The David Gillespie Blog

If you change nothing, nothing will change
September 12, 2012
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How seed oils increase Breast Cancer risk

By | Vegetable Oils | 10 Comments

The science has definitively demonstrated that the dominant fats in margarine increase our risk of developing breast cancer. But that science has been comprehensively ignored by the Health Authorities. Is their obsession with pushing margarine for heart health clouding their vision?

Breast cancer is the most common cancer in Australian women. One in nine women will develop the disease in their lifetime.

We are getting very good at detecting and treating the cancer (88 per cent of new cases survive five years or more). But there are no signs of any reduction in the numbers of women developing the disease in the first place. In the last 30 years the incidence has increased dramatically.

An Australian woman in 2012 was almost 50% more likely to develop breast cancer than her mother was in 1982. If the woman lived in the ACT, was white and is affluent, her risk is even higher.

Forty new cases will be diagnosed today. Forty women will discover they have breast cancer today that thought they were well yesterday. And tomorrow another 40 will join the list. And another 40 the day after that. Even more disturbingly three of those women every day will be under 40.

Despite its enormous impact, we know almost nothing about what causes the disease. The best the experts can tell us so far is what many would regard as the bleedin’ obvious – that we are more at risk if we are female, have relatives that have had the disease (or other cancers) or have previously had the disease (or other cancers) ourselves.

There is nothing in the official advice about the risks associated with polyunsaturated fat consumption. But researchers have known that there is a strong link between high polyunsaturated fat, seed oils (man-made oils extracted from grains and seeds such as canola, sunflower, grape-seed, corn and ricebran) and cancer for more than 40 years.

The Veterans Trial, completed in 1971, was conducted with a population of 846 Californian military veterans randomly assigned to two different kitchens. One kitchen replaced all animal-fat products with corn oil for the eight-year duration of the study. The other kitchen kept on serving a normal high-animal-fat diet.

The purpose of the trial was to determine whether animal fat caused heart disease, but it drew a blank on that front. Heart-disease-related events were slightly less than expected in both groups, and not significantly different from each other. But the researchers noticed something of far more concern. There was the dramatic difference in cancer deaths between the two groups. The incidence of fatal cancers in the corn-oil group was nearly double that of the normal-diet group by the end of the trial.

Ethical approval for more trials on humans was in short supply after that study saw the light of day. But rat studies performed in the 1970s and 1980s consistently noted that mammary (breast) cancer was formed more often in rats fed corn oil (high in polyunsaturated fats) than in those fed coconut oil (high in saturated fats). And a truly disturbing study published in 1997 showed that feeding the rat equivalent of a breastfeeding mother a diet high in polyunsaturated fat (43 per cent corn oil) doubled the rate of mammary cancer in her daughters, caused cancers to appear among them earlier and caused earlier onset of puberty.

In 1996, Swedish researchers decided it was time for a human study to provide some hard data on breast cancer. Scientists from the Karolinska Institute recruited 63,870 women aged 40–76 and monitored their diet and the occurrence of breast cancer for an average of 4.2 years. The dietary questionnaires used in the study enabled the researchers to determine exactly how much saturated, monounsaturated and polyunsaturated fat the women were consuming.

They found no association between the total fat or saturated-fat (the dominant fat in animal fats) intake and a woman’s risk of developing breast cancer. Monounsaturated-fat (the dominant fat in Olive Oil) consumption reduced the risk of breast cancer by 20 per cent but polyunsaturated-fat consumption did exactly the opposite. Just as the rat studies had predicted, the women consuming the most polyunsaturated fat were 20 per cent more likely to develop breast cancer than the women consuming the least.

Since that study, further human studies have found significant associations between dietary polyunsaturated fat consumption (in particular the omega-6 fats which dominate seed oils) and the risk of developing breast cancer. A review of the studies conducted by the Université Joseph Fourier (Grenoble, France) concludes “there are several recent and concordant studies that strongly suggest that dietary omega-6 [polyunsaturated fats] … increase the risk of breast cancers.”

