Back from the blood glucose brink
A diagnoses of out-of-control diabetes was a shock for Stuff writer John McCrone. But is this how we can all fight back?
Whoa. Not just diabetes, but completely redlining it. Fair to say that as a slimmish, fittish, 60-ish, white male, I wasn’t expecting the diagnosis.
Perhaps skin or bowel cancer. Those would seem more my risks. Yet here I was.
My surprise was mixed with guilt and embarrassment. Somehow I had screwed up. But where exactly?
My doctor appeared lost for a ready answer. He was muttering something vague about a ‘‘decompensation’’ – a stressed body finally giving out – as he pushed a diabetes guide across his desk.
Absorb the shock, he advised. Then come back for the pills and likely the insulin pump, which could be my lifetime companion now that I had succumbed to this nasty disease.
Type 2 diabetes mellitus. A sugary rot produced by an excess of blood glucose adhering to the body’s proteins, gumming up its works in every direction.
Kidney failure, blindness, gangrenous sores, limb amputations. Possibly also the strokes, coronary artery disease, Alzheimer’s, maybe Parkinson’s, which are now all being linked to the condition.
I would be falling apart by stages for about the next 20 years – if a diabetes-prompted heart attack didn’t carry me off rather sooner.
How could it have happened? In the mirror, I had to admit to about 5kg of middle-age spread. And in particular, there was a bulge, a distension, just under the rib-line.
Better informed, I can now read that as a fatty liver. However, nothing seemed that out of control. I could still stand up straight and mostly suck my gut out of sight.
And while I had always indulged freely with cake and chocolate, I believed I was compensating with healthy food too.
Lean cuts of meat, tons of vegetables, and enough of the good carbs – the recommended ‘‘food pyramid’’ foundation of potatoes, bread, rice and pasta – on my plate.
I had also exercised hard all my life. Given the calories in/calories out principle, my feeling was I would have been burning off the worst of any excess dietary sugar along the way.
So an unlikely candidate for diabetes. However, confession time. My annual blood test had shown an HbA1c reading – the measure of your average blood glucose – that had crept up into the official pre-diabetic zone.
My last result had hit 46 millimoles per mole (mmol/mol). On the coloured ‘‘speedometer’’
chart that doctors use, this was still in the green, but paling towards a cautionary yellow.
The warning had been easy enough to shrug off. I reasoned the change looked a gradual thing. There would be plenty of time to do something about it. Check back in another year.
Yet now, barely six months later, my HbA1c had rocketed to 99 mmol – straight into the screaming red zone.
I was broken. And the clue to how bad was that the diabetes speed dial actually topped out at 100. So off the road, down the ravine, tumbling into oblivion, I had to guess.
I was looking for a better explanation than just a decompensation – something snapping. But my 10-minute appointment was over. The doctor had his ‘‘time’s up’’ face on. The essential news had been delivered.
Being a journalist and science writer – used to getting answers – I went straight home and got stuck into researching my diagnosis. Thank goodness for Google, YouTube and internet discussion forums.
Three months later I was back at the surgery for a follow-up HbA1c result. My blood glucose had dropped to 56. Down from panic stations to merely serious alarm.
Another three months and it was right down to 35. Not even prediabetic anymore. Normal range. To all intents and purposes, fixed.
I was disappointed that my doctor didn’t fall off his chair in amazement, only furrowing his brow in mild curiosity.
Conventional wisdom says there is no cure for diabetes. You just use drugs to mask the worst of its symptoms.
However, I had been lucky with my timing. With diabetes reaching epidemic proportions across the world, it looks like our medical understanding of it is also being turned on its head.
As diabetes is basically a lifestyle disease, a drastic lifestyle change can – if not fully cure it – put it into remission. Or at least that is what my own story appeared to prove.
THE LOW-CARB SWITCHEROO
What did I do? The short answer. After poring over the many contrasting opinions offered up by the internet, I arrived at the low carbohydrate/high fat (LCHF) diet. Or as some prefer to call it, the low carb and healthy fat diet.
Simply put, take away the fuel of diabetes. Get rid of all dietary sugar. Even your fruit intake needs to be limited.
