Sugar Sugar Baby, Get On Down the Line, Part 2

Now where were we? Ah yes. We were talking about insulin. Let’s talk more about insulin. A lot more. Because if we don’t, you might come away with the idea that there’s something more important to talk about. There isn’t. Not Brexit. Not Trump. Not Climate Change. It’s not Kevin we need to talk about: it’s insulin. Again.

The Elastic Band Snaps

So, as we touched upon in part one, our bodies are complex federations of systems that need to work in perfect harmony if we want to enjoy fun stuff like staying healthy and reproducing. If we occasionally stretch one of these systems to the limit – or even beyond – then, fortunately, it usually bounces back. Our bodies are mercifully patient at correcting problems and reverting to homeostasis.

Nice word, homeostasis: those of us with systems good at course-correcting tend to cope with the occasional blow-out, with pushing ourselves a bit too hard, with getting a bit stressed, drinking a bit much, missing a night’s sleep, and yet recovering pretty quickly. Others aren’t so lucky, and one little stretch too far of the metabolic elastic band snaps it; and then, everything falls apart. And I do mean everything: we stop apportioning energy properly, so we get fat, and feel hungry even when we should be full. Our reproductive cycles cease or go mad (hello PCOS!). Our cellular corrective systems start to play up, and cancers get a foothold.

Nobody’s happy with a snapped metabolic rubber-band, but it’s a state so many of us do find ourselves in when we suffer from the so-called diseases of civilisation. And, surprisingly often, one thing underlies this snapped rubber band.

Insulin: Use and Abuse

One surefire way that even the best of us can smash our homeostatic elasticity is to abuse our insulin signalling system. As I discussed last time, insulin is an ancient hormone, a kind of master-switch between our store-and-build vs spend-and-expend modes. Evolutionarily, it seems that our bodies expect insulin to operate via quick, occasional pulses. Just enough to course-correct for any particular change in energy circumstance, but not so much that it leaves the body sloshing about in the stuff.

Think of your pancreas like a perfume dispenser – a tasteful little quirt of Eau du Insulin every once in a while, and everything’s fine. Store. Burn. Replenish. Store. Burn. The circle of life, an intricate concerto with insulin the subtle conductor. That’s the way things are supposed to work, and it’s the way they do work for generally healthy worms, wallabies or people. And I do mean worms. Some of the most fascinating data on this came from a brilliant researcher named Cynthia Kenyon, who noticed that the less saturated with insulin were her worms, the slower they aged and the longer they tended to live. And guess what: it’s the same with humans. The one thing that unifies centenarians is their low circulating insulin.

Pancreatic Stench

Though worms and people behave strangely similarly in this metabolic regard, let’s assume for a moment you’re a person. What happens if, instead of occasionally spritzing a bit of insulin into your system, you regularly demand your pancreas keep its insulin pump flowing pretty constantly?

Let’s think about perfume. What would happen if instead of spraying yourself once or twice a day with a nice fragrance, you of-a-morning realise you haven’t showered and are a bit whiffy. Instead of washing, you simply open the perfume bottle and pour its contents all over your head. And then you do it again, an hour later, with another bottle of perfume – just to be sure you “cover up” the shame of your unwashed state as the day progresses. What should have been just an agent of subtle fragrance becomes, via misuse as an emergency hygiene regimen, the conduit of a horrible stench itself!

If you’re lucky, olfactory fatigue will kick in and you’ll stop smelling it. But the slick of perfume will still be there, that stinking, overbearing bottleful, and you’ll be reeking of it, whether you realise it or not. And maybe your inability to smell it any longer won’t be such a blessing after all, because you’ll keep dousing yourself with yet more of the stuff, assuming that the smell has worn off, when really it’s just your nose’s receptor cells giving up in disgust.

Worse, the perfume’s strong essential oils will probably be burning your scalp in their unprecedented concentration. So, instead of treating the perfume as the expensive and subtle enhancement to your life, you’ll be rueing the consequence of treating it instead as if it were a weird body-wash.

