Metabolic Syndrome XX



Starting Protocol may be a good way to begin to reverse insulin resistance and regain muscle cell insulin sensitivity, but in the most stubborn cases, especially with the insulin resistant variant of PCOS I call Metabolic Syndrome XX (because men can get it too, besides being the genetic carriers) sometimes that’s not enough. As someone with Metabolic Syndrome XX, I had good reason to do exhaustive research and testing on how to ameliorate it. Unlike regular Metabolic Syndrome X, which is characterized by low HDL, high Triglycerides, high fasting insulin and blood pressure readings and obesity, MSXX sufferers have excellent HDL and Triglycerides, and perfectly normal fasting insulin and blood pressure. About the only thing they have in common with Metabolic Syndrome is excess belly fat, which is why it is almost never diagnosed by regular doctors. They’re looking in all the wrong places. As you will also see, following either Paleo and Atkins diets can sometimes be a disaster for folks with MSXX.

People with MSXX have great insulin levels, but that insulin is bone lazy and insufficiently active to handle normal glucose consumption. A dead giveaway to this condition is having 2-hr PP’s consistently higher than 1-hr PP’s – when it should be in reverse. That’s because insulin activity fails after an initial leap. The second condition of MSXX is generally high Cortisol and runaway Gluconeogenesis. Gluco = glucose. Neo = new. Genesis = birth.

Gluconeogenesis is an evolutionary species survival adaptation and usually benign. It allows our bodies to create glucose from the protein we eat, when we have consumed insufficient carbohydrates for our brain’s needs. This was great for our hunter/gatherer forebears, and works today for Peoples who still eat their traditional very low carb diets, like the Inuit. Since humans are not nocturnal animals, it allows our brains to get the glucose it needs at night, when we do not normally consume food.

In folks with MSXX however, gluconeogenesis often takes place without need, and continues long past fulfilling our brain’s requirements. This is often accompanied by persistently high cortisol at night, which keeps you up or wakes you in the middle of the night, and then suppresses insulin, which raises blood sugars. Think of that as MSXX’s Triple Whammy. You don’t eat sugar but make it anyway from your protein, your cortisol lowers your already lazy insulin, and your lazy insulin, unable to handle even normal glucose intake efficiently – now has even more glucose to handle!

You can see how this is a recipe for getting fat and staying there, despite changes in diet. And why any diet that emphasizes lots of protein and very little or no carbohydrate will not work for these people, or at least not for long. Which tends be (but is not always) women, who often write on Paleo or Atkins blogs that although the diet/s worked for them for a brief while, progress has stalled. Occasionally for years. Replies sometimes cruelly insist the OP must be “doing it wrong” but that is not the case. The problem is MSXX.

Wait, it gets worse. Because gluconeogenesis involves the liver, which needs ample supplies of ferritin (storage, as opposed to serum iron), runaway gluconeogenesis plays a role in Thyroid Hormone Resistance – a particular form of Hypothyroidism. Folks with MSXX tend to have extremely low ferritin levels, and they are the very ones who have trouble taking Cytomel, an excellent hormone treatment for THR, without raising their blood sugars sky-high. Every medical study on this issue concludes that ingested thyroid hormones raise blood sugars, and that diabetics should consult doctors before taking any, but none of them investigated why this should be so.

I have. Just as Cortisol suppresses insulin, thus raising blood sugars, so too do thyroid hormones suppress insulin. When I tried to take Cytomel to raise my T3 and lower my high Reverse T3, my fasting blood sugar, normally 89-93, rose to 105 within five days. I stopped taking the hormone, but increased my research. A blood test showed my ferritin level to be 11 – the sub-basement. Thyroid blogs indicated that ferritin levels needed to be between 70-90 in order to take thyroid hormones effectively, but none of them said why. It took me a while, but I finally figured it out. Just as improperly folded leptin pools in the bloodstream and never reaches the brain with its ‘fat messages’ — so too ingested thyroid hormones must pool in the bloodstream (where it suppress insulin, thus raising blood sugars) because there isn’t enough ferritin to let it reach the liver.

What I know about medical research is that researchers don’t generally look at the big picture of anything, but tend to think in silos. Straight up and down one narrow area. My hypothesis was that whenever they tested thyroid hormones on women and came up with increased blood sugars, they never bothered to test ferritin levels first. What if I could raise my ferritin level — thereby providing my liver what needs to create T3 despite MSXX and lazy insulin — and then take Cytomel? Would that allow my liver to finally utilize it, so that it wouldn’t pool in my blood and lower insulin/raise blood sugars?

In order to test this hypothesis I first needed to find something that would specifically raise ferritin levels (as opposed to regular iron supplements, that tend to raise iron serum). I already ate liver on a regular basis, and my low ferritin levels said that wasn’t enough. What I needed was some kind of super food. It took a while, eventually I found one. Molasses. As you can read by clicking the link, this food has everything a metabolically challenged person would need to help with insulin and thyroid hormone resistance. On paper, anyway.