And then restrict anything starchy as well. Potatoes, bread, flour, oats, rice, noodles, pasta – all the stuff which is one step away from being converted to sugar.
Even if standard dietary wisdom is that these are necessary staples, the message is starve the disease.
Yes, I found it a daunting thought too. As humans, we are our habits. I couldn’t even imagine mealtimes with these basics missing.
However, I got started. Out went marmalade and toast for breakfast, my morning routine for any number of years. In came a couple of eggs scrambled with a large knob of butter. Just that. It looked rather naked and alone on the plate.
Lunch became more eggs – usually fried with bacon or some other protein – laid on a crunchy bed of green veg and salad. At least on an LCHF diet you can still eat all the broccoli and cabbage – lowdensity carb – you could possibly want.
Dinner continued to be roasts and stir fries. Just reinvented to be without potatoes, rice or pasta.
Dessert was reduced to a single square of 90 per cent dark chocolate. Snacks were a handful of nuts or a cracker piled as high as I liked in peanut butter.
A blessing of the LCHF diet is that fat is back on the menu. It is how you fill up. And as the LCHF pundits promise, the diet is naturally satiating. So you shouldn’t end up overeating.
Sugar only turns your appetite on. After one biscuit you are always ready for another. It is an evolutionary thing.
Our hunter/gatherer ancestors were hard-wired to gorge on fruits and berries when they became available during a brief few summer weeks – a once-a-year passing treat.
But protein turns our appetite off. We know when we have had enough. So once the habit of having sugar and starch at every meal is broken – that built-in expectation – there is no particular nagging craving.
I didn’t believe it would be the case either. Yet I discovered it was true after I tried.
As well as seeing my blood sugar plummet back to safe levels, I found my waist band shrinking by whole sizes. I was having to punch new holes in my belts, cinch in my trousers, then eventually just go out and buy a new wardrobe.
Another unexpected bonus of joining the LCHF club was it appeared to put me in the middle of everything trendy.
Keto monitors, barbell training, intermittent fasting, bio-hacking, sleep tracking, even turmeric, coconut oil and apple cider vinegar. I was part of the cool crowd for a change.
Of course I was only what lowcarbers call an n=1 experiment – a single patient clinical trial. Fair warning. My experience might not be your experience.
But how could I doubt the evidence it was working? And the more I looked into the theory behind low carbs, the more it seemed to make perfect sense.
FALLING OUT OF BALANCE
YouTube was a great resource. You get to look over the shoulders of scientists as they present their latest research findings in lectures and conference sessions.
And YouTube certainly seems flooded with low-carb advocates. The likes of Professor Ben Bikman, Professor Tim Noakes, Dr Jason Fung, Dr Michael Eades, Dr Ted Naiman, and the ‘‘fat emperor’’, Ivor Cummins, stood out for me.
New Zealand has its own community, led by Professor Grant Schofield at Auckland University of Technology (AUT), along with others at his Human Potential Centre, like Dr Catherine Crofts and Dr Caryn Zinn.
Schofield helped host a Low Carb Down Under meeting in Auckland in 2014. And the pace has picked up so much that Australia ran six Low Carb Down Under events last year.
It has also been moving from the medical fringes – a subject largely for physiologists, nutritionists, sports scientists and family doctors – to the mainstream.
In 2018, the reinsurance giant Swiss Re teamed up with the
British Medical Journal to put on ‘‘Food for Thought’’ in Zurich. LCHF as an answer to diabetes is on the map.
I listened. And what I picked up about my own plight was that after years of silent abuse, I must have finally burnt out my pancreas.
That decompensation was an abrupt failure of the pancreatic beta cells which produce the body’s insulin. And it could have been a collapse 20 years in the making.
My diagnosis actually came in August 2017. I was 60 and had just returned from a trip around Europe – a holiday dedicated to scone teas and cake stops at every museum cafe. The only symptom coming home was a thirst. I couldn’t wait to gulp down glasses of Christchurch’s pure tap water. But also I was suddenly shedding weight. A kilo a week without trying.
A first hopeful thought was that it was the delayed effect of tramping hours a day around European capitals. The truth was my pancreas was shot and the insulin regulation of my blood glucose had just given out.
I was peeing out excess glucose by the bucket-load. The kilos were simply calories overflowing the kidneys and splashing their way down the toilet.
