In the scheme of things, I’m probably a non-compliant, uncooperative patient.

Having recently moved to another state, I now have the arduous task of convincing doctors that I’m not always going to be compliant, particularly when it comes to filling a bunch of scripts for medicines I know I’m not going to take, and running eagerly to a bunch of new specialists, just because I have diabetes.

I’m not altogether unconvinced that drug companies shouldn’t be non-profits, formed for the good of the patient, and that their research money should come from elsewhere. I am thoroughly convinced that profits push the whole industry way too far, and that we take many drugs that often do more harm than good. We sometimes forget that we do have choices.

Putting aside those drugs that actually cure, much of what is pushed at us is band-aid therapy at best – some stick, some don’t. Most that I have tried, well, it’s like ‘the cure is worse than the disease’.

Take, for example the drug that is supposed to protect the kidneys of people with diabetes – ACE Inhibitors. I tried several, all with varying, very unwanted side effects.

Around the same time, I spent about two years being constantly dizzy. Went from one doctor to the other and the best I got was that my Meniers disease had returned. Needless to say I don’t think had it in the first place, but thats another story. The dizziness, however was driving me crazy!

One fine day, I ran out of the ACE inhibitor. It took me a few days to get another script, and a small country pharmacist had to order it in. And then something unexpected happened. I noticed I wasn’t dizzy anymore! Could it be? Could it possibly be?

After some research I discovered that it was very probable the dizziness was from the ACE inhibitor. Now why couldn’t all those doctors have told me that? Probably the same reason i’ve been misdiagnosed with a bunch of diseases countless times, most notably with the wrong kind of diabetes. Nit an uncommon story.

I filled that script and threw it in the bin when I got home. I haven’t had any dizziness since! That was about 18 months ago! Try Ace inhibitors again? Hell no!

Statins do my head in. With the super-high cholesterol I’ve had since I was a teen, I probably should have been long dead by now, if you can believe the hype.I refuse to take them, having been through the gamut of what’s available here and suffering through the muscle aches and raised CPK. Now the new doctors want to start that trip all over again! Hell no!

So, just last week, I was having a hard time convincing my family doctor that I don’t need to see a podiatrist. Saw one a couple of years ago. I’ve never had much of anything wrong with my feet other than a tiny bit of neuropathy in two toes, most of which has now resolved.

So the last one I saw started lecturing me about why I shouldn’t go barefooted and how I could be doing myself great harm, like I’d been living under a rock for the last 30 years with diabetes and I hadn’t heard this before! Groan!

So my doctor was saying that the podiatrist would remove some minor callousing on my heel. Um, why would I want to do that? I am convinced that it protects my feet – objects have a much harder time getting through thickened skin than baby-soft feet! I’m the original Princess and the Pea. If there’s a grain of sand on my foot, I’ll know! I do a proper, regular pedicure and have comfortable shoes and sandals. Yes I’ve had broken toes – once with shoes, once without. Clumsiness more than anything. Take a scalpel to my heels? Hell no!

Do I really have to get to know and love going to see someone who actually chose a career in feet? Eeeew! Hell no!

Anyway, I’m having a hard time with new doctors and all the specialists I’m supposed to see. I have much of the paperwork and I can’t tell you how unmotivated I am to pick up the phone and make appointments because I know what’s ahead – lots of telling my story over and over again, and explaining why I’m not going to go where I’ve been before.

As this year goes, it’s been a pretty horrid one, culminating in an even more extremely blah birthday.

Yes, I had some calls from my wonderful friends who’ve been around me for 20 and 30 years. It’s always a delight that they remember. Most of them are 10 hours drive away. If I could afford to fly them all up and we could go out and do daft birthday things.

It was my 50th when we were all last together. A riot of a party with a Middle Eastern theme and I did a beached-whale-belly-dance in full (but modest) costume! It was more than fun and fabulous. It all went a bit downhill from there. I miss them but I know I could never live back in Sydney. Too busy, to crazy, too everything for me.

Of my other close friends, 1 died early this year and 3 more are overseas with only 1 returning later this week, 1 over there for a few years and 1 coming to visit for 3 months, but nowhere near me.

Birthdays have morphed into days that I take stock. The more psychologically challenging stock-taking is still being mulled over.

Of the more mundane stuff…  What fashion item, shoes or makeup do I now need to throw in the bin because it has ‘mutton dressed as lamb’ written all over it? When do I have to get my hair cut short because I’m over 50? When do I have to go to bed at 10pm, have an afternoon nap, and have a fibre-filled breakfast?

When will I accept that the wrinkles and sags are here to stay and that I’ll probably never fit into the kind of fabulous clothing my 21 year old daughter wears, let alone look ok in it? (Oh, how shallow! Right?)

As I write this, I’m channel surfing and happened to land on the Fashion Channel. It always makes me want to throw up or cry. Wow those girls look fantastic! I was probably never that reed-thin or that gorgeous, but 20 years and more ago, I could certainly wear almost anything out of my mother’s clothing boutiques and get away with it.

