Taking the challenge

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Today’s edition of Noosa River Living magazine is running a story about the book.  You’ll be relieved to know that, for once, it’s not just me banging on about fructose.  

Alan Hubbard, the journo who wrote the story, weighs in at 124.9 kgs and is Type II Diabetic.  Rather than take me at my word on what should happen to you once you stop eating fructose, he’s decided to put it to the test.  
Alan tells me the story is the first in a series that he plans to write documenting his trials and tribulations following the Sweet Poison message.  I’ll keep you posted as he updates his progress (as long as it’s positive, otherwise forget I even mentioned it).

Low Fat Diet = Heart Disease?

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I know most of you will have already read Fructose intake is a predictor of LDL particle size in overweight schoolchildren (published in the American Journal of Clinical Nutrition last October for those of you who missed it), but dust off your copy because I want to take a closer look. Grab a coffee, this is a long one.

I think the schoolchildren paper explains exactly why many things we have been told about Cholesterol could be wrong and why many of the people taking medication to lower it may be simply doing so for no better reason than to line the pockets of some underprivileged drug companies (a noble cause in itself, I admit).   The current treatment of arterial disease is based on restricting the intake of animal fat, with or without drugs.  But, there is mounting evidence that fructose plays an important role in modifying the fats in the blood in ways that block your arteries a lot more quickly.

That having been said, nothing in this post (or on this blog) should be taken to be medical advice.  Don’t rush out and cancel your medication (or your prescibed diet) unless your doctor tells you to.  But do by all means discuss the studies presented here with your doctor.

Ok, disclaimer over, let’s start from the start. Contrary to popular belief there is only one kind of cholesterol. There is no good, bad or even ugly cholesterol. There’s just cholesterol. Cholesterol is a fat and is therefore not soluble in water. Since our blood is a water-based solution this presents a bit of problem in the logistics department. Cholesterol needs to be transported from the liver (where it is made) to the places where it is needed (pretty much everywhere in the body – it’s used to make cell membranes). That’s where lipoproteins come in. The body packages the cholesterol with some proteins in a bundle of molecules ready for shipping.

Lipoproteins are the transport system for cholesterol (and other fats). There are five major groups of lipoproteins but I want to focus on the group that the doctors sometimes call ‘bad cholesterol’.

Lipoproteins are grouped by size. Low Density Lipoproteins or LDL particles are loosely packed (hence ‘low density’) and as a result, relatively large. LDL particles transport cholesterol manufactured in the liver out to the cells.

When a doctor says you have a bad cholesterol reading, she is talking about LDL being outside a target range (2.6 to 3.3 mmol/L). If you get too far out of that range (greater than 6.5 mmol/L), out will come the ‘script book and there is a good chance you will be prescribed a class of drugs called Statins (more on them in a later post) to lower your LDL cholesterol levels.

LDL particles also come in a range of sizes and people can be divided into two main groups according to which size is most common. Some people have mostly large LDL particles and some people have mostly small ones. The folks with the large particles are called Pattern A and the others, Pattern B. Whether you are Pattern A (large) or Pattern B (small) is largely a matter of genetics. If both your parents are Pattern A then you are more likely to be Pattern A and vice versa if they were both Pattern B.

Which pattern you are matters because if you are Pattern A, your LDL reading is not an indicator of the risk of heart disease. But Pattern B people are at considerable risk. It seems the small size of the Pattern B LDL particles means they are more easily embedded in the walls of blood vessels and this ultimately leads to the development of blockages.

In June 2000, Dr Krauss and his team over at the Lawrence Berkeley National Laboratory, Department of Molecular Medicine at UC-Berkeley published some very interesting results on experiments they had been doing on low-fat diets. What they found was that if you put a Pattern A person on an extreme low-fat diet (less than 25% of the Calories come from fat – the Pritikin diet for example, is 10%-15% fat), they change to Pattern B.

Let me just restate that because it is important. In June 2000, a study was published which showed that if you put some people on a low fat diet you INCREASED their risk of heart disease. This happened because you convert them from Pattern A (large) LDL to Pattern B (small) LDL particles. Did the media health experts forget to mention this as they merrily recommended low-fat foods?
As far as I can tell, Dr Krauss wasn’t concerned what else was in the diet, just that it was low fat. And this is where the article that started my little detour comes in. The schoolchildren paper from 2007 concludes:
“In school-age children, greater total and central adiposity [fatness] are associated with smaller LDL particle size and lower HDL cholesterol. Overweight children consume more fructose from sweets and sweetened drinks than do normal-weight children, and higher fructose intake predicts smaller LDL particle size.”

In other words, a child on a high fructose diet will have small (Pattern B) LDL particles and a child on a low fructose diet will not. Maybe the reason that Dr Krause’s low-fat diet was so destructive was not because of the fat itself but because the diet was by definition high carbohydrate (and therefore high fructose in our modern world)?