Getting back from the doctor’s, one of the other things I immediately did was invest $30 in a blood glucose monitor and test strips. I needed to know exactly what was going on.
The idea of pricking your finger for beads of blood was another psychological hurdle. But easy to brush aside. Realising why you see so many one-legged people in wheelchairs these days – it’s the diabetes, not the car crashes – served as encouragement enough.
HbA1c readings give you a three-month rolling average. With a glucose monitor, you can check what your levels are doing right at the moment, before and after each meal.
A healthy baseline number on this type of reading is between 4 and 6 mmol/l. My scores soon confirmed my red-lining status. I was tracking along all day at between 16 and 20.
Fellow diabetics I chatted with were almost impressed I had managed to achieve such catastrophic levels. The only good news was that I found out so soon after my insulin-producing collapse.
As I said, glucose does its damage by sticking to cellular tissues. That is how the HbA1c measurement itself works. It is a calculation of the percentage of your red-blood cells that have haemoglobin molecules which have become glycated.
This glycation of proteins erodes delicate structures like capillaries, nerve endings, the filtering glomeruli in your kidneys.
It also turns cholesterol particles – the body’s fat transporters – shrivelled and toxic. The body can no longer recognise the particles to recycle them, so they get lodged in the walls of your arteries, creating inflammation.
That is how diabetes becomes a cause of strokes and heart attacks too.
It does take a good few years of this syrupy marination for bits of you – your eyes, heart, feet, kidneys – to start to fall off.
But that was a disturbing thought too. Apart from a continual dry mouth, I had no particular symptoms telling me my blood sugar had got so high. I felt pretty fine overall. I had no fatigue, high blood pressure, itchy skin, or other of the signs that can be tell-tales of diabetes.
THE BODY’S HYBRID MOTOR
So what had happened inside me to bring me to my sorry pass? And why did a drastic diet change make such a rapid difference?
Following the science, I learnt the key thing is that the human body is evolved to have a twin fuel system. It is like a hybrid car – energy-efficient and fuel-flexible – designed to alternate between glucose-burning and fat-burning.
The pancreas in fact secretes two hormones – insulin and glucagon. While insulin is produced by groups of beta cells, glucagon is released by neighbouring islets of alpha cells.
When the level of one is high, the level of the other is low. That way there is binary control over which mode of metabolism is dominating at any time.
Insulin rules when the body is in energy surplus – when food is
coming in and we are busy digesting. The pancreas senses this and pumps out an insulin signal telling the body to start using the freely available glucose.
Insulin molecules actually act like a key in a cell’s door, binding to receptors on its membrane and letting blood-borne sugars flow in.
But most meals deliver more energy than we immediately require. The whole body only needs a teaspoon of circulating glucose at any moment. So insulin also acts to direct the excess into longer-term storage forms.
First, the muscles and liver are prompted to convert glucose into glycogen – the animal equivalent of plant starch. The body can hold enough of this as a local reserve to fuel itself for a few hours.
After that, the rest of the excess glucose has to be turned into fat for proper long-term storage. The liver processes it into triglyceride molecules which are taken up by our adipose tissue, our body’s fat layers.
So insulin runs the body in a glucogenic state. We are concentrated on burning or storing glucose. But then we have to flip into our other fuel mode to begin burning the fat stores we have accumulated.
In nature – back when our ancestors were living by hunting and gathering – it would have been normal to be short of food for a day or two, and often even weeks. Switching into a ketogenic state was the way we survived.
Glucagon takes over as blood glucose drops. This is a signal to the liver to start breaking down fatty acids into ketone bodies – smaller acetone-like molecules like beta-hydroxybutyrate.
Our mitochondria, the powerhouses of our cells, can accept either these ketones or glucose molecules as their fuel. So it makes for an exquisitely balanced system.
Either we are generally building up our fat stores, or else we are generally breaking them down. And as long as we spend enough time in each distinct metabolic zone, everything should be fine.
The trouble with type 2 diabetes is that we don’t. Instead, the modern diet leaves us stuck on the glucose half of the cycle and eventually this causes a collapse in our insulin regulation.