And that perfume-dousing outside is pretty much how “civilised” people treat insulin inside.

Riding Insulin River to Disease Dam

We’ve already discussed in part one the problems that happen because of the constant “storage mode” that insulin’s presence keeps turned on. But that actually understates the problem. You see, having your body constantly marinated in insulin is a problem all on its own. Insulin’s pretty “corrosive” stuff, so to speak. We force our pancreas to produce ever-more of it to deal with the dietary gluts of glucose that our cells increasingly refuse to deal with. This leads to having ever more insulin in circulation. And that insulin, swilling about, becomes a problem in its own right. Instead of treating the hormone as that precious spritz of metabolic perfume, we’re sloshing ourselves in it. And it burns.

We term this constant gush of insulin a state of “hyperinsulinaemia”, which literally means “too much insulin in the blood”. Its twin, “hyperglycaemia”, means “too much glucose in the blood”. Just as having too much glucose in the blood is, effectively, corrosive, so is having too much insulin. One beckons the other, and neither is a guest we wish overstay its welcome. It’s insulin Peter robbing to pay sugary Paul: if your cells are insulin resistant, and you have lots of glucose molecules waiting in line to leave the bloodstream, and you have lots of insulin hysterically banging on the cell doors to let those sugar molecules in, you have two corrosive problems, not just one. It’s no better to have lots of insulin in the blood than it is to have lots of glucose. And if you happen to have both most of the time – known as Type 2 diabetes – then Lord help you.

This is why people who smugly conclude that the way to deal with diabetes, or PCOS, or any other related disease, is “to lose weight” have got it quite the wrong way round. Putting on weight is a symptom of hyperinsulinaemia: your body starts crazily sequestering energy in its fat cells. Getting PCOS is a symptom of hyperinsulinaemia too: the hyperinsulinaemia completely dysregulates the delicate hormonal clockwork that drives fertility. Obesity and PCOS: they’re both symptoms of the same underlying dysfunction.  Some silly doctors say “you need to lose weight to cure your PCOS”. Balderdash! You need to solve the problem that gave you both PCOS and deranged fat storage.

There’s another very quick way of realising how silly it is to blame the disease on obesity, rather than the other way round. There’s a rare genetic disorder where people cannot lay down any body fat. They’re utterly emaciated, no matter what they eat. And, guess what – they all have diabetes! These people have nowhere to buffer the glucose but some muscle cells, and so most of that sugar stays in the blood, no matter what insulin has to say about the matter. So not only is obesity not a primary cause of problems, it actually acts as a safety buffer for many years against some of the truly terrible problems of the underlying disease: hyperinsulinaemia. Eventually, even your fat cells give up, become diseased and add to the problem. But they certainly didn’t start the fire!

Cure the hyperinsulinemia, and you let the body regulate its cycles and its processes once again, whether that cycle is related to fertility, or that process is in allowing the body access to its energy stores.

“Losing weight” cures almost nothing. Find the root cause of the weight-gain in the first place and target that! And thus also, perhaps, regain fertility. And put diabetes into remission. And help to prevent Alzheimer’s (type 3 diabetes, as some now call it). And radically lessen the likelihood of many cancers (especially breast cancer). And.. And.. And…

A Doctor a Day Makes the Diabetes Stay

It might surprise you to know how few doctors actually understand that too much circulating insulin is itself a problem. So if you understand it by this stage, pat yourself on the back. Go on. Do it. I’ll wait.

Even experienced clinicians and researchers often get it upside down. Perhaps it’s because much funding and training comes from the drugs-companies that sell bags of profitable exogenous insulin. These corporations ensure that few “stakeholders” join the dots from “cure” to “scourge”: there’s a reason why the ancient Greeks had the same word for antidote and poison – Pharmakon! Of course, all doctors know the acute problem of an insulin overdose. But distressingly few understand the chronic problem of too much insulin.