Now count me in with weight-gaining insulin, post menopausal pounds and a penchant for good food and you get beached-whale – almost. Not quite in the BMI obese category but hovering and at times, falling in.

These days, I can’t wear heels (sore feet and lack of balance), and designer clothing is made in one size either way of reed-thin and often priced out of my league, so that’s out too. In fact, this past week, I’ve been hobbling around with a fractured toe on my left foot (the middle one), wondering why I still don’t have a car with automatic transmission (because they’re always $2,000 more than I can afford) or special shoes for broken toes.

But there was one good thing amongst a few others today – cake!

I was going to makeanother Persian Love Cake, but yesterday, time got away from me. Here’s the one I made last year for my husband’s birthday.

Theoretically, if you have insulin, you can eat whatever you want. On the other hand, theoretically, if you have diabetes, if you keep the carbs down, you can control the diabetes much more easily and blood glucose spikes can be reduced. Both theories are true. I like a combination of the two.

If your diabetes is out of control, lower the carb intake to start with. It goes a long way to help the control.

On birthdays, all that flies out the window.

I have cake-eating with insulin-taking down to a fine art. And while a store-brought piece of cake doesn’t come with carb instructions, I’m pretty good a guestimating after the first bite.

So, tonight my fancy was taken by what was labelled as a Jaffa Chocolate Cake. Yes indeed – carbs multiplied by carbs!

The first bite was heaven. I could taste the dark chocolate, orange and the surprise of coconut. It was unexpectedly moist, with a measurable layer of thick chocolate ganache on top.  As cakes go, this one took the cake!

With an insulin pump, if you get the carb-guestimate right, it’s so much easier than trying to manage a fat-laden (read: long-absorbing), high carb slice of heaven with injections, although certainly it can be done.

A combo bolus over 2.5 hours did it. At 4 hours post ingestion, I was a tad high at 9.0 mmo/l (162 mg/dl), but all things considered and without an exact carb amount per slice, I think I did ok. A quick correction bolus and I was done.

Maybe it wasn’t such a bad birthday after all! Did the cake make up for the absence of close friends? Um.. I think the right answer is ‘no’, but my honest answer is… kinda… yeah it did, for a few scrumptious chewing and tasting minutes!

Eating a Mediterranean diet rich in fish, olive oil, legumes, fruit and vegetables may strengthen the heart but the cost strains the wallet and may deter healthy eating, according to Spanish researchers.

They’re not kidding! While a healthy Mediterranean diet has more carbs than a low-carb diet, try doing low-carb on a tight budget!

Don’t you love how doctors with six-figure incomes can sit there and pontificate about what we should and should not be eating. They haven’t a clue or any advice about how some people are going to afford to do so.

Consider a loaf of bread, often the whiter the cheaper, at say $2.50. Add to that some cheap toppings. The bread and the toppings most likely can last several days for lunches. So say $7 for all that. I’m dealing in Australian dollars, but would equally apply anywhere.

Consider a large bowl of salad. The lettuce alone would be $2-$3. The whole salad could easily cost $15-$20. Lettuce, tomatoes, cucumber, avocado, parsley, witlof, bell peppers, pea sprouts and more. No root vegetables. Or I could make a high-carb potato salad for a few dollars.

Add to that meat, chicken or fish, and you’ve got a very expensive meal. Multiply that for other meals in a week and you’ve got a healthy diet that is definitely too expensive.

If you’re on a pension or are a low-wage earner, trying to feed a family, it’s totally impossible.

Instead, it’s fine for governments and medical insurers to fork out millions in trying to fix the problem instead of being proactive and preventing it in the first place. Not sure what the answer is, but food production somehow needs to be subsidised. It’s getting far too expensive to eat well.

Not to worry, we can atone for our eating sins (amongst others) at Yom Kippur, just 10 days later, with a 24 hour fast.

It’s also no secret, however, that I’m a bit of an atheist, despite my background, my involvement with my local Jewish community (on the board), and my very sentimental tie to my cultural if not religious heritage.

Rosh Hashanah is traditionally accompanied by lots of sweet food, so you’ll have a sweet year. That’s the theory, or close to it. It’s nice to have an apple dipped in honey, and challah (bread, sweet at this time of year), also dipped in honey, and carrots drowning in honey, or kugel with a double dose of sugar and honey.

Almost everything you eat on Rosh Hashanah is ether dipped in or drowned in something sweet. Just a bit of overkill. Seriously folks, did the Rabbis not ever consider people with diabetes? It’s all just not the same with Splenda!

My mouth waters just thinking of the food that will be laid out tonight in a community event for Rosh Hashanah, that expects around 150 people. I had a hand in preparing some of it today and will continue tomorrow afternoon. Not sure my aching legs can take any more but there’s no way I’m not going back to that kitchen!

