The David Gillespie Blog

If you change nothing, nothing will change
March 30, 2013
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We owe our kids more than a future full of transplants

By | Sugar | 10 Comments

According to a report released this week, liver disease now affects more than six million Australians.  The doctors who commissioned the report want the taxpayer to give them more money to manage sufferers.  Fortunately we now know what causes the vast majority of liver disease and that it can be reversed simply by telling people not to eat sugar.  But I won’t be holding my breath waiting for that to become the recommended treatment.

Liver diseases fall into two main groups, those caused by viruses (Hepatitis – currently afflicting about 518,000 Australians), and, accounting for the other 90 odd per cent of cases, those caused by ‘lifestyle’ (5.5 million people).

The lifestyle group is usually further divided into drinkers (who have the same symptoms but have a history of consuming  more than 2 standard drinks per day for women or 3 for men) and everybody else.  According to the report, Alcoholic Fatty Liver Disease now affects 6,203 people but Non-Alcoholic Fatty Liver Disease (NAFLD) afflicts a massive 5,538,677 Australians.  That’s a pretty big number for a disease was first identified just 30 years ago.

As the name suggests, NAFLD starts out as an accumulation of fat in the liver.  It can then progress through various disease stages and ultimately end in cirrhosis requiring a liver transplant (if you’re lucky enough to find a donor).   There are very few symptoms until the later disease stages, so most people are unaware that they have it all.

NAFLD is frequently described as the liver component of the metabolic syndrome (elevated blood fats, insulin resistance and obesity), because it’s rapid growth has paralleled the same runaway growth in each of the diseases which are a consequence of the syndrome.  More than 90% of obese people and up to 70% of people with Type II Diabetes have NAFLD.

The number of people with NAFLD is accelerating at a tremendous rate.  Even worse, the age of onset is declining rapidly.  A study published last week revealed that the number of US teenagers with the disease more than doubled in the last 20 years and now affects almost 11% of US children aged 12-19.  If those rates translate to Australia (and there’s every reason to think they might) this means the average high school classroom now contains three children suffering from chronic liver disease.  Every classroom.  Three kids.

Even though one of the liver’s functions is to make fat from any excess carbohydrates we consume, the fat is normally exported for storage in all the places that make our jeans too tight.  NAFLD starts when the liver’s ability to export fat is overwhelmed.  The excess fat remains in the liver and begins to create the human version of foie gras.  The best way to make this happen in ducks and geese is to overfeed them (by shoving a metal tube down their throat) with carbohydrates (like corn or dried figs).

Humans get a little twitchy if you reach for the tube and corn, so overfeeding us has to be accomplished with a little more finesse.  In people, all but one carbohydrate triggers an insulin response which (unfortunately for those expecting to make a bit of human foie gras) shuts down appetite and stops us eating too much.

The one carbohydrate which subverts this handy appetite control feature is fructose.  So you might expect that a bit of effort has been put into seeing if fructose (and its primary modern delivery vehicle, sugar or sucrose) might be the source of the sudden explosion in NAFLD.

And you wouldn’t be disappointed.  In the last five years research that proves that sugar is the culprit has been pouring in.  Scientists have of course shown that you can give ducks (hmm, I wonder why they chose that experimental animal) and rats NAFLD using fructose.  And a recent series of human studies have also shown that the consumption of soft drinks is strongly associated with the onset of NAFLD (and I don’t think we can blame the water or the bubbles).  But if that wasn’t enough, a pair of very recent trials from Scandinavia have put the icing on the cake.

The first trial involved feeding four groups of people four different drinks (Coke, skim milk, Diet Coke and a still mineral water).  After 6 months of this, the Coke group had massively (140%) increased liver fat (as well as significantly increased blood pressure, cholesterol and blood triglycerides).  The folks knocking back Diet Coke and water were pretty much the way they were at the start (just in case you thought it might be the water or the bubbles) and the milk drinkers had even slightly improved their liver fat status.

A similar story unfolded in the second trial.  Some very unfortunate volunteer humans were put on the path to NAFLD (27% increase in liver fat) in just three weeks by overfeeding them chocolates, pineapple juice, soft drinks and sports drinks.  The good news is that the disease was easily reversed with diet (although it did take 6 months).

The trials are done, the evidence is clear.  Fructose consumption causes NAFLD in exactly the same way that alcohol causes Alcoholic Fatty Liver Disease.  NAFLD’s alcoholic cousin can be usually be reversed by ensuring the patient avoids alcohol.  So are the experts demanding that GPs be told to adopt a similar practice for fructose?  Nup.

No, what they want is for the government to spend more money on, well, them.  This week’s report calls for a $6 million dollar a year program (run by the doctors who commissioned the report) to increase awareness of liver disease and a $7.5 million dollar a year community care program to help people who are suffering with liver disease.

Now I’m sure these are admirable programs and I’m sure they’ll go some way to alleviating a little bit of the suffering caused by the overwhelming epidemic of chronic liver disease.  But when the cause is clear and the solution even clearer, we can do much better than throw a bit of cash at some liver doctors.

NAFLD currently has at least a quarter of the population on an expressway to a liver transplant (if the rest of the metabolic syndrome doesn’t get us first).  Yet it can be easily and effectively reversed with a pathetically simple piece of advice – don’t eat sugar.  Those charged with keeping us well, need to immediately start giving that advice rather than lobbying for a better ambulance  to park at the bottom of the cliff.

January 31, 2013
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A day late and a dollar short? – Australia’s peak health bodies decide sugar is unhealthy (but only when added to fizzy water).

By | Conflicts of Interest, Sugar | 20 Comments

The week before last the Heart Foundation, Cancer Council and Diabetes Australia declared war on sugar. But before you break out the party poppers you should know that it wasn’t so much an all-out assault as a slap with a wet tram ticket. And the Dietitians Association couldn’t even be bothered getting out the tram ticket, moist or otherwise.

Don’t get me wrong, it’s great to see such august bodies uniting behind an anti-sugar campaign. It’s just a pity the message is so riddled with caveats, exceptions and contradictions as to render it almost completely ineffective. Or was that the point?