One thing even forgetful or well-schmoozed doctors know is that their diabetics need to bring down their blood glucose. They train such patients to “cover” the floury-baps they eat by injecting a concomitant amount of the aforementioned profitably-sold insulin. Hey, if the pancreas is going crazy, producing insulin at its absolute factory limit, and the stubbornly piggy cells still refuse to let the Big Bad Sugary Wolf in – well, the best course of action is to huff and puff and inject some more insulin to blow the doors down, wouldn’t you say? Well, you might not now say so, but most doctors and dietitians do. After all, the alternative might be something truly horrific, like having to forgo Special K. Or questioning a drug-rep and his generous dinner offer. Cynical, moi?

So doctors prescribe expensively-produced insulin in a syringe for when the ocean of endogenous pancreas-delivered insulin is still not enough to blow open the cell doors. Or, if the patient is a Type 1 diabetic, then their pancreas is effectively caput, and can’t produce any insulin at all.

The more insulin you inject, though, the more you stoke the insulin vs cells arms race. Doctors have to make their patients inject more and more insulin over time to get their blood glucose to drop below a certain level. This sad state of affairs is called “well controlled” diabetes, by the way. And doctors term diabetes itself a “progressive” disease, because despite the treatments, it gets progressively worse. Of course, you now might be coming to the hideous realisation that it’s not despite the treatment that the disease worsens so predictably, but because of it!

So “progress” the disease does, with the “treatment” pushing its foot down hard on the accelerator. Even with blood glucose “well controlled”, the illness continues, with heart problems, impotence, kidney failure, amputations, blindness, cancers, dementia and heart attacks following with depressing predictability. The doc doesn’t realise that the very treatment – the injection of yet more insulin – solves the short term glucose glut by exacerbating the long term corrosive crisis of hyperinsulinaemia.

So yes, I’ve been banging on about insulin for a while now, but it’s important. No, it’s even more important than that: it’s IMPORTANT. Indeed, I am convinced that the major key to healthful longevity is to treat insulin as a precious, pulsile resource, not as an inexhaustible lake of glucose scouring-agent! Our addiction to hyperinsulinaemia – either via pancreas or injection – is a very big problem. Again, most of the major diseases of civilisation: diabetes, heart disease, cancer, fertility problems, dementia and alzheimer’s, depression and other mental illnesses, inflammatory illnesses and more, have the abuse of insulin at their causal nexus.

Sweet Measurements, Bitter Ignorance

So how diabetics get treated is bad enough. But a horrifying and horrifyingly-increasing number of us suffer from this insulin dysregulation and hyperinsulinaemia without even knowing it. You see, one way that doctors determine whether you’re diabetic is by getting you to take an Oral Glucose Tolerance Test (OGTT). In this test, they ask you to gulp down some sickly glucose solution. They then take several blood tests over the next hour or two to see how quickly that glucose clears from your blood. If the glucose shoots up high and takes its time to come down then alarm bells ring, rightly, in your doc’s head, especially if the glucose level actually dips significantly below baseline before it bobs up again. But if the blood glucose level doesn’t seem to spike that high, and the sugar clears away nice and quickly, without too much of an under-dip, your doctor will assume you’re good to go, and nowhere near diabetic.

But if you’ve been following the story carefully, you’ll already have an inkling your doctor could well be wrong to be so blithe! You now know that he or she is missing half the story, because he or she only usually measures glucose in your blood after that sugary drink, but does not measure insulin!

It’s all very well being pleased at how nicely your bloodstream seems to dispose itself of glucose after a “happy” OGTT, but this ignores a very important question: what exactly did the pancreas need to do to get you that “lovely” glucose clearance? If all it had to do was give you a quick spritz of insulin, then yes, everything is probably fine. But what if it effectively had to open up the sluice-gates and gush your body with a torrent of insulin from hell in order to get you that same glucose clearance? The spritz would be calm metabolic normality. The gush would be a hysterical metabolic system at the end of its endocrine tether, sluicing rivers of corrosive hormone into every artery and vein.