To put it to the test, I first needed to find a concentrated form that wouldn’t require downing tablespoons of black strap syrup a day. Luckily, some excellent Molasses powders are now available. You can get already made capsules (with regular iron that often causes constipation), or as I prefer, the pure NGO powder itself (without fillers) that with the use of a capsule machine let you make a thousand capsules for a fraction of the price.

1. Empty Capsules.

2. Molasses Powder, small. Molasses Powder, large.

3. Capsule Machine by itself. Capsule with empty vegetarian (not gelatin) capsules. I use only vegetarian capsules because they never ‘melt’ or get bent out of shape in summer’s high humidity. I can make two dozen 00 size caps in about five minutes with this.

4. Capsule Refills. Since the machine lets me buy all sorts of supplements in bulk and make my own caps for a far lower cost, I use it for a lot of things. I even buy fermented cod liver oil in the bottle (cheaper than the caps) and fill my caps with that, too. They never leak. If you need vegetarian capsule refills, I recommend these 00 caps, and not NOW Foods, since they appear to be made a fraction too small to get the cap tops on easily. I’ve tried several batches, and no go.


Long story short – it did! I took two molasses caps daily with water first thing every morning for three months, and then had my ferritin tested. It was 75. So yes, molasses powder did raise my ferritin. But . . .  would increased ferritin prove my original hypothesis, that my liver would now be able to absorb Cytomel, instead of having it pool in my bloodstream where it suppressed insulin and raised blood sugars?

I took the Cytomel, using the regime I’ve created to raise body temps to normal, increase T3 and lower reverse T3. After a week, my fasting glucose remained steady. After two weeks my body temps began to rise, but I noticed something strange. My fasting glucose had dipped a bit. After two months I had ‘captured’ a normal average temperature of 98.6 – but – my average daily fasting glucose had lowered to 79-83, a full ten points lower than I’d ever managed, even with Protocol. I discontinued the Cytomel, no longer needing it, but have continued to take the Molasses powder daily. And my fasting glucose has remained rock solid. So my initial hypothesis – that raising ferritin would allow absorption of T3 without raising blood sugars, thus disproving every medical study on this issue – was correct. And my hypothesis that molasses would raise ferritin levels was also correct.

But it led to a greater mystery. Why did molasses lower my fasting glucose by a statistically significant amount? I’ve been taking molasses for well over a year, and during that time I tried to disprove this by stopping the powder for a few weeks, during which my fasting glucose slowly rose to its previous levels. When I took it again, my FBG dropped again. I did this several times just to make sure. The results were always the same. Clearly, there was cause and effect

Then I wondered – was molasses actually doing a bad thing by raising insulin levels, which would lower my fasting sugars, but not in a good way? For the last several years my fasting insulin level had been 4, which is true normal (though not as excellent as < 2). I went for an insulin test and the results stunned me: < 2. Which means that the molasses powder had actually made my insulin more, not less, efficient. Which is what lowered my FBG!

I immediately recruited a few Protocol Participants to try this. They had the same results: higher ferritin, increased insulin efficiency, and lowered fasting blood sugars. What great news for them, and for everyone with MSXX.

The problem was, and this is why I have not written about this here until now – I didn’t know WHY molasses was doing this. What property did it possess, aside from the ability to raise ferritin, that would increase insulin efficiency? It took my discovering some older research (now gaining new medical and research prominence) on another substance altogether to let me put in the final piece of the puzzle.


A member of the Vitamin B family, inositol is a key intracellular signaling molecule responsible for, among other things, optimal cellular glucose regulation by modulating insulin sensitivity. And a deficiency of which is related to the pathology of both insulin resistance and hyperlipidemia and PCOS, to name a few. Just those three items alone should set off light bulbs in the heads of anyone reading this. It certainly did in mine.

The research above was fascinating, a sort of reverse of the serum leptin craze that Big Pharma went through when leptin was first discovered in 1994, and found to be missing in enormously obese people. But as Big Pharma found out, what those folks (often upwards of 400 pounds) were actually missing was the enzyme that allowed fat cells to make leptin. Which is why, only after they spent millions of dollars on trials to inject leptin into merely fat people, they discovered that the injections were useless. Fat people have more leptin in their bloodstreams than slim people, not less. Any reader of my blog knows why: insulin resistance interferes with the ability of the ‘chaperone’ protein, the endoplasmic reticulum, to help leptin fold into the correct three-dimensional shape to cross the blood-brain barrier and reach the hypothalamus. The leptin pools in the blood instead, thus making the brain believe its body is skinny and starving.

