you’re not supposed to be here, get out of here, get into the cell.” As a result of sensing an invader (not an antigen per se because antibodies aren’t released, but more of an immunogen), the immune system releases inflammatory cytokines in a looped cycle, that over time, cause tissue damage, leading to inflammation.5

Blood sugar and white blood cell activity

For a technical example, CD33 immune cells are a type of protective sheath for white blood cells. While the CD33 system is functioning and blood sugar levels are under control, white blood cells behave themselves. However, when glucose levels stay elevated, CD33 expression is reduced, the white blood cells go haywire, and the production of inflammatory proteins called cytokines are the result.6 Cytokines such as TNF-a cause damage to cells and increase levels of oxidative stress, which in turn damage fats, protein and even DNA.

Blood sugar, glycation and oxidative stress

Think back a minute to the glycation discussion above. The binding of sugar to the hemoglobin proteins in the blood also cause inflammation as “glycation end products” are produced. This throws off more oxidative stress, which leads to more damaged fats, proteins, etc. Glycation and the damage sugar can do when it binds to fats and proteins is one of the arguments nutrition scientists like Dr. Rhonda Patrick offer as the cause of heart disease. To simplify, sugar damages fats and those damaged fats get into lipoproteins where they wreak havoc at the artery wall. This is why meals that combine high fat and high sugar are particularly damaging, they oxidize the flood of fat making it effectively radioactive to our endothelial cells.

I’ve written previously about how oxidized phospholipids (plant fats) have been shown to bind preferentially to dangerous lipoproteins such as Lp(a), so the theory makes sense. The question is what level of glycation is damaging?

In sum, chronically elevated levels of sugar in the blood cause an inflammatory cascade in the body which is why it is worthwhile to study ways to keep our HbA1c and blood sugar spikes under control.

Blood sugar after a meal vs. chronically high blood sugar

When is elevated blood sugars bad for us? Is it the chronically elevated numbers that are the true bad guys, or do the quick spikes after higher glycemic meals cause trouble as well?

Blood glucose levels after a meal are called postprandial levels. There is some evidence that the spikes in blood sugar after a meal may be an independent task factor for certain diseases, especially heart disease.7 This is kind of a scary proposition as most people have no idea what their post meal blood sugar data looks like. Longevity experts like Dr. Peter Attia have expressed preference for a two hour oral glucose tolerance test (OGTT) over HbA1c, presumably because of the importance of the post prandial period.

As such, the idea is to keep blood sugar under control over the course of weeks and months, but also to prevent major spikes during the day.

Ok, now on to my actual test results.

My blood sugar numbers (HbA1c, Glucose, Insulin, and More)


Ok, so let’s do a quick walk through of each metric. Of course, we have already covered HbA1c, so we will leave that out.

HOMA-IR – HOMA-IR, or the homeostasis model assessment-estimated insulin resistance, is a calculation clinicians use to measure insulin resistance. It is calculated by multiplying fasting plasma insulin by fasting plasma glucose, then dividing by the constant 22.5. When HOMA-IR is greater than 3.80, it is thought to be evidence of insulin resistance.

Glucose – This one is pretty straightforward. How much glucose is hanging around in the blood after going without food for at least 8 hours? Levels of between 70 and 100 mg/dl are considered normal, 100-125 mg/dl are believed to evidence of prediabetes.

GSP – Ok, here is where I hit a snag, and I think I have a SNP to pin it on as well. GSP stands for glycated serum protein, as the name suggests, it measures the amount of protein that has been glycated (bound to sugar) in the blood over the previous two weeks. Less than 200 umol/L is optimal, but I sit above that in the 230s.]


I believe it is due to a diet that has traditionally not paid much attention to glycemic load (yes, I will main line mega doses of ice cream or cookies from time to time, at least in the past) as well as an unfavorable SNP in a gene that we see as regulating post prandial glucose levels, ADCY5. I am homozygous for the risk allele, and as a result, I may be seeing large spikes in blood sugar after meals that are quickly brought back to earth by other favorable pathways. However, as we have discussed above, the post prandial period is one in which damage can be done, so writing this post has me much more focused on my insulin sensitivity post meals.