Oh what a hypocrit I must be – a Jewish Athiest who cooks for and partakes in traditional Jewish Holiday meals? You know what? I don’t care! Call me names but I love it all! I love the craziness around this time. I love seeing people I might not have seen all year. I love the spirit of community and the happy flavour (excuse the pun) of the holiday. I especially love it when the Israelis all start to sing, much to the delight of the rest of us who are too shy to get into such merriment.

Weighing up options is a fact of life with diabetes. I can let my BLGs go to hell in a handbasket, (insulin pump or not – there’s no way I can account for every last carb) or I can sit there like Miss Goody-Two-Shoes and pick a piece of dry chicken and some nutrient-free lettuce and maybe a tomato.

Maybe I don’t have to do all-or-nothing. Maybe I can have it all, in very tiny portions?  My carb-load will probably still go to blazes but it’ll be slightly easier to manage. Missing out totally is a very poor alternative.

What would you do?

Entering your BGL during the day, and then entering BGL with the grams of carbs you’re about to eat, will allow the pump to accurately suggest how much insulin it should give. It’s done on an incredibly complicated algorithm and it also knows how much bolus insulin you still have active at the time. This is called Insulin on Board (IOB). It figures this amount into the insulin-suggestion calculation.

On some pumps, you can just accept the suggested amount. On the Animas 2020, you have to enter the amount yourself. I rather like this idea because the pump has no idea what I’m going to do next – exercise, sleep, eat more, suspend the pump after the bolus and many more possibilities. I can then give less or more according to my needs over the next 3 hours.

The pump can be set to remind you to test your BGL. I have mine set to remind me every two hours after entering my BGL, which I test several times a day. After any entry, the reminder comes on screen for you to confirm it or change the reminder time – 1 hour, 2 hours and so on. When I sleep, I set the reminder to zero hours, so it doesn’t do the reminder alarm and wake me.

Because of what the pump records and the reports it produces, I have not yet needed to record anything manually.

Once a week, I upload the data from the pump to my computer via an infra-red cable. I produce the reports as PDF documents that I email to my medical team. They can then see trends, averages, total insulin and more, and perhaps suggest  adjustments.

The sample report below is just one of a number of reports available. It’s the one most people with diabetes will recognise – it’s very similar to a handwritten log. Yes, it’s my log for last week, with reasonably OK numbers (only reason I’m sharing).

Looking at the report, I see if any adjustments need to be made to any of the pump settings. Of course I’d probably look at a week or more of data, not just a couple of days.

Last week, I made a huge effort to keep my carbs fairly low, lower than my usual under 120 grams per day. It certainly paid off for me.

You’ll see the following:

The time of day across the top. Each day has 3 lots of data: BGL, Grams of Carbohydrates Eaten, Insulin Bolus.

At the far right, you’ll see the average BGL for the day, the total carbs for the day and the total insulin bolus for the day.

At the bottom of the report, the last 3 rows are the averages for the time of day, and the averages for the week on the right.

Note that the BGL measurements are in mmol/L, the standard in Australia. To convert to the USA standard, multiply by 18, or see the chart at the end.

There’s another report hat shows all the BGL testing data. You might test more than once an hour, eg if you’re low, or after a site change. The log book only has BGL value in any given hour – the average of all tests done in that hour. You can’t see in the chart below how many times I might have tested for any one BGL shown.

I’d love it if my HbA1C would be done on just the four days showing! Now, wouldn’t that be nice! Almost everyone I know in the diabetes world, has highs and lows. The days shown aren’t typical for me. I’m still having a problem going high between 11pm and 1am. I’m slowly tweaking the pump to take care of this. It’s not easy because I tend to go low in the early hours of the morning. I don’t want that to happen while I’m sleeping, so any insulin I have between 11pm and 1am will still be active 2-3 hours later.

I wanted to share because it was something I wanted to know and see before I decided which insulin pump to get. As you may have already read, I totally love my pump and I’m extremely happy with the choice I made.

This chart shows HbA1c and what your average BGL would be in both mmol/L and mg/dl. It’s such a handy chart, I use it all the time!

I thought I knew a lot until I started the preparation for going on an insulin pump earlier this year. Since then, I can’t tell you how much more my poor brain has been filled with extra information. Every week it seems I learn something new. Whether it’s about managing the disease, research, reading other people’s experiences, it’s still learning.

My averages had been creeping up over the last couple of weeks. I can put it down to a number of things including another kilo on my already overweight frame (I still manage to just scrape in to the ‘overweight’ category with Body Mass Index (BMI)).

We had visitors and were eating out a lot, in places where whatever was on my plate was sometimes difficult to carb-guess. And the kicker was the extra exercise. Like some, I’m not textbook when it comes to exercise. I don’t do enough of it (knee needing replacement) so I go high during exercise – contrary to text book advice – and have to bolus more. More bolus = more insulin = more weight for me. Going high during all the walking we did meant extra insulin.

So, whatever the reason or combination of reasons for my averages going up, I felt I had to break the cycle. Three days last week, I did very-low-carb. This week, I’m doing lower-carb. It’s done the trick. Don’t take this as advice – it’s just my experience.