Meanwhile the Australian Heart Foundation is busily telling ‘Mums’ that they should be replacing butter with margarine. They are doing this because for the last 30 years they have been telling people that plant fats reduce the risk of heart disease. Unfortunately there is no evidence that this is true. Indeed it is likely that the omega-6 fats in margarine significantly increase the risk of heart disease and death. Even more unfortunately the margarine they want all our mums to eat is made from the very oils the French review concluded “increase the risk of breast cancer.”

This evidence is compelling. It demands critical discussion. It demands widespread publication. And it demands public warnings. But none of this is happening. The folks charged with safeguarding our safety are asleep at the wheel (I’m being generous). And the folks with a buck to make from selling us seed oils appear to be running the show.

We are not talking about a rare disease afflicting tropical fish. Breast cancer is a blight upon the community. There is not one person who will not be personally affected by the tragedy of this very modern epidemic. Our mothers, sisters and daughters (and even very occasionally our men folk) deserve better. Somebody wake the watchdogs – please. And while you wait for them to stir, stop eating seed oils.

Graphic designed by Freepik

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

April 23, 2012
3

Stop it or you’ll go blind

By | Vegetable Oils | 18 Comments

Macular degeneration is the primary cause of blindness in Australia today.  And evidence is mounting that the likely cause of the disease is consumption of vegetable oils.  But once again Australia’s Dietitians Association is on the side of the processed food industry instead of the consumer (or in this case, the patient).

Our eyes are exquisitely complex pieces of machinery which work much like a camera.  Light from the outside world hits the the retina at the back of our eye.  The macula is the centre of the retina. It is responsible for our detailed vision.  If our macula is damaged, we can no longer see fine detail, drive, read or recognise faces.

Macular degeneration begins in a layer of cells underneath the retina called the Retinal Pigment Epithelium (RPE). The RPE is responsible for transporting oxygen and other nutrients up to the retina and moving waste products down to the blood vessels underneath. It also contains a specialised immune system which reacts to some of the more dangerous waste products produced by the macula.

When the RPE wasted disposal system fails, junk from the retina builds up underneath the RPE. These junk deposits, known as drusen, appear as yellow spots on the retina and are visible in a normal eye examination.  As the disease progresses, vision loss happens because the RPE cells die (‘dry’ macula degeneration) or because the RPE cells fail to prevent blood vessels from growing into the retina (‘wet’ macula degeneration) from below the RPE.

The macula contains a high concentration of some of our most specialised hardware, the rod and cone cells that allow us to see in fine detail and in colour.  These cells are unusual in that they use polyunsaturated fats in their membranes rather than the saturated and monounsaturated fats used by most of the remainder of our cells.

If you’ve ever wondered what an essential fat (like omega-3 DHA) is essential for, there’s a big part of your answer.  The omega-3 DHA fats make up the outer segments of the light sensitive cells in the retina and are the most frequently replaced cell membranes in our body.

When these molecules are exposed to light they oxidise rapidly (this is thought to be an important part of how our light sensing cells work).   Normally oxidation is a very bad thing because of the waste products it produces (broken bits of fat molecules and free radicals).

But our body didn’t fall off the back of the potato truck yesterday.  The special immune system built into the RPE does a magnificent job of getting rid of all the junk, so the oxidation is not normally a problem.  That is unless we use the wrong kind of polyunsaturated fats.

Researchers have consistently found that people with macular degeneration have abnormally low levels of Omega-3 fatty acids in their retina.  This has inspired many studies which look at the dietary fat breakdown of the participants.

As expected a lot of those trials have shown that when people are eating a diet high in fish (the principal dietary source of the correct omega-3’s) they tend to have less macular degeneration.  But closer analysis of the figures has unearthed a very worrying exception.  They are only better off if they are also NOT eating omega-6 fats.  Indeed, people eating a diet high in omega-6 fats are twice as likely to have macular degeneration as those eating a diet low in those fats (regardless of how much omega-3 they are consuming).