However, I should point out that GSP as a metric is thought to be most relevant in cases of T2D, and in cases of elevated albumin, and my albumin numbers are low at 4.5.8

Insulin – again, fairly self explanatory. This test looks at the insulin in your blood, lower is better because it signifies your body doesn’t have to work as hard to get glucose in your cells. High fasting insulin is a sign of insulin resistance.

Triglycerides – call them sugar fat or energy fat, both are basically correct. For our purposes here, it’s important to reemphasize that the body converts glucose into triglyceride fat when it has stored as much glycogen as possible for a “rainy day.” Anything below 150 mg/dl is considered normal by most labs, and my TG have been as low as 66.

Is it all in my genes? The genetics of blood sugar

We touched on the ADCY5 gene, but how much of blood sugar metabolism is genetic? It is certainly top of mind when we categorize nutrition plan customers into their diet types.

For this part of the post I have brought in Aaron to run through my genetics, which definitely give us a clue as to why my blood sugar numbers generally look to be in good shape, ADCY5 SNPs notwithstanding.

Thanks John, on to the genetics of blood sugar, a topic we delve deep into in the custom nutrition plans. For starters, our scoring algorithm place John in the Mediterranean diet type category, which is marked by a higher tolerance for higher glycemic foods.

As you can imagine there are masses of proteins which modulate the glucose level in the body, and many of the genes which encode for these proteins have been shown to contain SNPs which influence T2D risk, circulating glucose and a whole host of other factors.

Simply put the answer to the first question is yes, for a whole host of key SNPs John carries no risk alleles, or is at worse a heterozygote. Let’s break that down a little and have a look at some of the individual effects.


MAP kinase-activating death domain protein (MADD) is an adaptor protein which interacts with another protein TNF-alpha receptor 1 to activate mitogen-activated protein kinase signaling within cells regulating controlled cell death.  There is some interesting work which has linked a SNP in MADD with elevated blood glucose levels, by altering the conversion of pro-insulin to functional insulin. Although this effect is modulated is unknown as MADD has no known glucose related functions. The SNP is detailed in the table below along with my own genotype. As you can see, John does not carry any risk alleles so score one for him.

rs IDRisk alleleNon-risk alleleRisk effectMy genotype
rs7944584TAIncreased circulating glucose.AA


Alpha-2A adrenergic receptor (ADRA2A) has been shown to be involved in regulating circulating glucose levels and there is a proposed association with T2D (R, R), and the SNPs are detailed below. As you can see John is homozygous for the non-risk alleles. What’s interesting about this gene and the two SNPs is a complete lack of a mechanism linking the protein with changes in glucose levels, given the quite strong effects observed. There is some suggestion that the risk alleles lead to increased expression of the ADRA2A protein could increase T2D risk and that this may be something to target therapeutically, but this is the limit of current understanding. One other interesting finding is that while each SNP alone is important, carrying risk alleles for both together further increased T2D risk and levels of circulating glucose.

rs IDRisk alleleNon-risk alleleRisk effectMy genotype
rs553668AGIncreased risk of developing T2DGG
rs10885122TGIncreased circulating blood glucose.GG


Adiponectin (AdipoQ) is a protein hormone which regulates pathways related to fat storage and metabolism. Secreted exclusively from fat cells AdipoQ modulates sugar and fat metabolism in the body by increasing insulin sensitivity and fatty acid breakdown, so as you can imagine low levels are associated with an increased T2D risk and increased circulating glucose levels. There is one SNP of interest which is detailed in the table below. But again as you can see John is homozygous for the non-risk allele so another potential reason why his blood sugar numbers are good. For this SNP the risk ‘C’ allele is associated with increased circulating glucose levels and an associated increased risk of developing T2D through alterations in AdipoQ activity (rather than expression). Importantly the authors didn’t discriminate between heterozygous and homozygous carriers of the risk allele, rather grouping everyone together.

rs IDRisk alleleNon-risk alleleRisk effectMy genotype
rs17366743CTIncreased circulating glucose and increased T2D risk.TT

Three important SNPs and for each one John sits square in the positive effect category, which goes some way to explain his good blood sugar scores. But there are some where the story isn’t quite as rosy.