Under no circumstances did I want to increase my TDD of insulin, which would put on more weight. What I did, worked nicely for me. I’m back to carb-watch-eating and my numbers are way better. In the process, I also shed a couple of pounds, for which I’m very grateful. The extra weight seems to be super-glued to me, and getting it off is a battle.

In passing, my endo, a few weeks ago, told me not to worry about the extra weight, considering how well I’ve done since I went on an insulin pump. I didn’t think much of it at the time. My thoughts were of fashion and vanity.

In a twist of fate, I subsequently read about some latest studies which suggest that BMIs under 18 and over 30 are associated with a greater risk of death. What was apparently surprising to the researchers was that the overweight category BMI: 25 to 30, was NOT associated with any significant greater risk. And the most surprising was that the underweight category BMI <18, was.

We all thought that calorie restriction was the way to go. Apparently not. From what I’m reading, going into the twilight years with a little extra padding, isn’t all that bad. What is vitally important, is your fitness. If you are normal weight and not fit, you do worse than someone overweight and fit.

If you have the time, watch the video below. It outlines some of the latest research.

Obesity: Ten Things You Thought You Knew

So maybe my endo had seen these same studies.

That still doesn’t let me off the hook as far as off-the-hook fashion goes. And yeah, I’m not all that fit. I hope to change that.

While I haven’t lately had anyone tell me anything that irked me, I see it and hear it all the time.

Please folks, if you don’t have diabetes yourself, unless you’re a medical person (and they are sometimes wrong too),  don’t presume you know anything about how to manage anyone’s diabetes!

Just a few tidbits… if you have diabetes, as you know, this list can get a mile long. Here are just a few that come to mind.

• Because I’m a few pounds overweight (thank you insulin), don’t presume I have Type 2. I don’t.
• Because something worked for someone else, don’t presume it’ll work for me… and above all, stop shoving it down my throat.
• Don’t tell me that if I don’t look after myself, I’ll die. That’s the first thing we learn. Then it’s OUR choice.
• Please stop being the food police!!! I have insulin. Theoretically, I can eat whatever I want as long as I can manage it effectively with insulin. (Doesn’t mean I do or I can.)
• If I look like I’m not motivated to manage my diabetes effectively, motivate me gently, suggest a counselor who can help, or just plain hold your tongue! You probably have no idea why I’m not motivated.
• Don’t talk to me about low-carb, high-carb, low-fat or whatever other combination of foods you think aren’t good. Studies have shown that both a low-carb/high protein/high fat, or high-carb/low fat diet/low protein (in whatever combination you want) are equally effective for losing weight. If you can manage your diabetes well on high carb, then that’s your choice. If you manage on low-carb, that’s your choice too. If you manage on a mix of both, fine too.

I can’t stress this enough, EVERYONE IS DIFFERENT in terms of their management of diabetes and what works for them, and what they’re willing to do. If just one thing worked, everyone would be on the same diet, with the same amount of insulin/pills, taken at the same time of day, via the same method. Nice try, but no cigar!

If everyone was motivated the same way, there’d be no issue – everyone would have perfect A1Cs, right? Even then, diabetes doesn’t always behave the way it’s expected to all the time. Just doesn’t happen unless you’re a total creature of habit (eating the same thing every day, same exercise, same everything, stable hormones, no illnesses and so on)! Even then everyone gets curve-balls at one time or another!

What I want to stress above all else is that it’s people’s personal choice about how they manage their diabetes, whether you think it’s right or not.

If you find someone who’s not motivated, then try gently once or twice, then LEAVE THEM ALONE, and don’t judge. Support them in other ways. It’s not your place to be judge and jury for anyone else’s life.

Even if you think you know better, please don’t lecture – more often than not, it’s more unproductive than helpful.

Been saying the same thing it for years!!

Whether you’re Type 1 or Type 2 or anything in between, if you can’t keep your blood glucose within your target range most of the time, try cutting the carbs!

On lower carbs, diabetes is so much easier to control – on insulin and even more so, without insulin!

If you are on any medications for diabetes, please check with your doctor before embarking on any change of diet.

Primal Coconut Pancakes and Waffles (link to original, including video, which shows you how)
2 eggs
1/2c or 56g almond meal
1c or 68g shredded coconut, unsweetened, unsulphured
1 can or 400mL/g Coconut Milk
1/2t sea salt
1/2t baking powder
1/2t or 1g cinnamon (to taste)
vanilla, optional (to taste)

Nutritional Info
Servings Per Recipe: 8 (divide by 8 to get nutritional info for 1 pancake)

Amount Per Serving
Calories: 209.4
Total Fat: 19.7 g
Cholesterol: 46.8 mg
Sodium: 141.4 mg
Total Carbs: 6.1 g
Dietary Fiber: 2.2 g
Protein: 3.6 g

I knew some of the theory, but this explains it in detail.