We have known for at least two decades that our body isn’t that picky when it comes to omega-3 and omega-6 fats.  If we need an omega-3 polyunsaturated fat and the only one handy is omega-6 then our body just goes ahead and uses that.  And there’s no reason to suspect that our body isn’t doing exactly the same thing in our eyes.

A number of researchers have speculated that what is going on in macular degeneration is that when we eat too much omega-6 fat, our body is simply using that instead of the preferred omega-3.  When the omega-6’s are oxidised, their waste products are different to those produced by the omega-3’s.  This waste is not recognised by the RPE, not cleaned up by its immune function and accumulates as the drusen which lead to macular degeneration.

The only place we are likely to encounter significant quantities of omega-6 fats in our everyday life is in, well, everything.  Over the last two decades, the Australian Heart Foundation and the Dietitians Association of Australia (DAA) have been busily ensuring that the dominant health message in this country is that we should be eating those fats (rather than ‘unhealthy’ saturated fats).

The omega-6 fats occur in large quantities in ‘vegetable oils’ made from seeds (canola, cottonseed, soybean, sunflower, safflower, rice-bran and grape-seed).  And it is exactly those oils which now form the basis of every margarine, every fried food, every ‘ovenfry’ food, most biscuits, most breads, and most ‘heart-healthy’ products on sale in Australia today.

Faced with this research, the DAA’s response is exactly the same as their response to research that sugar is an extremely dangerous addition to our diet – denial.  Worse than that, their official position appears to be a rerun of a press-release provided by the Australian Oilseed Federation (the folks representing those with money to make out of seed oils).

Macular Degeneration is a debilitating disease which now affects a significant proportion of our population. The average Australia is four times more likely to suffer from macular degeneration than they are to suffer from Dementia.  One in seven Australians over the age of 50 (a little over a million people) has macular degeneration and this number is likely to increase by at least 70 per cent by 2030.

There is now significant evidence of the role of seed oils in the development of the disease.  But once again, the folks charged with looking out for our health are squarely on the side of their corporate sponsors.

Luckily there is something you can do without their assistance.  Don’t eat seed oils.

Image courtesy of dream designs at FreeDigitalPhotos.net

March 2, 2012
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It’s time to stop mainlining anti-cholesterol drugs

By | Big Fat Lies | 19 Comments

In Australia, statins (the class of drugs used to lower blood cholesterol) now chew up 13 per cent of the money paid out by the Pharmaceutical Benefits Scheme (PBS), and the amount shelled out for them by the Australian taxpayer (via the PBS) grew by a third in just the last year alone.

That’s a worry for taxpayers, but with one in three Australians over the age of 50 now taking them, a greater concern is that new research suggests statins significantly increase the risks of Type II Diabetes and dementia.

The United States Food and Drug Administration is worried enough about those little ‘side-effects’ to require that statins immediately carry warnings about diabetes and cognitive impairment.  But here in the land of nod, we’ve happily become the world’s biggest statin pill-poppers.

Don’t get me wrong.  Statins do work. The studies have shown that they do lower LDL cholesterol and they do reduce heart-disease in younger men who’ve already had a heart attack. But there’s a good deal of evidence to suggest that the benefits for these folks had nothing to do with the cholesterol-lowering and quite a lot to do with their blood-thinning properties.

Unfortunately (for drug marketers) ‘younger men who’ve already suffered a heart attack’ (and lived to tell the tale) is a very, very small market. The only way to turn a buck from statins was to convince doctors to prescribe it (and the PBS to fund it) for ‘prevention’ (among people whose only sign of illness is being diagnosed with a higher than ‘normal’ blood-cholesterol reading).

A comprehensive review published in 2007 of all of the major high-quality trials on statins concluded that for these not-sick people (who make up the overwhelming majority) taking statins did not alter the overall risk of dying at all.