The campaigning trio called for action on sugary drinks by “governments, schools and non-government organisations such as sports centres.”

Kellie-Ann Jolly, acting CEO of the Heart Foundation urged the Federal Government to “implement restrictions to reduce children’s exposure to marketing of sugary drinks.” She went on to suggest that State governments should also limit the sale of sugary drinks in schools and sporting grounds.

The CEO of Diabetes Australia, Greg Johnson, wanted even more direct action, calling for a tax on sugar-sweetened beverages.  The call to action was because these drinks are “associated with a range of serious health issues including weight gain and obesity, which in turn are risk factors for diabetes, cardiovascular (heart) disease and cancer.”

The sugar in soft drinks must be magic. You see when it’s mixed with water it apparently makes you fat and gives you diabetes, heart disease and cancer. But when the very same sugar constitutes 72% of a children’s lunch box snack it is so healthful that it deserves a great big Heart Foundation Tick of approval. And when it makes up almost a third of Uncle Toby’s Oat Gourmet Selections or Kellogg’s Just Right breakfast cereal it gets a tick as well.

But the real sign of its magicness is that it is not always dangerous even when the only other significant ingredient is still just water. Fruit Juice is sugar and water but that is not on the radar of the newly minted crusaders against sugary drinks. Apparently sugar molecules that were once part of a piece of fruit are not evil but those that were once part of a piece of sugar cane (despite being chemically identical) are deserving of taxation and prohibition.

Soft drink is an easy target. No-one is suffering under the impression that a can of Pepsi is health food and not even the Beverage Association at its most brazen would attempt to convince us that it is.

Confected rage on the part of the magnificent three is token (at best) for as long as they continue to ignore (or endorse, in the Heart Foundation’s case) the vast majority of sugar we are sold under the label ‘health food’.
Sugar is sugar. It’s just as dangerous when it’s the primary ingredient in a Heart Foundation approved children’s snack as it is when it’s sloshing around in a bottle of Coke. The Heart Foundation in particular robs this campaign of any shred of credibility for as long as it accepts payment from the processed food industry to endorse their sugar filled ‘health’ food.

The evidence supporting the campaign has been available to these organisations since at least 2007. Despite this, the Heart Foundation in particular has publicly and actively denied that sugar presented any health problem at all. Indeed as recently as 2011 they said“based on the current level of evidence, sugar is not directly linked to [heart disease], diabetes, or obesity.” That’s right, the exact opposite of what they now say about the sugar in soft drinks.

They must have found their library card because now it appears they’ve finally caught up with decades of research and mustered the gumption to acknowledge (some of) that evidence – albeit in half-hearted and non-revenue-endangering fashion.

The research on dietary sugar intake is just as damning as the evidence that has now convinced them to act on soft drink. Sugar doesn’t suddenly become dangerous when combined with water and bubbles. It’s dangerous all the time.
How many people million more people need to suffer from the lifelong debilitation (of Type II Diabetes) caused by the sugar added to everything we eat before Diabetes Australia is prepared to accept that evidence. How many more deaths from Heart Disease need to occur before the Heart Foundation is prepared to bite the corporate hand that feeds it?

Until those who are supposed to care, stand up and acknowledge the obvious, the suffering will continue. Until the Heart Foundation are prepared to say no to corporate sponsorship and demand action on all sugar, their gormless flailing at the easy targets will render them less and less relevant. In this age of profit driven, processed food we need real, independent advocates not corporate flunkies.

Image courtesy of Paul / FreeDigitalPhotos.net

July 10, 2012
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The Australian Diabetes Council needs to clean up its act.

By | Conflicts of Interest, Sugar | 15 Comments

It’s Diabetes Awareness Week.  But the Australian Diabetes Council continues to advocate a solution that the science shows will make the disease worse rather than better.  Is their position mere negligent incompetence or is there something more sinister afoot?  Either way it is ordinary people who will pay the price.

Type II Diabetes (90 per cent of all diabetes is Type II) is a disease of carbohydrate metabolism.  Sufferers can no longer properly convert the carbohydrates they consume into energy.  The result is that their blood glucose level is permanently too high.

A permanently high blood glucose level leads to damage to the fine capillaries of the eyes and kidneys as well as the blood vessels transporting food and oxygen to our lower limbs.  Uncontrolled Diabetes will eventually lead to blindness, kidney disease and lower limb amputation.

Every day in Australia nine limbs are amputated because of this disease. Worse than that, it affects more than twice as many people today as it did in the nineties.  And that number is likely to triple in next fifteen years.

You don’t need to be a scientist to figure out that if a person has trouble dealing with carbohydrates they should eat less carbohydrates.  After all that is exactly the approach taken with other similar problems.  For example people who can’t properly digest fats (because their gall bladder is compromised) are advised to eat a lot less fat.

And if that was your hunch you wouldn’t need to look too far for science to back you up.  In 2010 the Harvard School of Public Health published the results of its meta-analysis of the research on the relationship between sugar sweetened drinks and diabetes. They reviewed eight high quality studies which involved 310,819 participants and 15,043 cases of Type 2 diabetes. Each of the underlying studies was significant in its own right and all had been concluded between 2004 and 2010.

All but one of the studies revealed a strong (and significant) association between sugar and diabetes. Taken together they showed that consuming one or more soft drinks (or fruit drinks or vitamin waters) per day would increase your chance of contracting type 2 diabetes by 26 per cent.As convincing as this meta-analysis is, it just confirms what a very strong series of studies (on the link between soft drinks and diabetes) have been saying for the last decade, sugar consumption significantly increases the incidence of type II Diabetes.

Two decades ago (when there were half the number of sufferers there are today) reducing carbohydrates in general and sugar in particular was exactly the advice given.  But strangely the Australian Diabetes Council’s  (ADC) advice to Type II Diabetes sufferers today amounts to advocacy for increasing the amount of carbohydrate.