Considering the process of Type 2 Diabetes starts long before it becomes obvious medically, it might be why two people can have exactly the same diet and the one prone to Type 2 Diabetes will be the only one piling on the weight, long before they are diagnosed. You also have to have the genes for Type 2, otherwise every overweight, obese and morbidly obese person would have diabetes. Not all do, in fact, go look at the statistics.

It’s yet another reason I think much of the medical community has it backwards – being overweight DOES NOT cause diabetes. Being overweight is the result of the disease process – you pile on the weight, often well before you are diagnosed.

In Type 1, you don’t produce insulin. End of story. But many people find that taking insulin puts on weight.

Below is an excerpt from an interview by Norman Swan, who chairs the Health Report on Australia’s ABC. The guest is Dr Robert Lustig, Professor of Pediatric Endocrinology at the University of California, San Francisco.

Dr Lustig, also a researcher, “claims that the reason for the obesity epidemic is more than just the calories we eat and the lack of exercise. It’s a substance that food manufacturers are widely using.”

They are, of course, talking about high-fructose corn syrup. But the discussion focuses on fructose in general.

The part of the discussion that I’ve reproduced here, also highlights why exercise is important and why staying away from fructose is also important. Yes, fructose, as in fruit, although eating fruit isn’t that bad because you’re eating fibre with it. If you have diabetes, and you really want to eat fruit, please eat fruit with a protein (eg a piece of cheese), which will slow down the absorption and not give you such a big BG spike. If you can’t control your blood glucose levels well, think about not eating so much fruit along with reducing your carb intake to under 100 grams a day. It works for me. Try it to see if it works for you!

As an observation, fruit will make my blood sugar go sky high, even with my usual insulin to carb dose ratio. Clearly, for me, fruit is in a category of its own. I might as well be taking the equivalent in spoons of sugar or honey with some lettuce as fibre.

Yes, fruit is yummy, but I find I just can’t eat it without all the problems of managing high blood sugars, even if I eat it with a protein. I rarely eat fruit for this reason. Easy in winter but not so easy in summer with cherries, mangoes, nectarines, peaches and apricots – summer fruits that are amongst my favourites.

Now if you think you can eat sugar and not fructose, think again. Sugar is half fructose (or thereabouts).

Can you burn off that Big Mac? Find out why exercise is important for reasons other than burning calories, and why it’s really important if you are overweight – even slightly.

Why are the Japanese, who eat so much high carb white rice, not fat? For the answer, read on.

The science is there – we just have to pay attention.

The original transcript can be found here. My apologies if I’ve infringed any copyright. The material presented here is the property of the ABC, and I reproduce it here for the purposes of my subject matter and with a link to the original.

It might be worth reading the full interview. This is the last part of the interview, but the most relevant to my interest.

The obesity epidemic – July 9, 2007

Continued….

Robert Lustig: Exactly, in fact exercise is the best treatment. The question is why does exercise work in obesity? Because it burns calories? That’s ridiculous. Twenty minutes of jogging is one chocolate chip cookie, I mean you can’t do it. One Big Mac requires three hours of vigorous exercise to work that off, that’s not the reason that exercise is important, exercise is important for three reasons exclusive of the fact that it burns calories.

The first is it increases skeletal muscle insulin sensitivity, in other words it makes your muscle more insulin sensitive, therefore your pancreas can make less, therefore your levels can drop, therefore there’s less insulin in your blood to shunt sugar to fat. That’s probably the main reason that exercise is important and I’m totally for it.

The second reason that exercise is important is because it’s the single best treatment to get your cortisol down. Cortisol is your stress hormone, it’s the hormone that goes up when you are mega-stressed, it’s the hormone that basically causes visceral fat deposition which is the bad fat and it has been tied to the metabolic syndrome. So by getting your cortisol down you’re actually reducing the amount of fat deposited and it also reduces food intake. People think that somehow exercise increases food intake, it does not, it reduces food intake.

And then the third reason that exercise is important, which is somewhat not well known, but I’m trying to evaluate this at the present time, is that it actually helps detoxify the sugar fructose. Fructose actually is a hepato-toxin; now fructose is fruit sugar but we were never designed to take in so much fructose. Our consumption of fructose has gone from less than half a pound per year in 1970 to 56 pounds per year in 2003.

Norman Swan: It’s the dominant sugar in these so-called sugar free jams for example that you buy, these sort of natural fruit jams.

Robert Lustig: Right, originally it was used because since it’s not regulated by insulin it was thought to be the perfect sugar for diabetics and so it got introduced as that. Then of course high fructose corn syrup came on the market after it was invented in Japan in 1966, and started finding its way into American foods in 1975. In 1980 the soft drink companies started introducing it into soft drinks and you can actually trace the prevalence of childhood obesity, and the rise, to 1980 when this change was made.

Norman Swan: What is it about this, it’s got more calories than ordinary sugar weight for weight hasn’t it?