The studies showed that we would need to treat 67 otherwise healthy people with statins for five years in order to prevent just one of them suffering a heart-disease event. This puts the drugs in the category of being almost completely ineffective. By way of comparison, we need to treat 11 people with antibiotics in order to completely cure 10 of them.

When the data were broken down by gender and age, the results became even less impressive. Statins delivered absolutely no benefit for women at all. And men aged over 69 (those most at risk of fatal heart attacks) enjoyed no benefits either. The only people the drug appeared to help were men aged 30–69, and then only by a very small absolute margin.

The reason for the disappointing results may be that statin drugs work by shutting down the enzyme we use to manufacture cholesterol.  Unfortunately we also use that same enzyme to manufacture one of our primary anti-oxidants, co-enzyme Q10. Shutting down cholesterol production also means shutting down Q10 production (and thereby impairing our ability to fight heart disease and other types of inflammation).

This might be why (although these drugs have a big effect on cholesterol levels) they have very limited effect on heart-disease outcomes. It might also be that although statins lower cholesterol, this has nothing to do with why they lower risks for people who’ve already had a heart attack. Just like aspirin, statins reduce clotting. And just like aspirin, the people who benefit the most from statins are those who’ve already suffered a heart attack. But no one will make a fortune selling aspirin at 97 cents a box.

However they are not merely harmless profiteering.  A series of studies has suggested relationships between statin usage and increased diabetes and cognitive impairment (dementia to you and me). And a significant independent analysis of the trials, conducted in 2011 by the ever reliable Cochrane Review, concluded that becasue of this doctors to be cautious in prescribing statins to people who hadn’t already had a heart attack.

Statins are powerful drugs that alter the function of important liver enzymes, and the evidence suggests that the only class of people who benefit are younger men who’ve already had a heart attack. The only people who should be given statins should be this very small group (and then only if their doctor feels the benefit outweighs the risk of diabetes and dementia).

The US regulators are ringing the alarm bells.  But here the Australian Heart Foundation is more concerned that not enough people are taking preventative medication.  The Australian Medical Association is much more cautious.  They say statins should only be prescribed to high risk patients.  Good advice, but clearly someone isn’t listening.  Heart disease rates are high but don’t come anywhere near needing to put a third of the over fifties on statins.

Meanwhile millions of Australians continue to take a drug they don’t need and which the evidence says significantly increases their chronic disease risks.  We need to stop slavishly following the drug marketing agenda.  The practise of mass (and accelerating) prescription of statins must stop immediately.

Note: Parts of this blog post were ‘borrowed’ from my new book Big Fat Lies.

Image courtesy of Paul / 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.

November 21, 2011
1

Are Mums really United in their love of Margarine?