Yesterday, their Chief Research Officer Dr Alan Barclay told the Today program that Australians hoping to prevent the onset of this terrible disease should eat less fat, less salt and more fish.  He gave no advice about sugar either during that interview or in the similar one he also gave to Alan Jones.  Neither does a word about sugar appear in the detailed booklet on preventing diabetes published by the ADC yesterday.

The official position of the ADC on sugar is that it has nothing to do with Diabetes.  Indeed it “want[s] to end the myth that sugar causes diabetes.” It’s a position which is (strangely) almost identical to the one maintained by CSR Sugar and Nestle Australia.  The ADC instead recommends “that people with diabetes choose at least one serve of a low G.I. food at each meal and snack.”

Sugar is a moderate to low GI food and pure fructose (which is one half of sugar) is the lowest GI carbohydrate available.  It shouldn’t therefore come as much of a surprise that foods high in sugar feature heavily in lists of processed food awarded Low GI certifications.  One type of pure sugar (made by CSR) has even managed to have itself certified as being low GI.

Besides being ADC’s Chief Research Officer (and oft-quoted spokesperson), Alan Barclay has some other strings to his bow. He is also a director and vice-president of the Glycemic Index Foundation (GIF). GIF exists to dispense GI Symbols.

Prospective supplicants submit their fare for testing, pay the ‘testing fee’ and, if adjudged worthy, receive a little blue G that they can display on their labels.  They can leave the proclamation of healthiness on the label for as long as they continue to pay for the privilege with a percentage of their product sales.   Some currently certified foods include, Nestle Milo (46% sugar), a range of Nestle muesli bars (around 25% sugar), USANA Meal replacement shakes (around 27% sugar), CSR’s Low GI Sugar (100% sugar) and of course Danisco pure fructose (100% fructose).

When the ADC exonerates sugar and steers sufferers in the direction of Low-GI foods, they are driving demand for the services of GIF, and the products certified by them.  Doctor Barclay’s involvement in both organisations is a clear conflict of interest (which should, at the very least, be disclosed with every appearance he makes on behalf of the ADC).

The studies linking sugar and diabetes are large, well conducted and reliable yet they are ignored on both the ADC website and in Dr Barclay’s most recent public advice to those seeking to avoid diabetes.

People with type II Diabetes will heed the ADC’s advice.  They will seek out low fat foods (which are usually high in sugar).  They will ignore the sugar content of foods and they will look for foods which bear a Low-GI certification.  This will inevitably increase their sugar intake and the science says they will significantly increase their risks by doing so.

If this was about increasing the risk of your fingernails going green then I would say, so what.    But far more is at stake in this game.  Almost 300 Australians will contract an appalling, life destroying, disease today.  And they’ll be joined by another 300 tomorrow, and another 300 the next day. They will suffer every remaining day of their (foreshortened) life even though the science on how to avoid it has been clear for at least a decade.

I don’t pretend to know ADC’s motivations, but telling at-risk people that it is ok to eat sugar is an extraordinary abuse of a position of trust.  Real people are suffering because of the ADC’s incompetent advice. It needs to clean up its act and it needs to do it now.Type II Diabetes is not a game.

Image courtesy of pat138241 / FreeDigitalPhotos.net

February 14, 2012
2

Why eating sugar impairs your ability to conceive.

By | Sugar | 11 Comments

Female infertility is increasing at an astounding rate in Australia.  The rate of increase of Type II diabetes is strapped to the same rocket.  Now a series of new studies suggest the cause for both is the humble fructose molecule found in every teaspoon of sugar added to your food by your local processed food conglomerate.

As many as one in five Australian women of reproductive age now have PolyCystic Ovary Syndrome (PCOS). Exact data on the numbers affected are hard to come by because up to 70 percent of PCOS cases have not been medically diagnosed.

The symptoms usually include acne, the appearance of male patterns of hair growth (and male baldness) and irregular or absent periods.  Ok so it’s not pleasant, but the big impact is on fertility.  PCOS is the primary cause of female infertility in Australia today.  The reason that doctors suspect that the syndrome goes largely undiagnosed is that pretty much the only time it’s tested for is when a woman seeks fertility treatment.

A recent Swedish evaluation concluded that women with PCOS were 9 times as likely to need access to IVF as women without the syndrome.  IVF is the last resort in fertility treatment.  It is used when everything else has failed.  And it is being used increasingly frequently.  In Australia today approximately one in every 30 children is born as a result of IVF.

IVF is not a path women choose lightly.  It’s an experience that comes bundled with significant psychological and emotional costs.  And at a monetary cost of approximately $32,000 per birth it’s an increasingly expensive burden on mothers, families and the public health system as well.  The number of IVF treatments grew by 50% between 2004 and 2009 and is currently increasing by about 14% every year.

As you might expect from a glance at the symptoms, PCOS is a result of there being too much testosterone (the male sex hormone) in circulation.  Testosterone is not an exclusively male hormone.  Women have it too, but generally circulating at about 10 percent of the male level.

Doctors have long known that women with PCOS not only have higher circulating testosterone, but they also have extremely low levels of very important protein, the charmingly named Sex Hormone-Binding Globulin (SHBG).

One of SHBG’s jobs is to keep testosterone out of circulation.  By binding to testosterone, SHBG controls the amount of free (and therefore active) testosterone in our bloodstream.  Having low levels of SHBG seems to result in there being too much free testosterone in women.

It’s also well established that people who are obese or who have insulin resistance or Type II Diabetes have extremely low levels of SHBG.  In fact low SHBG is such a reliable indicator of insulin resistance that SHBG testing is being proposed as a good early indicator of the development of Type II Diabetes.

Hormones are complex things (and that’s an understatement) and sex hormones are the big daddy of complexity.  Because they are constantly produced and their actions depend on the presence or absence of other sex hormones and what sex you are, it’s very hard to tease out the cause and the effect.

For a long time researchers have believed that insulin resistance is the cause of the low levels of SHBG.  That would mean that PCOS is a consequence of being insulin resistant but a January 2012 study has shown that is not the case.  It turns out that insulin levels do not affect the level of SHBG, but the presence of fat around the liver affects both the insulin level and the SHBG level.