Fat mass and obesity-associated protein (FTO) is probably one of the most well-known genes/proteins, as it is often termed the “obesity” gene and is widely investigated. However despite been so well known what FTO actually does to regulate body mass, and how SNPs alter this activity, remains unknown. One proposed method is that FTO regulates hunger and so SNPs may lead to increased eating even when full,9 whereas another mechanism proposes that FTO changes expression of another protein IRX3 which regulates fat metabolism, and may, therefore, impact on fat storage and glucose metabolism.10 So because of this unknown activity, we don’t place great emphasis on FTO in our analyses but show it here more because it’s so well known. There are many SNPs in FTO that are thought to impart an effect but the most well known is rs1121980 which is detailed below.

rs IDRisk alleleNon-risk alleleRisk effectMy genotype
rs1121980AGIncreased risk of gaining weight, and risk of associated disorders including T2D.AG


Looking good so far, but there is one SNP where John does have some issues.  Adenylyl cyclase type 5 (ADCY5) converts ATP, the cells energy currency, into another molecule called cyclic adenosine monophosphate which in this case regulates the release of insulin from cells in the pancreas in response to elevated blood glucose. Two copies of the risk allele ‘A’ of the SNP rs11708067 detailed below are associated with a 50% reduction in expression of ADCY5 compared to heterozygotes (no data shown for non-risk homozygotes).11 This reduced expression is thought to lead to an impaired pro-insulin to insulin conversion meaning blood glucose levels remaining higher for longer.12 Together these effects have been linked with an increased risk of developing type 2 diabetes.13 So we have a mechanism and an effect what about John’s SNPs? Well as you can see in the table not quite as good for this gene. although John’s theory about ADCY5 and elevated GSP is just that a theory. There isn’t much to prove that connection as of now, hence the very low science grade.

rs IDRisk alleleNon-risk alleleRisk effectMy genotype
rs11708067AGIncreased circulating glucose and increased risk of developing T2D.AA

John’s Genetic Summary

This is an excellent case of why not to analyze your genes individually. If you look at ADCY5 alone you’d probably panic: well defined negative effects, being homozygous for the risk allele puts John in the worse possible place etc… But this isn’t borne out by his actual blood sugar numbers which are uniformly good (with the possible exception of the GSP number). But when you look at his sugar/carbohydrate-related genes as a whole you can maybe see an explanation as to why John’s blood sugars are consistently good.  This can be seen in his nutrition report where he was scored into a higher carbohydrate category. This doesn’t mean he can go nuts and binge on sugar as even the best genes in the world won’t help with that, but it does mean that he can more readily deal with a higher carbohydrate intake which gives him more flexibility in other aspects of his diet.

Ok, thanks Aaron, I am now taking back the mic for a few closing thoughts.

Closing thoughts

In my experience, keeping blood sugar top of mind is beneficial. It blunts that voice in my head which tells me its fine to tear into a pint of ice cream or a bag of cookies. Now, of course I still get into the junk food drawer on occasion, but knowing the science of how spikes in blood sugar impact my health does help me reserve my sugar intake to the occasional treat.

I also believe there is benefit in using food preparation techniques to make foods like white rice, oats and potatoes lower on the glycemic scale and therefore healthier.

As with any of the topics we touch on on the blog, the idea is not to fear glucose, but rather to learn how our bodies use it and make food choices that go with the metabolic flow, as opposed to against it.

There is a very real public health threat posed by diabetes and greater awareness of our own metabolic state, is I believe, a good thing.

John O'Connor

John O'Connor is the founder of Gene Food, host of the Gene Food Podcast and a health coach trained at Duke's Integrative Medicine Program. Read his full bio here.

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