Type 2 diabetes used to be almost unknown. Now it is an epidemic. The Ministry of Health says 250,000 Kiwis suffer full-blown diabetes – double the number of 20 years ago.
A further quarter of the population is then pre-diabetic. So on their way to getting diabetes soon enough if they don’t do something about it.
Diet is the issue. Anyone of my generation will have been witness to how much the way we eat has changed.
In the 1970s, junk food and sugary snacks went from being occasional treats to standard fare. The food industry had discovered it could make addictive products from dirt-cheap ingredients.
Fructose – a variant of sugar – could be factory-produced for next to nothing by running a truckload of corn through a bath of acid and enzymes.
Likewise cheap fat – hydrogenated vegetable oil – could be
churned out by the barrel by heatcracking and solvent-treating a low-cost crop like soybean.
Two industrialised ingredients to then jazz up anything, including your ‘‘healthy’’ morning bowl of muesli, or the sweet and greasy caesar dressing swamping a takeaway salad.
But also, official dietary advice changed too. Due to medical fears about saturated fat and heart disease, the public health emphasis went on cutting back on meat and dairy. People were urged to fill up their plates with ‘‘good carbs’’ instead.
Through the 1980s and 1990s, I was hearing this message like everyone else. So my wedges of butter became guilty smears. It became automatic to reach for the leanest cut at the supermarket, while just also reducing the amount of protein altogether.
The compensation was being liberal with the carbohydrates. When it came to starch like potatoes, rice and spaghetti, or sweetness in the form of apples, bananas, melons and other fruit, any amount seemed allowed. They were nature’s bounty, packed with energy and nutrition.
Indeed if, like me, you were out running every evening, playing tennis all weekend long, then carbloading was the thing to do. The way to train.
So apart from the cakes and biscuits, I thought my own diet was pretty much a model of the going Heart Foundation guidelines. And what a laugh that turned out to be.
DISCOVERING TOFI SYNDROME
It is at this point of the story that things get properly controversial. The old colliding with the new.
Current mainstream dietary advice – even for diabetics – remains ‘‘heart-healthy’’.
A sensible diet is meant to have a balance of macronutrients where about 50 per cent of our daily calories come from carbohydrates, then some 30 per cent from fat and 20 per cent from protein.
The diabetes management booklet handed to me by my doctor toed this line. It said cut out the processed food, the sugary snacks and fatty treats, of course. Perhaps go easy on the starch and ramp up the greens. But breakfast could still be porridge, Weet-Bix, or baked beans on toast. Standard carbs.
An LCHF diet tilts the ratios the opposite way. Carbs become 20 per cent of the calories, protein 20 per cent, and fat 60 per cent.
The even more aggressive ketogenic diet – Keto to its advocates – reduces carbohydrate to 10 per cent and takes the fat level to 70 per cent.
With LCHF, you can still get in your healthy five fruit and veg a day. Starchy tubers and grains are carb dense. However, it takes an awful lot of kale, cauliflower, courgette and capsicum – the green and fibrous stuff – to reach the diet’s 20 per cent goal.
And the low-carb argument is that the modern diet is just wrong once viewed in an evolutionary light. We now eat sugar the whole year around. And starch of some kind with every meal. On top of this, we also graze continuously, snacking our way through the day.
It is a pleasant enough way of existing. But the result is we are always on the glucose side of the equation, never much on the ketone-based, fat-burning side.
This sets up an invisible war in our bodies. The beta cells of our pancreas have to be in constant overdrive to flush the excess glucose out of our bloodstream and into our glycogen and fat stores.
Yet that starts to provoke its own response of insulin resistance. Our muscles say they have already got enough. And our fat cells – even though they are designed so they can swell 8000 times in volume – eventually become full up too.
These tissues react by becoming deaf to the urgings of the pancreas. They reduce the number of insulin receptors on their membranes, making them insensitive.
This causes the pancreas only to shout even louder. Insulin levels soar as the beta cells redouble their efforts to clear the bloodstream of glucose. It becomes a vicious circle – a state called hyperinsulinemia.
But at this stage, the pancreas is still managing to force the glucose away. So your HbA1c readings might seem fairly normal. Or just a touch pre-diabetic.