One really sure way to create a fatty liver is to consume large amounts of fructose.  Because fructose is (directly and immediately) converted to fat (by our liver) it’s the single most efficient way to get the job done.

The best way to prove that theory is of course to try feeding a healthy person high quantities of fructose and see if they develop fatty liver, insulin resistance and PCOS.  Because volunteers for that kind of fun might be a bit thin on the ground researchers have had to resort to rats as the model.

You can’t use any old garden variety rats.  To be certain you need to use rats that have been bred with the human gene for the production of SHBG.  Before you get out the rat breeding equipment (whatever that might be) you might like to know it’s already been done.

In 2007 a group of Canadian researchers tried feeding so-called transgenic rats glucose and fructose to see what happened.  They found both sugars suppressed SHBG production but fructose was twice as effective (glucose 40%, fructose 80% suppression) and fructose was especially quick, causing its damage after just three days.  They found the SHBG effect was caused by the accumulation of the fats created as a result of processing the fructose.

Joining some dots here it does not seem like a big leap to say that insulin resistance, Type II Diabetes, fatty liver disease and PCOS are all part of the same bunch of joy you can expect from consuming fructose.

Fructose directly increases the amount of circulating testosterone in women.  More testosterone directly impairs a woman’s ability to conceive.  The single most effective way for a woman to increase her chances of having a baby is for her to stop eating fructose.

When fructose is removed, hormone levels return to normal, PCOS symptoms disappear and fertility is restored.  It really is that simple.  There is no reason (other than financial) that the first words out of a fertility doctor’s mouth shouldn’t be “Stop eating sugar.”

 

Photo by Ⅿeagan. Distributed under the Creative Commons License.

October 31, 2011
0

Let those who cause the pain, pay the tax

By | Sugar | 8 Comments

Sugar causes tooth decay. No sane scientist would argue that simple statement. It is about as controversial as saying day follows night. But treating tooth decay costs Australians $7.7 billion a year. Why are we not looking to the folks who sell sugar to help pay for that?

Certainty is a hard thing to come by in science. It is very rare indeed to find a group of scientists agreeing without exception to a cause and effect relationship. But there are some examples. You will not get a fight from anyone if you say that antibiotics cure most bacterial infections. And you’ll encounter even less resistance if you say that smoking causes lung cancer.

The statement that sugar causes tooth decay is even more certain. The statistics are clear. Populations exposed to sugar for the first time go from ‘background’ levels of decay (of around 4 cavities per 100 teeth) to ‘modern’ levels of around 24 cavities per 100 teeth. The mechanism is known and the science is uncontroversial. Not even Coca-Cola dares deny that sugar and tooth decay go together like peas and carrots.

Researchers have known since the 60s that tooth decay is caused by a little chap called Streptococcus Mutans (S. Mutans). It is one of the two to three hundred species of bacteria that inhabit our mouths.

Like most bacteria, S. Mutans loves a good feed of sugar. As it chomps down on the sugar molecules it produces lactic acid as a waste product. It’s that lactic acid that does the damage to our teeth. But under normal circumstances we are up to the task of protecting ourselves and avoiding tooth decay. Our saliva quickly neutralizes the acid and we regenerate any damaged enamel.

This is fine if the only sugar in our diet is glucose or carbohydrates that are converted to glucose (which is almost all of them). But, if there is some fructose available as well as glucose (oh, such as in table sugar – half glucose and half fructose), then through a quirk of evolutionary biology, S. Mutans has the upper hand.

S. Mutans can build itself a saliva proof home if fructose is also present. We call this little anti-saliva shield, plaque. Plaque binds S. Mutans to each other and to the tooth enamel. It traps the lactic acid against the tooth surface, protects it against the waves of saliva and gives it time to eat through the enamel.

If you really want to rot teeth, the most effective way is to give S. Mutans a constant wash of sugar solution (like soft drink or fruit juice) between meals. Eating sugar at mealtimes still works but it is nowhere near as effective.

S. Mutans has really enjoyed our change in diet in the last few decades. The amount of fructose laden, soft drink, juice and flavoured milk we drink has risen from virtually nothing prior to the Second World War to almost 1 litre per person per day. Consumption of soft drink alone has more than doubled in the last 30 years. And with this our need for dental services has also risen exponentially.

Every now and then politicians bow to public anger over the rising cost of dental services and mumble indistinctly about perhaps fixing the problem. Do they suggest limiting sugar consumption? Don’t be silly. How about asking the sugar purveyors to pick up the bill? Think again.

No, the politician’s answer is to make it our problem. First they try the chemical band-aid of dosing us all with fluoride, then, when that barely dents the costs, they reach for our wallet. The most recent go-round was Kevin Rudd’s ill-fated Denticare scheme, which suggested increasing the medicare levy by 50%. Heaven forbid a processed food manufacturer be presented with the bill.

Sugar rots teeth. The evidence is abundantly clear that, but for a constant wash of sugar between meals (topped up with some nice sticky fruit snacks), we would barely need to visit a dentist at all. So why are we not asking the folks who cause the problem to pay the bill? Or better still, stop creating the problem?

We have no difficulty asking the purveyors of cigarettes to kick in for the costs of treating the disease they cause. So why is the political response to the cost of dentistry a tug of the forelock and a scurry to collect more tax from us (whether we consume sugar or not)?

To be sure, $7.7 billion is a large bill to present to anyone. It represents about two and a half times the entire annual revenue of the Australian sweetened beverage industry. But it is also about 30 times the income tax they paid. Is it really fair that an industry contribute so pathetically to the cost of the damage they cause?

This is not a sin tax in disguise. It is repugnant for food nannies to attempt to make us healthy using the blunt instrument of taxation. If sugar is bad enough to require (at least) $7.7 billion of reparation every year then we should be removing it from the food supply. The level of harm it does is out of all proportion to its utility (is there any?).

But our governments clearly don’t have the moral and intellectual steel to bite that bullet. So let us at least insist that the most obvious part of the damage being caused (the part about which there can be no argument) be paid for by those profiting from our misery.