Robert Lustig: No, actually it’s not the calories that are different it’s the fact that the only organ in your body that can take up fructose is your liver. Glucose, the standard sugar, can be taken up by every organ in the body, only 20% of glucose load ends up at your liver. So let’s take 120 calories of glucose, that’s two slices of white bread as an example, only 24 of those 120 calories will be metabolised by the liver, the rest of it will be metabolised by your muscles, by your brain, by your kidneys, by your heart etc. directly with no interference. Now let’s take 120 calories of orange juice. Same 120 calories but now 60 of those calories are going to be fructose because fructose is half of sucrose and sucrose is what’s in orange juice. So it’s going to be all the fructose, that’s 60 calories, plus 20% of the glucose, so that’s another 12 out of 60 — so in other words 72 out of the 120 calories will hit the liver, three times the substrate as when it was just glucose alone.

That bolus of extra substrate to your liver does some very bad things to it.

Norman Swan: Dr Robert Lustig who’s Professor of Pediatric Endocrinology at the University of California, San Francisco. And you’re listening to a Health Report special here on ABC Radio National on how food manufacturers by adding fructose to our foods, either from corn syrup as in the United States or added sucrose as in Australia, may actually be making the obesity epidemic even worse, starting with damage to our liver cells, the hepatocytes.

Robert Lustig: The first thing it does is it increases the phosphate depletion of the hepatocyte which ultimately causes an increase in uric acid. Uric acid is an inhibitor of nitric oxide, nitric oxide is your naturally occurring blood pressure lowerer. And so fructose is famous for causing hypertension.

Norman Swan: High blood pressure. And what you’re saying here is that the liver cell itself gets depleted of this phosphate and then you’ve got this downstream reaction.

Robert Lustig: That’s right. And so when you have excess uric acid you’re going to end up with increased blood pressure and we actually have data from the NHANES study in America, the National Health and Nutritional Examination Survey in America which actually shows that the most obese hypertensive kids are making more uric acid and have an increased percentage of their calories coming from fructose.

Norman Swan: Are they getting gout as well?

Robert Lustig: Well not yet. They will.

Norman Swan: So what you’re saying in fact is that whilst we are clearly eating too much, we’re passively eating too much of the wrong thing, that the food manufacturing industry is putting stuff in which is fuelling the epidemic?

Robert Lustig: Absolutely, we’re being poisoned to death, that’s a very strong statement but I think we can back it up with very clear scientific evidence.

Norman Swan: There’s clear scientific evidence on this fructose pathway in the liver?

Robert Lustig: There’s clear scientific evidence on the fructose doing three things that are particularly bad in the liver. The first is this uric acid pathway that I just mentioned, the second is that fructose initiates what’s known as de novo lipogenesis.

Norman Swan: Which is fat production.

Robert Lustig: Excess fat production and so VLDL, very low density lipoproteins end up being manufactured when you consume this large bolus of fructose in a way that glucose does not, and so that leads to dyslipidaemia.

Norman Swan: And that’s the bad form of cholesterol.

Robert Lustig: That’s correct. And then the last thing that fructose does in the liver is it initiates an enzyme called Junk one, and Junk one has been shown by investigators at Harvard Medical School basically is the inflammation pathway and when you initiate Junk one what happens is that your insulin receptor in your liver stops working. It’s phosphorylated in a way that basically inactivates it, serum phosphorylation it’s called and when your insulin receptor doesn’t work in your liver that means your insulin levels all over your body have to rise. And when that happens basically you’re going to interfere with normal brain metabolism of the insulin signal which is part of this leptin phenomenon I mentioned before. It’s also going to increase the amount of insulin at the adipocyte storing more energy. And you put all of this together and basically you’ve got a feed forward system of increased insulin, increased liver fat, liver deposition of fat, increased inflammation — you end up with non-alcoholic fatty liver disease. You end up with your inability to see your leptin and so you consume more fructose and you’ve now got a viscious cycle out of control.

In fact fructose, because of the way it’s metabolised, is actually damaging your liver the same way alcohol is. In fact it’s the exact same pathway, in fact fructose is alcohol without the buzz.

Norman Swan: So this is the obesity related fatty liver disease that people talk about?

Robert Lustig: Exactly.

Norman Swan: Some people say, I’ve heard obesity experts say, well it’s surprising that will all the ready availability of food that we’re not fatter. In other words that we are actually controlling our appetite pretty well given that we’ve probably been evolutionary designed to eat anything that goes, and there’s anything that goes all around us, so why aren’t we actually fatter? It’s not so much why is there an obesity epidemic, why isn’t is worse, is what people say and therefore you don’t need to postulate fructose, it’s just the fact that we’ve evolved in the Savannah to eat in times of plenty.

Robert Lustig: I’ve heard those same concerns you know, why, if we have so many calories why aren’t we fatter. Well there are a few reasons why that might be. I do want to mention that the American food industry produces 3,900 calories per capita per day. We can only eat 1,800 calories per capita per day. In other words the American food industry makes double the amount of food that we can actually use. Who eats the rest? We do, through this mechanism, they actually know that by putting fructose into the foods that we eat, for instance pretzels — why do you need fructose in pretzels, why do we need fructose in hamburger buns?