So what did you get as a result of your OGTT? The spritz or the gush? You don’t know. Your doctor doesn’t know. Worse, he or she probably doesn’t realise that it’s something he or she should know! But you now do. It’s clear now, I hope, that if you want to know how metabolically dysregulated you are, you might think it’d make sense not only to measure how your blood glucose changed after downing a glass of Lucozade, but also to keep an eye on what your blood insulin was doing to get it there! And you would be right – it would make sense. The problem is, most doctors don’t seem to realise this, bizarrely, and are happy to give patients whose pancreases are screaming into the void a clean bill of metabolic health, just because their glucose-clearance curve looked pretty. They ignore the manic pancreatic wizard behind the curtain, having a nervous breakdown to make enough insulin to counter the body’s cells resistant to its storage demands! They ignore it, because they don’t think to peek behind that curtain. But one doctor did. His name was Dr Joseph Kraft. 

Kraft’swork

Dr Kraft, an American pathologist, tested over 14 thousand of his patients from the 1970s to the 1990s. Unlike most doctors, he didn’t just make them glug down a Lucozade and then test their blood-glucose. Instead, he also measured their blood-insulin periodically over 5 hours. As you will now understand, this allowed him to get the true, unvarnished metabolic truth, usually hidden from doctors who choose only to measure half the story. With that many patients, Dr Kraft also began to understand a clear pattern that was emerging from his data.

As with Goldilocks and the three bears, Dr Kraft noticed that a few lucky patients’ bodies were able to spritz a little insulin, and have the glucose nicely dispose of itself: “just right”. These people clearly had working metabolisms, and remained healthy in the years and decades that they remained his patients.

Sadly, the more frequent tale was one of dysfunction. Dr Kraft’s more unfortunate patients had gushed out torrents of insulin to deal with the same amount of glucose that had demanded a mere spritz in the lucky Goldilocks patient; or sometimes, blood glucose clearance responded sluggishly to even the strong insulin signal. Or, conversely, some pancreases seemed weirdly sluggish themselves in getting into gear to respond to the glucose hit at all. The curtain had truly been lifted, and the nasty truth revealed.

Dr Kraft plotted glucose and insulin over time on a graph for each patient. After a while, he noticed that those with “non-Goldilocks” patterns almost invariably returned some years later with full-blown diabetes. Or heart disease. Heart disease was the big one. So big, in fact, that Dr Kraft began to ponder whether pretty much all heart patients are effectively diabetic, even if they don’t realise it!

A normal doctor would never have had the opportunity to see these warning signs decades before the trouble became apparent. Dr Kraft did have that opportunity, though, because he had been uniquely thoughtful enough to run the tests others didn’t. He summarised the different shapes of graphs he got, and noticed they fell into five general patterns. And of those five patterns, only one actually represented unambiguously good news. A troubling proportion of the rest of his patients, without knowing it, were sliding down to metabolic Hades, along the slope of one of Kraft’s four “danger” graphs, whose curves slalomed each patient to an eventual metabolic crash.

When other doctors would have sent their patients away with a full bill of health, Dr Kraft’s four graphs of doom gave him a crystal-ball premonition of his patients’ unhappy futures. After being right several thousand times, anecdotes legitimately transformed into data: he came to the inescapable conclusion that a huge number of people suffered from what he termed “diabetes in situ”, where the pancreas was already quietly at war with the body’s other cells; years, or even decades, before a final diagnosis of diabetes or one of its partner maladies.