There’s a double whammy in all this. Most Low-fat foods you will encounter in the supermarket are higher in fructose than their full-fat equivalents. So whether it is the low-fat or the high fructose part of the diet that is causing the LDL particles to shrink, foods low in fat and high in fructose are probably not a good idea.

Unfortunately there are no cheap and easy tests for LDL particle size. But if this latest study is to be believed, maybe you don’t need to know.  Maybe all you need to know is that you can significantly reduce your risk of heart disease by not eating fructose. This is because this most recent study suggests that the amount of fructose in your diet so accurately predicts your LDL particle size (at least if you are a school age child).

This post has droned on for long enough so I won’t go into the studies that suggest that once again pre-menopausal women are protected from the effects of fructose on particle size. I’ll leave that for another day.

Image courtesy of Nutdanai Apikhomboonwaroot / FreeDigitalPhotos.net

Fluoride

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Experts continue to tell us that the solution to the obesity epidemic is to “reduce the consumption of harmful high-fat foods” and “encouraging people to walk more through consistent town and building planning“.  But not even the most insane of them will tell you that eating less fat and exercising more will stop tooth decay.  
Researchers have known since the 60s that tooth decay is caused by just one (Streptococcus Mutans, or SM) of the two to three hundred species of bacteria that inhabit our mouths. In hundreds of very well controlled studies, scientists were able to determine that feeding rats sucrose (table sugar) encouraged SM to produce decay, but feeding them pure glucose or fructose on their own did not.   
In Sweet Poison, I take a brief look at some of the studies which show that if you want to rot teeth, you need to use a constant wash of sugar solution (like soft drink or fruit juice).  The following article was left on the cutting room floor when the book was being put together but with the impending fluoridation of the drinking water in my home state of Queensland, I thought it was timely to share it with you.
The costs associated with treating the symptoms of the activity of SM have grown exponentially in the past five decades (strangely coincident with the growth of the soft drink and fruit juice industries). Governments, desperate to avoid the popular demand for them to pay the bill for a disease that affects everyone (that consumes sugar), have increasingly turned to the quick-fix solution of mass medication with fluoride. 
The chemical used most commonly for water fluoridation is fluorosilicic acid. It is produced as a co-product from the manufacture of phosphate fertilizers. In 2002, the World Health Organisation conducted a thorough review of the available data on the health effects of fluoride. The report concluded that there were clear reductions (12.5%) in the incidence of dental cavities in communities where water fluoridation occurred.   These numbers are borne out by a recent Australian study which show that the average six year old will have one less decayed tooth (which still leaves two) if there is fluoride in the water.  However, the number of decayed teeth in the mouth of a six year old increased by 11.4% between 1990 and 1999.  So the ‘benefit’ of fluoridation may be very short lived indeed.  If we’re lucky, we’ll halt the upward progress for a decade or so.  Not even the most wildly supportive research suggests that fluoridating drinking water completely cures tooth decay.  It is at most, a band-aid solution.  Nevertheless it is a band-aid solution which has it’s attractions to those we elect to administer our funds.
There is no denying that mass medication has an economic appeal.  Australia now spends 1 in every 10 health dollars on those white (well, yellowish) things in our mouths.  And it is estimated that in the decade between 1979 and 1989, the US saved $39 billion in dental health expenditure with water fluoridation which cost a fraction of that. 
But the WHO report also noted that the risk of dental and skeletal fluorosis was significantly increased in areas where the water was fluoridated.  The report noted that 90% of ingested fluoride is retained by the body, leading ultimately to an accumulation which produced fluorosis caused by the accumulation of fluoride in the structural matrix of bones and teeth. It causes the exact property (hardening) desired by the mass medicators and is very effective, when applied to the surface of teeth, at protecting them against the destructive work of SM (although there is some evidence that SM can mutate to avoid the effects of fluoride). 
The problem is that when it is swallowed it enters the bone (and tooth) internal structure. The risks associated with ingesting too much fluoride are so real that earlier this year the American Dental Association put out a warning to mothers not to mix infant feeding formula with fluoridated water.  For the rest of us, over time, the accumulation of excess fluoride creates extreme brittleness leading to crumbling teeth and easily broken bones.   The experts employed by governments will tell you that the evidence is inconclusive, and so it is.  The reason it’s inconclusive is that the damage is done over a lifetime and this is difficult to simulate with a chemical which has only been part of the food supply since the 50s in some states in the US, let alone less than two decades in even the most ‘advanced’ implementations anywhere else.
‘Fixing’ tooth decay by replacing an expensive dental treatment with an ultimately more expensive, treatment of elderly people suffering continuous fractures, understandably has political appeal to legislators with a three election time frame in mind.  Even then the ‘benefit’ appears to be that we simply delay the upward march of dental caries by one decade.  It is  uncontroversial of me to suggest that reducing or eliminating the constant intake of sucrose would almost completely eradicate the problem (and a few hundred much more serious health problems), but governments would prefer the easy way out.  
The benefits to government are obvious.  They can justify the closure of public dentistry facilities (such as school clinics) because they have ‘solved’ the problem.  They will tell us that there will be an immediate reduction in the need for dental services.  And there will probably be a consequent short-term reduction in the pressure on government to pay for or subsidise those services.  Best of all, the ‘treatment’ is administered without needing us to exercise any control or will-power.
It’s clearly a lot easier to mass medicate than to contemplate a ‘discussion’ with the soft drink and fruit juice industries but I know which I would rather the Government be doing …