By | Uncategorized | 10 Comments
The Australian Heart Foundation has found a new and even more devious way to entangle itself with the interests of the processed food industry. Its new “Mums United” campaign pretends to be a grassroots movement for healthy living. But it walks like a margarine advertisement and quacks like a margarine advertisement, so guess what it I think it is.
The Heart Foundation’s “Mums United” campaign asks mums to “change the shape of Australia.” No earth moving equipment is required so I suspect they mean they’ll change the shape of Australians. Apparently ‘Dads’ are not up to the task (or is it just that in the Heart Foundation’s world ‘mums’ do all the shopping?).
Putting aside its deeply patronising premise, mums can get going with their ‘fat-busting’ using some tips from the Heart Foundation. Tip #2 is to make sure mums use margarine instead of butter.
The campaign was only launched last month, but already it has received impressive media coverage and has a facebook group with over 4,500 followers. Selin Tas posted a link to her blog post which says “We finished our [Mum’s United] meeting pledging never to purchase butter again”.
And Selin is not the only one. The facebook page is full of mums posting stories of how they have organised groups of fellow mums and sworn off butter. The casual reader could easily come to the conclusion that the Heart Foundation has tapped into a throbbing artery of desire (among Australian mummy bloggers) to change the health of a nation (or at least to eat more margarine).
Except that (rather like the construction of sausages) it is better not to look too closely at the process. It turns out that Mums United is an advertising campaign.  Roberta Donovan, marketing director of the Heart Foundation explained to an advertising industry magazine “our campaign galvanises Mums into being part of an ongoing movement – one that sees Australians work together to achieve a healthy weight for the nation.”
The social media and word of mouth campaigns are being run through “conversation marketing agency” Soup. Their website tells us that they gave mummy bloggers “a $10 voucher” and asked them to “hit the supermarket and buy margarine instead.” Soup tells us that the “results were outstanding; most [mummy bloggers] reported … they have since made the switch to margarine …”
And Soup’s largesse doesn’t end there. Many of the bloggers report that Soup has sent them up to $350 of shopping cards to distribute as prizes to any readers who sign up to their facebook pages or comment on their Mums United blog posts.
It all sounds like a bonanza for the mummy bloggers and their readers (and at least according to Soup, its working). I asked the Heart Foundation who was paying for all of this. They told me that there are several social media campaigns being run by Soup on their behalf but they refused to say who was picking up the tab for any of them. All they would say is that companies entitled to use the tick can optionally get involved in “co-operative marketing” programs (like Mums United).
And this is by no means the only example of “co-operative marketing.” Last year the Heart Foundation was involved (judging by the prominent use of their logo) with a series of infomercial-type advertisements put together by Goodman Fielder (the manufacturer of Meadow Lea). The commercials featured a cardiologist who told us “what saturated fats can do to your child’s health”. He then goes on to suggest that we should switch to a margarine spread made with plant seeds.
You can still see the ad on a website called Spread the Facts which is “brought to you by Goodman Fielder” and which highlights the Heart Foundation’s recommendation that we swap margarine for butter.
The cosy relationship between margarine makers and the Heart Foundation is not new. In 2001, Bill Shrapnel (then a consultant nutritionist to Unilever Australia, maker of Flora margarine) pointed out that “Modern nutrition advice is one of the most negative influences on margarine consumption.” At the time, the Australian Healthy Eating Guidelines asked people to eat a low fat diet and this negatively impacted on margarine sales (as it is a visible source of fat).
But as Bill pointed out, things were improving (for the margarine manufacturers) because the Heart Foundation had just started recommending “an increase in the polyunsaturated fat content of the Australian diet of between 80 and 100 per cent.” He then suggested this represented “a rare opportunity” and that “[p]erhaps … margarine companies should consider assisting the Heart Foundation in its educational activities about dietary fats.” It looks like they listened to that very sage marketing advice.
The only trouble is that they Heart Foundation’s own analysis of the evidence does not support its “co-operative marketing.”  It is not hard to come away from the current campaign with the impression that eating less fat is good for your weight. But the Heart Foundation’s most recent (2003) position statement on the subject says exactly the opposite – “Dietary fat is not an independent risk factor for the development and progression of overweight and obesity. [my emphasis]”
And there’s absolutely no evidence that switching polyunsaturated fat for saturated fat will have any effect on weight whatsoever. That stands to reason. They are both fats, and they both deliver 9 calories per gram. As far as our digestive system is concerned they are identical.
Margarine can be legally sold in this country. And margarine companies are entitled to use every (legal) marketing tactic to sell their product. But why is our Heart Foundation rolling around in the marketplace with them? Why are they sneaking through the back alleys of the internet whipping up mummy blogger campaigns with gift cards? And why are they happy to create an impression about health benefits which they know not to be true? 
The Heart Foundation’s tick program generates money for a charity and I guess that’s a good thing. But it comes with a heavy price. Co-operative marketing means the Heart Foundation’s health halo is sullied by commercial interests. It means (whether they intend it or not) that the Foundation becomes a spokesperson for the processed food industry. And the result is that the foundation is less an independent umpire and more a player from the other team wearing the umpire’s uniform.
So do us all a favour Heart Foundation and give your tick (and the phoney campaigns that come with it) the flick.
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
3

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