Of course, you already knew about Dr Kraft, because he won the Nobel Prize for Medicine, and single-handedly changed the way we diagnose and treat the diseases of civilisation! That’s why the modern OGTT doesn’t just measure glucose, it measures insulin. Nah, only joking. It doesn’t. And he didn’t win anything. Science, sadly, doesn’t always work like that, thanks to a coagulation of profitably vested interests and blind groupthink. Dr Kraft did, at least, write a book about his amazing data, which few have read.

Joseph Kraft died recently in his 90s, and that would have been that. Fortunately, one online researcher, Ivor Cummins, discovered the Kraft treasure trove before it slipped completely into the mists of time, and brought it to public attention. Ivor even managed to interview Dr Kraft before he died, saving this unsung genius’s work from the tragic obscurity that otherwise would have been its likely fate. And now, happily, some PhD students have taken Dr Kraft’s data for crunching and publication, so they might yet have some of the impact they deserve.

How to Keep Insulin Special

Anyway, it’s all very well talking about this in theory: what about in practice? Well, firstly, you shouldn’t conclude that insulin is “evil”. It’s vital. Without it, we’d die. Ask a Type 1 diabetic how well they do when their pancreases cannot make any of the stuff. The take-home, then, should not be that insulin is evil, but that what we now demand of poor old insulin is evil. Don’t blame the bull for being in the China Shop. Blame whoever shoved him in and locked the door.

How can we properly respect the insulin we make, and limit the amount of insulin we must use? We want less of it sloshing about in our blood. Excess causes not only the obesity that remaining in eternal “storage” mode entails, but it inflames and upsets our bodies.  We’re pouring that bottle of concentrated perfume over our head. How do we put a stopper on the perfume bottle? Or, how do we make sure we stay on Dr Kraft’s happy slope, and not slip off piste onto one of his four deadly hills?

You can do a number of things to limit the amount of insulin your body needs to produce, and also to make sure that your body wrings the last drop of value from the insulin it does produce. You should find some of the prescriptions very familiar: make sure you get enough sleep (those who do not tend to become hyperinsulinaemic), do some exercise (exertion helps your body to use the insulin it has more efficiently), try to find ways effectively to manage your stress (responding badly to stress causes a cascade of hormones that can lead to chronic insulinaemia).

You can also limit your use of insulin by starving yourself, if you want. By eating less, you prod the pancreas less. This is actually how most calorie-restricted diets work (no, it’s not simple calories-in, calories-out!), and also why they stop working the moment you end them. You celebrate the end of your diet with a Krispy Kreme, the insulin pump turns back on and, what do you know, all the problems associated with hyperinsulinaemia flow right back in with the renewed gush of insulin!

So yes, the biggest elephant in the hyperinsulinaemic room is the one we put into our mouths. And, sadly, that elephant is often baked of flour and sugar. Simply put, no macronutrient other than carbs places so much rapid-response demand on your insulin systems. And whether you eat simple sugars, or “complex carbs” (which become simple sugars in minutes after hitting your gut, whatever propaganda you might have heard to the contrary), mainlining glucose can cause all sorts of problems.

Furthermore, whilst the other popular sugar, fructose, doesn’t itself require insulin for its metabolism, it does gum up the insulin machinery, so to speak, forcing your body to produce ever more of the stuff to compensate the next time you eat glucose – or something that turns into glucose, like a potato, some rice or a ciabatta. If you eat table sugar, which is a fructose molecule bonded to a glucose molecule, you get a double-whammy: the trouble-maker and the trouble in one fell swoop!

It seems simple, then. Stop eating so much stuff that demands insulin’s intervention: digestible carbs, in other words. Now, could you keep yourself off the Kraft danger-slopes whilst nevertheless eating a high carb diet? Yes, possibly. Some societies seem to cope with traditionally higher-carb diets. But they always come with certain important provisos which the modern supermarket milieu cannot replicate. Just because some group of tropical islanders seem to cope with guzzling tubers doesn’t mean you’ll thrive on doughnuts. And, once those doughnuts have done the early and rapid damage to your metabolism that Kraft identified, you may find no route back to that idyllic tropical island of happy tuber munching.