Norman Swan: Are you postulating here a fructose conspiracy, the way the tobacco industry had a nicotine conspiracy?

Robert Lustig: Well I can’t call it a conspiracy per se. I certainly know, and they certainly know that they sell more of it when they add the fructose to it. That’s why it’s in there, otherwise why would it be in there? Do they know that this is actually harmful? That’s what I don’t know. There’s no smoking gun, ultimately we found the smoking gun for smoking, you know we found the documents. I’m not prepared to say that about the food companies. I do not know that they know that they are hurting us. However, they definitely know they sell more, and it temporarily coincides with the advent of fructose being added to our diet.

Norman Swan: And of course you could argue that it’s going up because they are responding to the market and they’ve got sugar-free, fat-free etc. etc.

Robert Lustig: Well in fact fat-free doesn’t help, if anything as the fat content of our foods has gone down, and it has gone down, it’s gone from 40% to 30%, in fact our obesity prevalence has gone way up. So that’s not the answer.

Norman Swan: This is because they’re adding carbohydrates and sugars to it to replace the fat.

Robert Lustig: Absolutely, in fact fat does not raise your insulin but certainly sugar does. And fructose has been bandied about…because after all it doesn’t raise your insulin directly because there’s no fructose receptor on your beta cell in your pancreas. So people say well it doesn’t raise your insulin, but in fact it does because it’s a chronic effect not an acute effect. This has nothing to do with one fructose meal, this has to do with a year’s worth of fructose meals, or a lifetime’s worth of fructose meals, because as you become insulin resistant, which fructose clearly does and has been shown by many investigators not just me — that interferes with that leptin signal which causes you to eat more.

Norman Swan: Insulin-resistance increases your insulin levels because your pancreas pumps out more to get the insulin working.

Robert Lustig: Exactly, especially since your liver is not responding to it because of that effect on the serum phosphorylation of the insulin receptor. So that’s going to cause you to make a whole lot more insulin, that’s going to interfere with your leptin, that’s going to make you eat more so the whole thing just keeps going out of control.

Norman Swan: One way of proving this would be to put you on a fructose free diet, has anybody done that?

Robert Lustig: Well no one’s done it yet. In fact we’re trying to do that, in fact we’re actually going to be working with the Atkins Foundation here in America to actually do a fructose withdrawal experiment to try to actually answer that question directly.

Norman Swan: Well given that you’re not going to come to harm by reducing the fructose in your diet — somebody who’s listening to this — what’s the ingredient on the packet, or the jar, or the back of the tin that tells you there’s fructose in there because it won’t always say fructose will it?

Robert Lustig: Well high fructose corn syrup, it should say that, now in Australia for instance the sodas don’t have high fructose corn syrup they have sucrose. Well sucrose is half fructose. You know a lot has been made over this high fructose corn syrup being particularly evil. In fact high fructose corn syrup is either 42% or 55% fructose, the rest is glucose. Well sucrose is 50% fructose the rest is glucose. In fact high fructose corn syrup and sucrose are equally problematic.

Norman Swan: Basically table sugar.

Robert Lustig: Table sugar — that’s right. We were not designed to eat all of this sugar, we’re supposed to be eating our carbohydrate, particularly our fructose, with high fibre. Well the fact is we have 100 pound bags of sugar that go into the cakes, and the donuts.

Norman Swan: So we don’t need to get obsessed on fruit sugars, it’s sugar itself, sucrose.

Robert Lustig: Absolutely, it’s sugar in general. So people say oh does that mean I can’t eat fruit? No, let’s take an orange — an orange has 20 calories, 10 of which are fructose and has high fibre. A glass of orange juice has 120 calories, it takes 6 oranges to make that glass of orange juice and there’s no fibre. You tell me which is better for you, so by all means eat the fruit, just don’t drink the juice. Juice is part of the problem and there’s plenty of data, not just mine. Miles Faith had an article in Pediatrics, December 2006 showing that in toddlers, in inner city Harlem in New York, in toddlers the number of juice servings correlated with the degree of BMI increase.

Norman Swan: Where does this fit, I mean people at the University of Sydney who’ve pioneered the glycaemic index, the idea that you get some foods which actually boost your blood sugar very quickly and some which are slow. They kind of argue that it doesn’t actually matter terribly much what kind of sugar it is, it just depends on how fast your insulin is going to go up. Where does what you’re saying fit into the glycaemic index story?