The next stage comes when we hit our personal fat threshold. This is the bit that probably caught me out.
Diabetes is thought of as a disease of obesity. And while that is true, about 10 per cent of even severely obese people can remain metabolically healthy – at least in the insulin-resistance sense.
The reason is they can manufacture more fat cells. There is always more room for whatever their diets throw at them.
But other people have a strict fat limit. Once their available fat cells are filled, there are no more. And for slim body types like me – with a relatively thin layer of subcutaneous fat on the hips, trunk and back – it means maximum capacity may be reached that much more abruptly.
That does not mean the pancreas stops trying. Even when our subcutaneous fat cells are full – and now starting to burst and die, releasing their inflammatory contents – the insulin signal will continue, trying to drive fat into every other nook and cranny.
First we develop visceral fat – bloated deposits wrapped around our internal organs. Then the fat begins to invade our muscles and internal organs themselves.
We get the syndrome know as
TOFI. Thin on the outside and fat on the inside. The state I was in.
It is like hitting a hard wall as the organ fat builds. The liver clogs. And even the pancreas clogs. Then it is end game.
The beta cells cease to function. Insulin regulation of blood glucose collapses. Nothing is left to hold the sugar back.
You wind up at the doctor’s in a daze and find he is muttering something vague about a sudden metabolic decompensation.
LOSING A GRAM IN THE RIGHT PLACE
So goes the simplified version of my diabetic disaster. The full story of the body’s metabolic complexity could fill a book. I’ve read a few of those.
But the bodily mechanics explains how a dietary change can work – what you need to do. And there are in fact a number of fixes you can try.
Bariatric surgery – a gastric bypass – is one. For the seriously obese, a physical restriction on eating will cause fat levels to subside and ease the body back below its personal fat threshold.
Strict low-calorie diets can be effective as well. Losing the fat clogging the pancreas can get the beta cells going again, so long as they aren’t completely broken down.
Calorie-restriction diets appeal to the medical establishment because carbs can still remain half of the daily diet. You just eat less of everything.
But the low-carb claim is that it takes direct action. Carbs are the actual villain of the piece. Just cut them instead and get yourself into the ketogenic fat-burning zone.
It is about working with nature, working with your metabolism. Low carbers are big on other lifestyle changes like barbell exercises and high-intensity training. Kicking your body up a gear.
I already was active. But I got busy at the gym. I broke out the weights, the rowing machine, the chin-ups. I also went for long, glucose-burning walks directly after meals.
Intermittent fasting is another fashionable move. And one I liked more than I expected.
The goal is to give your insulin system as much rest as possible. And stretching out meals is as good as cutting way back on the carbs.
Now I often sleep my eight hours, skip breakfast and then have lunch around mid-afternoon, dinner thereafter. A fast of 14 hours or so. Sufficient time to shift into ketosis.
Again, it sounded like something I never could do, being apparently so addicted to food. And it was actually surprisingly easy when I tried.
BUT NO FAIRYTALE END
If you get right into low carb it can start to become cult-like. The internet is full of buff Instagrammers promoting their highly restrictive keto lifestyle.
Even with the LCHF, I only limited my diet to the degree it made sense. I would tighten my regime and check the result on my glucose monitor. Did blood sugars head in the right direction? Test and repeat until I got where I had to be.
I did start taking metformin tablets, the standard drug for type 2 diabetes. They certainly shaved a few points off my HbA1c early on. I got down to 35 mmol/mol with the help of those. Stopping saw a bounce back to 39. But that was good enough, I felt.
And as to the final outcome, it isn’t fairytale perfect. For some, their pancreas does recover after it has been unclogged. As far as I can tell, my beta cells were burnt out by being red-lined. Even shrinking every last gram of visceral fat hasn’t brought them back yet.
So I’m not actually cured. But being in remission for as long as I stick to an LCHF diet is a happy alternative. And I generally feel better in every way for doing so much about my metabolic health.
Once more, I am only another n=1 experiment. Results may vary from individual case to individual case.
However, it is worth knowing about the insidious damage too many of us are doing to ourselves through our existing eating patterns.
And that when we decide to make a radical change, it is perfectly possible to haul ourselves back from the brink.
MONDAY: What the experts say on the keto diet debate.