Media Tart, the Sequel

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A few people have heard that I appeared on A Current Affair last night and asked that I post a link to the video – so here it is.

While I’m at it and in an effort to confine all this self-aggrandisement to just one (well now two) posts, here’s a link to a segment that also appeared last night on Brisbane Extra.
There … done … now back to looking for more evidence in the case against fructose.

Agave

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It’s all the rage in California and now in London.  Agave is pitched as the ‘natural’ alternative to all that awful processed sugar.  But what is it?  

No so long ago, this Mexican desert plant’s only contribution to the betterment of mankind was as the basis for Tequila.  Agave Syrup (or nectar if you are from the right side of the tracks) is a different kettle of fish to the stuff fermented for imbibers.  If you just do a little bit of processing, you can turn Agave juice into a light syrup which is 90% fructose, making it very sweet indeed.  Voila, now food manufacturers can use loads of it in their ‘natural’ and ‘organic’ foods without that nasty word ‘sugar’ appearing in the ingredients list.  

Watch out for Agave Syrup – it might as well say ‘Pure Fructose’.

The Exercise Myth

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I know this is going to come as a real shock to you, but apparently Australians have gotten quite a bit fatter in the last decade.  A report released today reveals that in the last decade alone the number of overweight and obese Aussie’s jumped from 41.1% in 1998 to 59.3% now.  If we keep going at this rate we’ll no doubt all soon be visible on satellite pictures.

The usual response to this kind of report is that we all need to do more exercise.  One Federal MP even wants to make exercise compulsory at least two nights a week.  And oddly fitness instructors think that’s “a step in the right direction“.  
So if exercise is the answer, we must have just not been listening for the last ten years right?  Well, actually, no.  According to the Australian Sports Commission, in 2006, two thirds of us exercised at least once a week and almost 43% of us participated in sport three or more times a week.  These numbers were only slightly lower than their equivalents in 1999 (the first year the report was prepared), but should be treated with caution as they are based on self-completed survey forms.  Everyone tends to exercise more when filling out survey forms.
As with most things, money may be a more reliable indicator.  According to the Australian Bureau of Statistics, between 1998 and 2004 our spending on sporting equipment increased by 18.8% (in constant 2004 dollars).  A big chunk of this was because we spent more on swimming pools but there was also a 92% increase in gym fees! 
Even today’s report (accusing us all of being fatty boombahs) sheepishly admits that 69 per cent of children met the physical activity guidelines of at least one hour of moderate or vigorous exercise each day.

Even in the US, where all kinds of unwelcome records are being set for obesity, the figures don’t match the spin.  According to the National Federation of State High School Associations, the number of students participating in high school athletics has just increased for the 19th consecutive year.  And it’s not just the kids.  Their parents have been spending up big on sports gear.  Sporting apparel sales are up 35.3% since 2000 and sports shoe sales are up 44.2%.  But it’s not all about looking good.  Sports equipment sales more than doubled between 1990 and 2008 (from $30b to almost $70b).

Perhaps we are just enrolling in gyms and filling our cupboards with gym equipment and stuff to make us look like we exercise – it happens.  A better test would be a fitness activity that we pay for only when it is really used.  Personal training is a very high growth industry in the US and Australia.  In  1999 there were 127,310 personal trainers in the US.  That figure had almost doubled to 219,990 in 2007.  Australian data is a little less granular but shows a similar trend.  In the 2006 census, 13,800 people said there were employed as fitness instructors up from 7,669 in the 1996 census.

It looks an awful lot like we’ve been doing what the ‘experts’ tell us for quite some time.  And where has it gotten us?  Fatter and sicker and getting worse by the minute.  Time for a rethink, perhaps?

Goaties

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There’s a Goatie shortage where I live.  I hope it’s fixed soon.  