September 15, 2011
6

It’s time to stop drinking the Kool-Aid of Public Health Dogma

By | Sugar | 11 Comments

One of the big complaints about research on fructose (the dangerous half of ordinary table sugar) is that many of the studies are done on rats, not humans.  But a pair of recent studies have shown that sugar is just as dangerous for primates (including us) as it is for rats.

People defending our right to continue eating sugar (‘in moderation’ of course) frequently waggle their fingers at the studies and say just because it kills a rat doesn’t mean it will harm a human.  One defender of the white stuff, Dr Jennie Brand-Miller, recently went so far as to suggest that sugar doesn’t do us any direct harm at all.

There’s a good ethical (and legal) reason that human studies are few and far between.  The ones that have been done have inevitably resulted in immediate harm to the human subjects.  A study where the expected outcome is to harm the participants makes lawyers nervous.  I guess that’s why you don’t tend to see studies on what happens if you don’t open the parachute.

But the science needs to be done.  There really is no other way to combat the incessant ‘sugar in moderation’ chant of the processed food industry and its toadies.  Thankfully a few US Universities are prepared to push the envelope.

Just last week a team from Vanderbilt University’s paediatrics department published the results of their year-long study into the effects of fructose on Rhesus Monkeys.  Their stated aim was to “induce insulin resistance” (the first step on the path to Type II Diabetes) in a primate using the same methods which are so successful in rodents.

The Vanderbilt folks chose Rhesus monkeys because they are physiologically similar to us and they develop the same chronic diseases that we do (and they are far less picky than humans about being locked in cages for 12 months).  Dr Bremer and his team studied a group of 29 adult male monkeys aged from 12-20 years (approximately equivalent to human ages of 36-60).

At the start of the study, all the monkeys had perfectly normal blood glucose levels and were otherwise fit and healthy.  The diet for the duration of the study was standard monkey lab chow (designed to give them all the nutrients they need in a healthy mix which is 59% Carbohydrate, 30% Protein and 11% Fat).  They were also given access to up to 500ml per day of Kool-Aid.  The monkeys could consume as much (or as little) of the food and Kool-Aid as they wanted.

Kool-Aid is a fruit flavoured powdered sugar drink mix sold in the US.  The closest Australian equivalent is Tang (which is really just Kool-Aid with a multi-vitamin chucked in).  The Kool-Aid delivered up to 75g of pure fructose a day to the monkeys.  I say ‘up to’ but the reality was that the monkeys drank the Kool-Aid and then topped up their calories with chow.  They weren’t going to leave any of the good stuff in the tin.

Unfortunately for our furry friends, they were never healthier than when they hadn’t drunk the Kool-Aid.  Four of them developed Type II diabetes between 6 and 12 months after starting.  The rest of them were well on their way to the same destination (with blood glucose and insulin readings that would have had them on the latest anti-diabetes drugs if they had been humans).

They put on weight (an average of 9% of their starting weight), the percentage of their body which was fat increased by 15%, they ate more of everything, exercised less and their blood lipids were a mess.

Their fasting triglycerides (a strong risk factor for heart disease) increased by a whopping 87%, HDL (good) cholesterol decreased and LDL (bad) cholesterol increased (by 14% each).  In other words these critters were also on the fast track to a heart attack.

The experiment would have been better if they’d had 29 monkeys eating nothing but chow to compare the results to.  But there is no evidence to suggest that monkeys on a standard lab chow diet ordinarily develop these symptoms (and certainly not in less than a year).The researchers set out to give diabetes to a group of primates (with an almost identical metabolism to ours).  All they did was allow them access to a sugar which is plentiful in our food supply.  They didn’t test chemicals on them.  They didn’t inject them with drugs.  They just fed them with the same stuff we give our kids.  And they achieved their aim – four had diabetes and the rest were on their way – in less than a year!

Still not enough to get you to step away from the Froot Loops?  Still not ready to believe, ‘till they do this to humans?  Then you’re in luck, because a human study has also just been released.

This time, a team at the University of California convinced 48 healthy (human) adults to consume four cans of soft drink a day for two weeks (about the same as one in 20 Americans do every day of their lives).    Some of the soft drinks were sweetened with glucose, some with fructose (the two halves of sugar) and some with High Fructose Corn Syrup (55% fructose, 45% glucose).

And guess what?  That’s right, the result was exactly the same as for the monkeys.  The blood fat measurements (which point to heart disease) started going in the wrong direction for the fructose and HFCS groups (and nothing happened to the glucose group).  No-one was given diabetes, but it was just a 2 week study.

Try as they might, researchers have never been able to get results like these by feeding people fat or stopping them from exercising.  But these latest studies could barely be more definitive on whether there is danger in that thar can of soda.

Eat fructose and the only question is when you will develop diabetes and heart disease.  If you happen to be a Rhesus Monkey (well done, you, for being able to read this) you have as little as six months, if not, you might get a bit longer.  But have no doubt, it will happen.

July 13, 2011
0

The Glycemic Index has passed its use-by date

By | Big Fat Lies, Sugar | 16 Comments

The glycemic index (GI) is not just bad science, it has a dangerous loophole big enough to drive an ice-cream truck through. Its time it went to the place where old (and wrong) public health messages go to die.

Wendy’s Chocollo (with waffle cone), Bulla Light vanilla ice-cream, Nestle Milo, Uncle Toby’s Choc Chip Crunchy Muesli Bar and CSR LoGiCane Sugar all have something in common. Yes, they’d all look pretty good on the dessert menu, but they also share something else. The owners of each of these products (and almost a hundred others like them) have paid for the right to display a GI Symbol.

Much like its more famous cousin (the Heart Foundation tick), the GI Symbol is designed to guide confused consumers towards “healthier choices” in the supermarket.

The symbol alerts us to foods which have a low glycemic index. The GI is a measure of the amount that a food affects our blood sugar levels. Our body converts most of the carbohydrates in our food to blood glucose. This causes a spike and then a decline in the amount of glucose we have in circulation.

