WTF? How Do You Explain These Lab Values?

Isn’t reality fascinating — often so different from our expectations! My lab values are back and they are actually a bit mind boggling!

My just ended diet experiment:

  • Total fat:                  – decrease by 15%
  • Net carbs:                – increase by 33% (total calories stayed the same)
  • “Bad” fat:                  – decrease by 25%
  • Omega-6:                  – decrease by 40%
  • Reduce soy:            – from twice a day to once or twice a week
  • Reduce lactose:      – eliminated by end of period
  • Eliminate wheat:   – yes, I did totally eliminate bread!

The main goal of the experiment was to bring my non-HDLc from its previous  166 mg/dl down to a number that felt a little more comfortable. My experience heretofore was that my lipid numbers generally tracked my sat fat intake as predicted according to conventional medical wisdom (see my previous post) and  so I thought I had it all well understood. My expectation was that reducing my total fat and especially my sat fat would drop my non-HDLc down somewhere below 140. And, in exchange, since I raised my carb intake, I was expecting to see my blood glucose a little higher, but hopefully still within the “normal” range.

So what did I get?

Here’s my latest lab values (last line only) displayed within the context of the previous year while I was holding my percent bodyfat relatively constant and putting on a few pounds of muscle:

Diet, LP7

So, in case all those tiny numbers just spin your head and blur your vision, what happened to my lipid numbers (dark blue column headers) is ABSOLUTELY NOTHING! They’re so close to their previous values as to be considered unchanged. As for the A1c (last column on the right), it went DOWN not up!!

For anyone who is young enough to not have to worry about blood glucose (BG) and type II diabetes, A1c (or HbA1c) is a blood test that indirectly measures how high your BG has been over the last few months; you can read more about it here. When your BG is too high, it’s bad and, in the past, it’s gone up (worse) when I eat more carbs and gone down (better) when I do more exercise. It was absolutely GREAT that the A1c went down, but how did it improve with more carbs and less exercise?

How can these numbers be explained?

The A1c is the easiest to try to explain. I think it might be related to dramatic changes in how I was sleeping during this three month experiment..

For most of my life, I’ve been afflicted with a daily cycle closer to 26 hours than 24. Left to my own preferences, in the long run, each night I’ll go to sleep a little later and each day wake up a little later, eventually turning night into day. And when I can’t sleep to my preference, I get what the sleep pathologists call “sleep latency”, which is just another name for insomnia. To add to my sleep misery, during menopause, I began waking up every night with hot flashes. This version of insomnia did not resolve after the hot flashes were over, and continued up until just about three months ago when I started this experiment…

So what could it have been in my new diet that helped me sleep? Well, the extra carbs might have helped. At my previous carb intake (about 90g / day), I was keeping my glycogen stores really low — low enough to go hypoglycemic during hard or long exercise if I didn’t eat carbs beforehand. … And perhaps low enough to interfere with good sleep (??) – I’m not alone in this; google “low carb insomnia”:

Diet, LP6

But that can’t explain the whole story; I haven’t been low carb all my life – far from it! So let’s look at what else I did. I haven’t mentioned the last four items in the intervention list (reducing/removing w-6, soy, lactose, wheat). This part of the experiment was to try out bringing my diet more into line with standard Paleo to see if I could feel any greater health or wellness. The most obvious change was a huge reduction in overnight mucus. Amazing how much better one can sleep when not drowning in sinus secretion!

But even though I’ve been eating high carb most of my life and still sleeping poorly, I still can’t let go of the idea that the additional carbs had something to do with the sleep improvement. ‘Cause these last few months, I’ve been hitting the sack and just sleeping. No sleep latency. Just falling asleep like a normal person. I can attribute the staying asleep to better air flow, but not the falling asleep. Maybe there are two factors at work here: increased exercise plus enough carbs to avoid blood sugar problems on the low side? That is, the increased exercise would have produced better sleep all along, but keeping my carbs down was interfering. At any rate, the bottom line, for whatever reason, is that during these three months of the experiment, I have actually slept better than at anytime for the last almost 50 years.

Q: So, what does sleep have to do with blood sugar (BG)?

A: It’s vital! If you wake up hungry and go eat something every night, your BG never gets that overnight dip. From PubMed study, 2011, “poor sleep quality affects glycemic control, as assessed by HbA1c level” [2]

Well, enough about the mysteries of blood sugar; on to the lipid panel. The lipid numbers are harder to explain. Possibilities that come to mind (in order of decreasing likelihood) are:

  1. Despite the prevailing medical wisdom, on an individual basis, dietary sat fat is actually so loosely correlated with LDLc in many people that the connection is virtually undetectable. I may be one of these people.
  2. Some other factor (such as less exercise, higher carb intake, gaining weight, …) raised my LDLc during the period and thus masked the drop.
  3. Standard lab error
  4. The amount of sat fat in my heavily used fat sources is misrepresented by the USDA nutrition tables.

For the time being, I will dismiss the last two as unlikely to account for the magnitude of the difference. So, if the answer is item #2 in the list, a repeat of the experiment might have that random factor drop out or even go the other way. If the answer is #1, then the outrageously high lab numbers from a year ago (Jan 2012, total cholesterol = 328!!) are *** completely unexplained ***. I would have to fall back on blaming them on the result of hypoglycemic induced low thyroid activity [3],[4] (I will probably discuss this in a later blog). But the good news is I could declare my non-HDLc as non-amenable to dietary modulation, pop a statin and go back to eating more sat fat (YUMM!).

My thought at the moment is, the prudent experiment would be to raise my carbs even a little further (safe since my A1c is at a good place), drop my fat intake a little more and cut sat fat to the bare minimum to see if I can budge that recalcitrant non-HDLc.

So be it; let the next experiment begin.

References:

  1.  HbA1c explained
  2.  Association between Insomnia Symptoms and Hemoglobin A1c Level
  3. Could Thyroid Disease Lead To High Cholesterol?  “When the thyroid slows down (hypothyroidism), it also slows down the body’s ability to process cholesterol. This processing lag is largely explained by a reduction in the number and activity of what are known as LDL receptors. LDL receptors help remove bad cholesterol from the body; when the number of receptors decreases, LDL accumulates in the bloodstream, acting to increase both LDL and total cholesterol levels.”
  4. High Cholesterol — “The connection between hypothyroidism and cholesterol is simple: Without enough thyroid hormone, metabolism slows, making it harder for the body to metabolize cholesterol. As a result, the cholesterol lingers in the blood, where it can cause plaque buildup in the blood vessels. According to the AACE, the average cholesterol level for people with an underactive thyroid is 250 mg/dL, which is much higher than what is considered healthy, which is below 200 mg/dL.”
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About Dan Hunter

Retired software engineer wading through the obfuscation, confusion and contradiction that corporate and political funding of medical research along with ego over science has created.
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