Goaties are delicious sweets that I discovered shortly after deciding that I could never eat fructose again.  In Sweet Poison I suggest that its not that hard for food manufacturers to switch to glucose sweetened food rather than sugar/fructose sweetening.  Well Goaties are living proof of that.  
They normally reside in the health food section of my local Coles, but alas there appears to have been a run on the Goatie supplies.  Recent communiques from loyal readers suggest the supply problem is widespread, with Goaties missing in action in all corners.  
The company that makes them still appears to exist, so I hold out hope that the current problems are temporary.  Long live the Goaties!

Media Tart

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It’s been a busy week on the hustings for me (hey, let’s face it one interview would be busy for a media amateur like me) with three bits of media stuff (that’s a technical term) hitting the streets.
I spoke to Steve Austin on ABC Statewide (QLD) on Tuesday night.  Steve has very kindly posted a recording of the interview in his blog.
On Wednesday this month’s issue of Slimming and Health Magazine came out with a terrific (and lengthy) summary of some of the ‘how to’ aspects of the book.  It’s not available online, but you can get it from most supermarkets and newsagents.
On Thursday the Sunshine Coast Daily came out with this story with a nice photo of some the kids and I.

Fructose and Menopause

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In the book I briefly mentioned that there is research indicating that men and post-menopausal women are the ones most affected by fructose.  I theorised that perhaps what was protecting pre-menopausal women was oestrogen.  I based that thinking on a line of research which started with a 1966 study by Dr MacDonald from the Guy’s Hospital Medical School in London.

Dr MacDonald fed a mixed group of pre and post menopausal women and some men solutions which were either glucose or fructose loaded.  He noticed that the men and post-menopausal women on the fructose diet had increased fatty acids in the blood.  This confirmed what rat studies had shown at around the same time – pre-menopausal women (and rats) were in some way immune to the most dangerous effects of fructose.
I was very pleased to notice the other day that a very recent study has picked up on that line of research.  The study by the Lausanne University School of Biology and Medicine, Switzerland has just been published in the June edition of Diabetes Care, the magazine of the American Diabetes Association.
The new study confirms Dr MacDonald’s work but gives some even more detailed findings.  Not only are circulating fatty acids lower in pre-menopausal women, they do not develop insulin resistance.  Both these things happened as expected in the male counterparts.  
The researchers called for more research given this was a very small (16 people) and short (6 day) study.  But interestingly they speculated as to the reason for the difference and suggested that it might be that pre-menopausal women appear to be extremely efficient at converting the fatty acids created by fructose into leg fat.  This rapid creation of leg fat seemed to provide protection against the more dangerous aspects of fructose feeding (insulin resistance and tummy fat).
So in a nutshell, something about menopause (and I speculate it’s the sudden decrease in oestrogen) caused women’s bodies to start acting like men’s when it comes to fructose.  They stop storing leg fat, start storing tummy fat and start developing insulin resistance and blocked arteries.   A fat bottom may not be the most desirable thing in the fashion world, but as far as nasty little diseases go, its much better that the fructose make its way there than stay in the arteries (as fat).
Quite a few readers have emailed telling me that menopause became a whole lot more bearable as soon as they stopped eating fructose.  Strangely, male researchers have so far seemed disinclined to look too hard at associations between menopause and fructose.  But this latest research does suggest there is some kind of link between fructose metabolism and pre-menopausal hormones.  
There appears to be alot of anecdotal evidence suggesting women not consume sugar during menopause.  Various sites suggest keeping the sugar intake low will reduce the impact of hot flushes and other symptoms.  So far I haven’t been able to pin down any reputable scientific source for this thinking.  I intend to keep looking further at this.  I’ll post what I find … 

Losing weight the easy way

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Thank you to all the people who take the time to send me feedback about Sweet Poison.  I especially like hearing about how reading the book has changed people’s lives.  The email quoted below is an example of exactly that:

… just a quick note to let you know what has happened since reading your book.

I bought the book on the 31/08/08. I started to change my habits immediately. I only had to make some small changes as I don’t eat a lot of junk food, but here’s what’s happened.
 
I have been trying to lose a few kilos for about a year, I exercise most days and try to do all the right things but nothing. I have lost 2.5 kgs, lost 3cm of my waist and 2cm off my hips in only a few weeks!! I can’t believe it, and all I did was cut out a few things.

No more plain biscuits at work with my coffee, I have a selection of nuts instead. I tossed all my “low fat” muesli bars in the bin and changed my breakfast to oats as recommended by you.

That’s it, nothing else. I kept up the exercise but I  now do it because it helps me start the day not to lose weight.

I still have a little more weight to lose but at least I know that it can be done. It amazes me how something so “sweet” can turn evil once it hits your system. I can’t wait to jump on the scales in a few more weeks once I start to get a bit more savvy with reading labels on products. I’m sure more weight will drop off once I get the hang of working out what is actually in food.

Thank you for such a great book. I am actually reading it a second time. 

Keep up the blog, I love reading your updates.