But not all foods are equal. Some (like glucose) spike our blood sugar levels more quickly than others (like potatoes). This is because the carbohydrates in some foods are more quickly converted to blood sugar than others.

The glycemic index of a food is measured by comparing the way a healthy person’s blood sugar level responds (over a 2 hour period) to 50g of glucose and how they respond to 50g of carbohydrate in the food being tested (let’s say boiled potatoes). If the tested food produces an effect which is 70% of the one measured for the glucose then it is said to have a GI of 70. A low GI food is one which has a GI of 55 or less (meaning that the blood sugar response is 55% of that of pure glucose over a two hour period).

The theory goes that if we could make sure we were eating just the foods which have a low impact on our blood sugar, then we would keep our blood sugar levels more even (and presumably somehow be more healthy as a result). I say presumably because there is a real scarcity of credible evidence that the GI of a food has any measurable (positive) health impact.

GI may be a pointless academic exercise but it is not a harmless one. It has a hidden danger in that the carbohydrate it assigns the lowest (and therefore the best) rating is fructose (it has a GI of 19). Fructose is a very sweet tasting (almost twice as sweet as sugar) carbohydrate that does not produce a significant blood sugar response.

When this little quirk of fructose was first discovered (in the early 1980’s) it was pronounced a miracle sugar for people with diabetes. They could have sweets just like everyone else and their blood sugar would never spike as long as the sweets were made with fructose. Even some sugar was ok too (because, being half fructose, it also has a low(ish) GI).

Diabetes organisations the world over happily advised diabetics they could eat sugar or, even better, pure fructose. Unfortunately for sweet tooths everywhere, by about 2001, it was becoming abundantly clear that the ‘no free lunch’ rule applied (or was it no free pudding?). Fructose was even more dangerous for diabetics than sugar.

It turned out that the reason fructose didn’t have a big glycemic index was because it is converted to fat (by our liver) and not circulating blood sugar (like just about every other carbohydrate). Telling diabetics (or anyone else, but particularly diabetics) to consume a substance that was immediately converted to fat was a very bad idea (verging on the culpably negligent).

The American Diabetes Association quietly withdrew its recommendation in 2002, but the message never got through to Australia. The Australian Diabetes Council tell us they “want to end the myth that sugar causes diabetes”, apparently because sugar-free diets aren’t “much fun.”

And the folks selling the Low-GI stickers (the GI Foundation – a collaboration of University of Sydney, Diabetes Australia and the Juvenile Diabetes Research Foundation) still tell us it is “best to ignore the sugar content of a food and instead focus on the food’s GI.” A director of the GI Foundation (Sydney University nutritionist Jennie Brand-Miller) even went so far as to say recently that “Unlike saturated fats, trans fats, salt and alcohol, sugar doesn’t actually do any direct harm to the human body.”

For the last decade (at least), the research on fructose (and sugar) has shown again and again that exactly the opposite is true. Fructose consumption is a causal factor in obesity, heart disease, hypertension and Type II Diabetes. It is implicated strongly in cancer growth and it is highly likely to be behind the explosion in the number of cases of chronic kidney disease and fatty liver disease.

That all sounds pretty harmful to me. So perhaps that is why the American Heart Association recommended (after reviewing all the evidence in 2009) that Americans needed to dramatically reduce their sugar consumption. Men should consume no more than 9 teaspoons of sugar a day (about a can of soft drink’s worth). That’s less than half the current (vague) Australian recommendation (of about 23 teaspoons a day).

Just like skinny leather ties and big hair, the glycemic Index seemed like a good idea in the eighties. It held out hope (for a dessert filled future) to millions of diabetics everywhere. But science eventually found out what was really going on (as it usually does) and the world moved on.

In Australia we got stuck on the notion that GI should work (and to this day stubbornly refuse to acknowledge the fructose loophole). The food industry leapt on the marketing power of a ‘healthy label’ that meant they could still use as much sugar as they wanted. Positions became entrenched. Reputations were built. And as a result we now have folks like the GI Foundation and the Australian Diabetes Council telling us there’s nothing wrong with eating sugar.

This would all be mildly entertaining if we weren’t talking about real people with very real (and very life-threatening) problems. Every day in Australia nine people lose a limb to Type II diabetes (and 275 more people develop the disease). Every day the number of obese children grows like never before in human history. Every day the number of new cases of chronic kidney disease sets a new benchmark.

The science says all of this misery (and lots more) can be traced back to eating sugar. So how about we stop playing ducks and drakes with quaint scientific notions (that protect the processed food industry from having to face reality). How about we start caring about the people who follow the advice they see on a packet of food. How about we face the truth about sugar and demand that those we pay to care – do.

June 1, 2011
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How Fructose makes us Unhappy.

By | Sugar | 16 Comments

We don’t know what causes depression and we certainly don’t know how to cure it. But some interesting new research suggests that there may be a very strong link between depression and what we shove in our gobs.

Depression is a catch-all diagnosis for a spectrum of illness affecting our mood. The spectrum covers everything from a mild bout of feeling down through to the most severe Major Depressive Disorder.

We can become depressed because things aren’t going well. If having your cat run over doesn’t alter your mood (one way or the other depending on how you feel about cats I guess) then you were probably built by aliens. But the science suggests how long we stay depressed has more to do with biochemistry than the state of Fluffy’s road-safety skills.

Food makes us happy (I know, you’re shocked at this revelation). Even seeing food improves our mood. This is because the anticipation of a feed, fires up the hormones responsible for how we feel.

The sight (or smell) of food gives us a squirt of the pleasure hormone, dopamine. Dopamine focuses our attention, makes us think more clearly and helps us move faster and more effectively. It’s an important signal to our body that we are in for something good and we need to pay attention. And that was probably pretty handy in times gone by (when dinner was on the hoof rather than in the burger box).