There are other dietary problems too. Big ones. I’m pointing at you, “vegetable oil”. Those “healthy” seed oils were promoted as a good alternative to saturated fat. You know, the lurid yellow bottles of rancid-tasting swill you have in your kitchen which replaced the delicious lard, ghee or beef-dripping your granny would have used. Well, these abominable oils are full of unstable “omega 6” fats. Whilst we need a small amount of omega 6 fats in our diet, it turns out  that when you treat them as a staple, they are highly implicated in insulin dysregulation too, among much else. Oh dear. One despairs whether recent nutritional science got anything right!

So, if you want to avoid a tumble down the Kraft cliff-of-doom, or at least slide yourself onto the safe slope from your present perilous perch, you can’t rely on getting most of your energy from vegetable oils, and certainly not carbs. So if don’t get your energy from margarined bagels, rice, wraps or “whole grain” cereal bars, then where do you get your energy from?

Hmm. What energy macronutrient happens not to require insulin for the majority of its processing and storage? Fat! Dietary fat. Not omega-6 fat, of course. We’ve already encountered some of its problems. But monounsaturated fat, like that in olive oil. And.. saturated fat, as in meat, eggs and butter.

Saturated fat! The very devil!

“But saturated fat clogs your arteries and gives your heart disease! You’ve thrown me from the hyperinsulinaemic fire into the greasy heart-attack frying pan! And also, if I don’t eat carbs, I don’t get glucose, and my cells need glucose for fuel! My brain will die if it doesn’t get carbs! And I hear I will go into this devilish mode called “ketosis” which will turn me into an ill, fuming dragon! You murderer!”

Wait! All is not what it seems. Tune in next time to to find out why the meme of ArteryCloggingSaturatedFat(™) turns out to have been a big, fat lie. Learn about our amazing onboard glucose factory. Marvel at the miracle of cholesterol. And weep at what 50 years of dietary pseudoscience has done to our species.

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5 Comments

  1. Paul says:

    An excellent read as always from Nick. I would enjoy a more technical blog post but would settle for him haranguing John on rum doings.

    As a T1 diabetic I can attest to the double edge sword that is insulin and that navigating NHS advice/doctors around the subject is a minefield at best. You are forced into subtly reducing your carb intake and upping your fat with out triggering their poorly tuned cholesterol measures. Or more likely, upsetting your dietitian who will be utterly convinced that <150g of carbs a day is a starvation diet regardless of your calorie total.

  2. […] Check out Nick’s latest guest-post on hyperinsulinemia for https://baby.botherer.org called Sugar Sugar Baby, Get On Down The Line, Part 2 […]

  3. Now I know what I’ll be passing round to people when asked about the 101 of insulin

  4. Slipp Digby says:

    “Dr Kraft plotted glucose and insulin over time on a graph for each patient. After a while, he noticed that those with “non-Goldilocks” patterns almost invariably returned some years later with full-blown diabetes. Or heart disease”

    “After being right several thousand times, anecdotes legitimately transformed into data”

    Is there a citation which supports these claim regarding the long term predictive value of Kraft tests?

    Because in Krafts book ‘The Diabetes Epidemic & You’ only the OGTT and insulin assays are presented, there is no follow up of any kind, nor outcome data cited.

    Also, Catherine Crofts who did the Phd on the Kraft database and who has examined it has confirmed Krafts work was cross sectional only and there was no follow up of the patients at all (see https://youtu.be/pCtwgAAuyBE?t=708).

  5. Dale says:

    Excellent post Nick. Thank you, Thank you!

    I appreciate the simplicity. Now,I can add more layers of detail to understand these metabolic pathways more fully. Further, I can refer others to this post for a basic understanding of this process. And finally, your explanation is evocative, I could see you creating an animated video detailing this process with you as narrator.