But with inositol, it’s the opposite. Slim people with healthy metabolisms (fat burning, not fat storage machines) retain their inositol, which helps fat burn. People with excess adipose fat eliminate inositol via their urine, losing a vital piece of the fat burning machinery. This was shown by the research, which administered glucose load tests to normal weight and obese people. But instead of using the test in the regular way – checking on rising blood sugar levels – they checked inositol levels in the urine of the test subjects. And sure enough, normal weight people retained their inositol; overweight people eliminated almost all of it. Not a good thing.

Although a long analysis of inositol’s molecular structure and cellular makeup and interaction within the body is beyond the scope of this thread, there’s a lot more information here. What interested me was – could oral supplementation of inositol override the biological loss, just as oral T3 supplementation bypasses the T4 to T3 or Reverse T3 conversion? And if so, what form of inositol would work? There are several forms of inositol, but aside from plain inositol, the main three are: d-pintol, myo-inositol and DCI (d-chiro inositol). Some are more readily converted and utilized in the body. DCI is the most expensive (by far!) and ostensibly used for fat loss, myo-inositol is touted as best for fertility problems caused by PCOS.

Which brings us back to molasses. Because – surprise – molasses is loaded with inositol! Could this be the reason molasses not only raised my ferritin level but made my insulin more efficient while lowering my blood sugars? If so, would consuming straight inositol in addition to molasses help to burn additional adipose fat? I’ve been on Lifetime Maintenance for a long time, but although my weight and clothing size has been very stable, my waist was still a few inches larger than I would like. Since there’s nothing special about the stuff in molasses, I decided to do a trial with plain, inexpensive inositol.

When it came I put half a teaspoon in water and stirred. It totally dissolved and was tasteless. There was a very slightly sweet taste in the back of my mouth when done (it, like many forms of Vitamin B is essentially a sugar, though a very helpful kind), but even that disappeared if I used a bit more water. Would it spike my blood sugars? I took it either an hour before eating or at least two hours after eating, because it must be converted to be used by the body, and it competes with glucose for the same conversion enzymes. The problem is, glucose is fast, and inositol is slow. It is my (unproven) contention that this is why insulin resistant, overly fat people pee it out: if it goes unconverted because glucose (of which there is normally a lot in insulin resistant folks) got to the conversion enzyme first, the body probably has no further use for it and simply eliminates it. Upcoming inositol research may well show this to the be the case.

Two weeks after I began taking a single double-dose (half a teaspoon vs. one-quarter teaspoon on the label, though that says “two to three times a day) before bed, I made the following observations: my blood sugars remained stable, I lost another four pounds that has remained off, and a full two inches off my waist, which has also remained off. I continue to take a single dose of inositol every other night or so. I confess, I don’t always remember. 🙂 Though I do remember to take my molasses caps every morning.

But n=1 isn’t enough to recommend it to you. I turned to my son, who at six-foot tall and weighing 148, should have been seen as skinny, but was not. He had a belly, and it was fat, though every other part of him was thin. VERY thin. He was a TOFI – a new medical classification: Thin Outside, Fat Inside. Given his height, weight and waist size: 36 inches, his body fat percent classified him as overweight/obese. He had PCOS. That’s right, PCOS, right down to his 2-hr PP being higher than his 1-hr PP. It was that realization that sent me back to research, where I learned that the insulin resistant variant (which I’m sure you can understand my renaming to Metabolic Syndrome XX) has a genetic component, that men are the primary carriers, that they pass it down primarily to women — but that they can get it themselves. And my Protocol had not been sufficient to fix his, even though he’s lived sugar-free and high fat for years. In fact, nothing worked, not even weight training, though of course I knew that for folks with MSXX, exercise only leads to high cortisol, runaway gluconeogenesis and high blood sugars.

I put him on the same dose of inositol, for one month. At the end of that month, the following was true: he weighed 142 pounds (where he has stayed for several months now, despite continuing the inositol, which confirms my theory that fixing a problem stabilizes you at healthy levels) — and his waist was now 31 inches. He went down two pant sizes, and could actually pull his old pants over his new ones; there was plenty of room. He had to buy new belts, too, since he went past the last hole.

I asked a few former (now healthy) Protocol Participants to try it. The result was the same: a last few stubborn pounds and waist inches disappeared.

And I figured it was time to tell you all about it. 🙂


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4 Responses to Metabolic Syndrome XX

  1. Laurie says:

    Great article, SugarFree. Lots of information to absorb!

  2. Shani says:

    Wow – there’s so much work and detail in this, SugarFree. Very interesting; it keeps us learning!

  3. K. L. says:

    Good stuff, SugarFree – I feel so lucky I found you! I can’t wait to get started.


    • SugarFree says:

      Kristie, I’m glad you found the thread, and suspect a few ‘light bulbs’ went off for you. 🙂 I’m looking forward to your becoming a Participant in Protocol!


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