Once we actually start eating, serotonin kicks in. The serotonin makes us feel happier and less stressed. We relax, our mood improves (Fluffy will still be road kill, but we’ll feel better about it) and our minds can turn to less important things than eating (such as sex – the anticipation of which will give us another dopamine hit and the aftermath of which will give us a nice relaxing serotonin hit). While the cliché that the way to a man’s heart is through his stomach may be the G-rated version – it is largely accurate.

Researchers have known for a long time that severe depression is strongly associated with an inability to properly absorb serotonin in the brain. No (or low) serotonin absorption makes it much harder for us to come back from unhappiness. And this can translate into anxiety and depression if it’s sustained for long enough.

The primary anti-depressant drugs available in Australia (Cipramil, Luvox, Prozac, Lovan, Aropax and Zoloft) all work by targeting the serotonin system. They give the brain more time to absorb the serotonin. Some other drugs (Ecstasy, Amphetamines and LSD) work by enhancing the amount of serotonin we produce (but you might find it tricky to get a prescription for them).

If all is well with our hormone system then severe depression should be an extremely rare disease. But it’s not. Most studies suggest that one in ten of us is suffering some form of depression at any given time. So it won’t come as too much of a surprise to discover that one in every 30 GP consultations in Australia is now about depression.

Depression is a major chronic health problem and it is getting much worse at a very rapid rate. Something is messing with our serotonin system and the evidence is starting to mount that the something is fructose.

Fructose is the only carbohydrate which produces a significant spike in our cortisol levels. Cortisol is our stress hormone. It’s terribly handy for confrontations with unexpected bears (for example) because it ramps up dopamine (to focus the mind and sharpen the movements). It also rapidly increases the amount of dopamine we can absorb. But it does so at the expense of our ability to absorb serotonin.

We like dopamine. It is our reward drug. Frequent hits of fructose mean frequent hits of dopamine. This leads inevitably to fructose addiction and that is exactly the mechanism used by other man-made opiods (like nicotine and cocaine). The trouble is that it seems the upregulating of dopamine at the expense of serotonin can become hard-wired if we allow it to go on for long enough. And once we’re addicted, we cant help but let it go on for long enough.

We don’t run into that many bears on a daily basis (well, I don’t). Fructose was once about as common as a bear encounter, but is now embedded in almost every processed food we buy. And it has an addictive quality as powerful as nicotine (so it isn’t exactly going to harm sales now is it?).

We are now on a constant drip of fructose. That means we are on a constant cortisol (and therefore dopamine) high. This in turn continuously impairs our ability to absorb serotonin, the one substance that can turn our mood around.

Fluffy will still become a bumper sticker if he chooses an inopportune moment to cross the freeway and that will probably be a downer. But the science is suggesting that how quickly (or if) we bounce back from that may depend (to a large extent) on how much fructose we are eating.

In an environment of non-stop fructose infusion, the wonder is not that one in ten of us is depressed, it’s that nine in ten of us aren’t (yet).

Image courtesy of David Castillo Dominici / FreeDigitalPhotos.net

February 2, 2011
0

Heart Foundation says sugar isn’t relevant.

By | Sugar | 19 Comments

The Heart Foundation has finally trashed the last of its credibility.

Last week, (an ecstatic) Nestle announced that it had secured a Heart Foundation tick on 44 of the 46 breakfast cereals it sells in Australia.

The line-up of tick-approved products will now include some of the highest sugar breakfast cereals on sale in Australia. Milo and Milo Duo (both 29.7% sugar), Uncle Toby’s Oats Temptations (up to 34% sugar) and Uncle Toby’s Healthwise for Heart Wellbeing (30% sugar) will join the Kellogg’s Just Right (31.1% sugar) on the list of cereals the Heart Foundation says you should be eating.

The only two Nestle breakfast cereals now lacking the tick of approval are Nesquick (31.7% sugar) and Uncle Toby’s Plus Protein Lift (25.3% sugar). But don’t worry they’ll both be tickety-boo in no time. They’re currently being “reformulated”.

Nestle won’t have to worry about reducing the sugar content while it is reformulating. You see, the Heart Foundation doesn’t care about the sugar content of a tick-approved product.

A fan of my blog shared some his correspondence with the Heart Foundation this week and it revealed some interesting insights into the process.

The Heart Foundation said:

“Sugar is not a criterion because added sugar and natural sugars have similar effects on the body and based on the current level of evidence, sugar is not directly linked to [heart disease], diabetes, or obesity.”

Which is a really odd stance to take because even the briefest glance at the scientific literature would reveal that the cup of evidence against sugar runneth over.

Take for example the recent review of the evidence (published in theAnnals of the New York Academy of Science), which concludes:

“…recent data suggests that fructose consumption in humans results in increased [stomach fat], [fat] dysregulation, and decreased insulin sensitivity, all of which have been associated with increased risk for [heart] disease and type 2 diabetes.”

Perhaps the Heart Foundation forgot to renew its journal subscriptions because its “evidence” proves sugar is not dangerous. If (by evidence) you’re thinking about an extensive literature review (oh say, like the one I just mentioned), you’d be unfulfilled. If you’re thinking about a series of population studies, disappointment is in your future. Even if you’re thinking of a single rat study, you’re aiming too high.

No, the Heart Foundation’s “evidence” appears to be a single graph. The (unattributed) graph shows an increasing trend of obesity plotted against a decreasing trend of sugar consumption. There’s no sign of any evidence about heart disease or diabetes, but perhaps we just have to take those on faith.

Under further questioning, the Heart Foundation revealed to my correspondent that the source of the graph was the research conducted by Alan Barclay (the chap who helps the folks slapping low-GI stickers on packets of sugar). They referred him to theDietitians Association press release about Dr Barclay’s study for confirmation.

Unfortunately, Dr Barclay’s paper has not been published, so figuring out how he arrived at the graph is a little difficult. Just about the only thing that is clear is that the graph produced by the Heart Foundation bears no relationship to the data on sugar availability (there is no current consumption data) from the Australian Bureau of Agricultural and Resource Economics (a government department).

ABARE seems to think that Australian domestic sugar availability has gone the way we might have expected it to (from about 45 kilograms per person in the mid-‘80s to about 62 kilograms per person in 2009).