Robert Lustig: In fact glycaemic index is half the story, the other half of the story is the fibre. Here’s the way it works — carrots, let’s talk about carrots for a minute. Carrots are very high glycaemic index, what is the definition of glycaemic index? It’s how high your blood sugar goes if you eat 50 grams of carbohydrate in that food, that’s what glycaemic index is. So if you eat 50 grams of carbohydrate in carrots your blood sugar goes up very high and so that would be a high glycaemic index food. Fructose is a low glycaemic index food because fructose does not stimulate insulin, it’s all of these calories but it doesn’t stimulate insulin. So in fact a soda has a glycaemic index of 53 which is low. So you’d say oh wait a second, carrots are bad for you and a soda is good for you? Because glycaemic index is not the whole story, in fact what you really want to talk about is a related concept called glycaemic load.

Glycaemic load is glycaemic index times the amount of food you’d actually have to eat to get the 50 grams of carbohydrate, so in carrots you’d have to eat the entire truck in order to get that. Well you can’t do that, you wouldn’t do that, so in fact carrots, even though they are high glycaemic index are actually low glycaemic load. Carrots are fine, there’s nothing wrong with carrots. On the other hand fructose, I mean a soda, there’s a lot wrong with it but you wouldn’t see it in just looking at glycaemic index.

Norman Swan: So glycaemic index plus common sense?

Robert Lustig: Well it’s glycaemic index plus fibre. Fibre turns any food into a low glycaemic load food. In fact we are supposed to eat our carbohydrate with fibre, that’s the key. Processed wheat is white, when you go out into the field it’s brown but by the time it gets to your bakery it’s white. What happened? Well the bran was stripped off, well the bran is the good part, the bran is what we’re supposed to be eating.

Norman Swan: I’ve often wondered, I’ve heard of some processed stuff and the evil of the food industry etc. but explain to me a conundrum — why Asians are thin, or have been traditionally thin and for centuries they’ve eaten processed rice, they’ve eaten white rice, they don’t like brown rice and I don’t blame them.

Robert Lustig: Not a problem, I can explain it very simply. If you look at the Atkins diet, the Atkins diet was no-carb, high-fat, no-carb and it worked. We look at the Japanese diet, high-carb, no-fat, it also worked. When you put them together you get something called McDonalds and clearly that doesn’t work. So the question is what is it about the Japanese diet, even though they eat all of this white rice, that still allows this phenomenon to be OK? And the answer is very simple — it’s called fructose, because fructose is really not a carbohydrate. If you look at the metabolism, the liver metabolism of fructose it is just like a fat, it doesn’t stimulate insulin, just like fat. It causes all this de novo lipogenesis.

Norman Swan: Fat production

Robert Lustig: Fat production within the liver, it causes deposition of fat within the liver, it’s actually like alcohol and alcohol is like a fat. So here’s a carbohydrate that’s acting like a fat. So outside of the Japanese diet, when you eat a low fat diet what are you eating? Snackwell — and what did they do? They added sugar because otherwise it would be unpalatable. So in fact a low fat diet’s not really a low fat diet, a low fat diet containing fructose is really a high fat diet and that explains what’s going on. So a Japanese diet yes, they’re eating a lot of white rice but they are also eating a lot of fibre in all of their vegetables and they are not consuming any fructose. There is no fructose in the Japanese diet whatsoever, but there is now, and childhood obesity has doubled in Japan in the last ten years whereas adult obesity hasn’t moved.

Norman Swan: And the reasons?

Robert Lustig: Because the adults are eating like they used to and the children are eating like we do in America.

Norman Swan: So do you check your home garage floor for brake fluid every morning, I mean you can’t be the most popular person with the food industry?

Robert Lustig: Well I’m not, I am not, very much so. The Corn Refiners Association and the Juice Products Association have been on my tail, but the fact of the matter is the science is clear, the science is there and the science has to drive the policy.

Norman Swan: So what about the regulators?

Robert Lustig: Well we’re trying to work with them, we are trying to do something about it. They are not moving very fast. In fact you may be aware of the International Obesity Task Force that met at the Sydney meeting in October and they came out with something which they called the Sydney principles. The Sydney principles involved marketing and advertising to children and trying to get rid of that, and they basically said that you have to do something about this and it has to be statutory in nature, it has to be regulated, it has to be a law. In fact in Europe 52 health ministers from the World Health Organisation from all the different European countries got together in Istanbul in August and agreed that marketing to children had to stop. Well in fact that is not happening in America.

Norman Swan: Nor is it in Australia.

Robert Lustig: Well probably not, but I just met with the commissioner of the Federal Communications Commission, Miss Deborah Taylor Tait, and she mentioned that she expected that the food companies would police themselves, that regulation would not be necessary. In fact I said, excuse me but I disagree. In fact in 1978 the US Federal Trade Commission had an entire congressional hearings on marketing and advertising to children and the food companies actually lobbied congress to actually have that killed. And they knew why, they knew what they were doing then, and they are going to do it again because it’s not in their best interest. They couldn’t increase their profits by 5% a year if they didn’t advertise and market to children.

Norman Swan: Dr Robert Lustig is Professor of Pediatric Endocrinology at the University of California, San Francisco.

If you have time, sit back and watch a video by Dr Lustig (1:29 hrs) called Sugar: The Bitter Truth, here on YouTube.