But even if the Heart Foundation’s graph was entirely correct, what would it prove? Well, nothing really. No one is suggesting that sugar consumption today results in instantaneous population-wide obesity.

The science says that (one of the ways) fructose makes us fat is by interfering with our appetite control over decades of continuous consumption. The cumulative effect of this is steadily increasing weight and concurrent metabolic dysfunction (which make us prone to Type II Diabetes and Heart Disease).

The increase in obesity statistics we are seeing now is likely to be a result of the appetite disruption (caused by sugar) between the Second World War (or even earlier) and now. So comparing today’s obesity statistics with today’s consumption is a pointless academic folly (even if it were accurate).

That would be rather like looking at this graph of lung cancer death versus cigarette consumption in 1980 and concluding that there was no correlation (because the lines had gone in opposite directions since 1960). But this is exactly the scientific method that the Australian Heart Foundation has deployed in justifying its stance (that sugar is not a relevant criteria for its tick program).

That’s not just bad logic, it’s not even bad science, it’s just straight out deceptive. I guess this all raises the question, why would anyone (least of all the Heart Foundation) be attempting to prove we eat less sugar now? One glance at the local supermarket (especially the breakfast cereal aisle) will tell us that is patent nonsense, so what would motivate someone to suggest it is so?

I hope it’s not just the lousy few million smackeroos the foundation makes every year from this little jape. Because if that’s the sole motivation behind this pathetic denial, then it is a dreadfully low price to pay for the health of a nation. The cynical lawyer in me suspects somewhere, somehow, someone is making real money out of this, but the father in me just wants the deception to stop — now.


December 24, 2010
0

How Fructose makes you AGE.

By | Sugar | 3 Comments

The fructose half of sugar causes irreversible cellular damage. And this damage may just be the thing which links most of the diseases of the Western World (oh, and makes us prematurely elderly as well). But there is a way to limit the damage. No its not a drug (although plenty of people are trying to find one). All you have to do is stop eating sugar.

Enzymes control chemical reactions in our body. If we need a sugar (like glucose or fructose) to be attached to a protein for some purpose, the appropriate enzyme will make sure the sugar gets attached to exactly the right part of the protein (or fat). The process of attachment is called glycosylation and we are only just beginning to understand the enormous array of uses our body has for glycosylated proteins (such as fending off disease and even inhibiting the development of Type II diabetes).

It is however possible for sugars to accidentally attach themselves to proteins without an enzyme’s help. When that happens, the process is called glycation. Glycation can result in sugars being attached in all sorts of unpredictable (and haphazard) ways.

Glycation happens by accident and is really only likely to happen when our blood sugar levels are high (the more sugar molecules there are floating around the more likely some of them are likely to crash into a protein). The good news is that in normal circumstances glycation is reversible. As soon as blood sugar levels drop, most of the sugars and proteins will disengage and no harm is done.

But if blood sugar stays high (as is the case with someone who is diabetic or pre-diabetic), the sugar-protein combo will undergo a series of reactions that will result in the creation of an Advanced Glycation End-product (AGE).

All sugars can form AGE’s, but the glucose half of sugar is the least reactive of all sugars. This is a good thing because it is the primary sugar in our bloodstream. The bad news is that the fructose half is ten times more reactive than glucose.

Eating sugar gives us a big shot of fructose and a big (and immediate) increase in AGE production. Making things much worse, fructose consumption also leads to an increase in insulin resistance. Over the long term the insulin resistance creates an environment where our blood glucose levels are persistently elevated. And this creates a second major source of AGE’s.

If your doctor suspects you of being diabetic, they will often test your HbA1c (or A1c for short) level. The test measures the level of a glycated form of haemoglobin (the protein which transports oxygen in your blood). A high A1c level indicates that there are significant AGE levels. That is taken as a sure sign that your blood sugar is persistently too high.

Our body’s are used to garden variety (glucose-produced) AGE’s. And we are pretty good at breaking them down and disposing of them. But even so, over time they accumulate in our organs and tissues and we, well, age (the acronym AGE is very much on purpose).

Unfortunately the AGE’s made with fructose molecules are resistant to our disposal system. So not only they made at 10 times the rate, they hang around like John Farnham on a comeback tour.

AGE’s are junk, litter on our body’s interstate highways. But this is not a burger wrapper chucked out the window. This is more like the (exploding) roadside litter our troops encounter in Afghanistan. AGE’s are dangerous because they bond easily (and randomly) to each other and to other proteins in a process called cross-linking.

AGE’s accumulate pretty much everywhere in the body, but in some places they do much more damage than others. When they pile up in the lens, cornea and retina of the eye they result in cataracts and macular degeneration (the leading cause of blindness in Australia). They also accumulate in the fine tubules of the kidneys – resulting in loss of kidney function.

They cross-link the collagen which otherwise gives our arterial walls (and our skin) their elasticity (hence the term, hardening of the arteries and the ‘aging’ of the skin). They cause the oxidation of LDL cholesterol particles, making them much more likely to become trapped in arterial walls (leading to heart disease and stroke). And they accumulate in the brain.

Neurons ideally last a lifetime. This means they are much more likely to accumulate AGEs. When researchers start looking at the tangles of twisted proteins which accumulate in the neurons of Alzheimer’s patients, they discover AGEs in abundance. This is likely to be the reason why other researchers have picked up on the association between Alzheimer’s (and other dementia) and high blood sugar.

Observational and controlled studies have linked fructose consumption to Type II Diabetes, Heart Disease, stroke, blindness, kidney disease and even Alzheimer’s (to name just a few of the more delightful ones). AGE research has come a long way in the last decade (and is still in its infancy), but it might just provide a unifying mechanism which explains why the incidence of these diseases is exploding in the Australian population – we eat way too much fructose.

So if aging slower (than you otherwise might) will be top of your to-do list in the New Year, you could buy a tub of hand cream sourced exclusively from the sweat of left-handed, French, mermaids – or you could just ease back on the fructose this Christmas.