Fructans (inulin)

By | Sugar | 7 Comments

If you’ve been anywhere near a naturopath or a health food store in the last five years, you will have probably come across the message that fructans are good for you.  A few people have asked me how or if they are related to fructose and what I think of them.

In a nutshell, the answer is that (like most things) I am happy to eat fructans au naturelle (in the original vegetables that contain them), but I don’t want them added to everything else just to get a ‘healthy’ looking label.  I will be avoiding things that have fructans added and here is why.

Plants convert sunlight to energy by creating sugars.  The two primary sugar molecules are fructose and glucose.  To store this energy, plants join these simple sugars together in long chains.  Chains which are mostly glucose are called glucans.

Cellulose, the hard stringy indigestible bits of plants we usually call fibre is a glucan.  Starch is another important glucan which we encounter most in our daily diet.  It forms the foundation for most of the carbohydrates, we eat.  Animals (like us) also store energy as glucans.  When we have too much glucose in our blood, we create glycogen (a glucan) and store it around our livers as a short term supply of glucose (to get us through between antelope kills).

Chains which are mostly fructose are called fructans.  Nobody knows why some plants store their sugar as fructans and others as glucans but researchers speculate that given the types of plants that do it, it might have something to do with drought tolerance.  Fructans are most common in Onions and other tubers like Chicory but they are also in Barley, Wheat, Artichokes and Asparagus.  They are present to some degree in about 15% of plants.

Fructans are less well known, but one that you might have seen popping up on the ingredients list of some foods is Inulin (yes, inulin NOT insulin).  Inulin is a chain of about 60 fructose molecules and one glucose molecule.

Humans (and most other mammals) do not have the enzymes (chopping shears) necessary to cut up a fructan like inulin.  We do have enzymes for sugar, fructose, glucose and starch, so when we eat those sugars, they get dealt with immediately in our small intestine (with disastrous consequences in the case of fructose).

But when we eat inulin it sails straight through our small intestine and becomes pet-food for the bacteria that inhabit our large intestine.  Our little passengers love the stuff, chomping away furiously on it and converting it into fatty acids (which we then absorb into our blood stream) and gases (which we … well, you get the picture).

Because feeding gut bacteria encourages them to multiply, inulin is sometimes described as a prebiotic (something that increases the number of good bacteria in our gut).  Prebiotics are different from probiotics (like Yakult) which are just more bacteria in a bottle.

Inulin has been very thoroughly researched because food manufacturers want to include it in many foods.  All of the research to date suggests that at no point does the fructose get liberated by our digestive system.  We just don’t possess the required cutting shears.  Our gut bacteria do, but they use the fructose to fuel themselves rather than us.

Because we can’t digest inulin (directly at least), food manufacturers have managed to convince food regulators the world over (including Australia and the US) to allow them to describe inulin as fibre on food labels (rather than as a sugar, which is chemically what it is).

Manufacturers want to put inulin in our food for one very good reason.  Health? No.  Flavour?  No.  Marketing?  Yes.

Inulin tastes slightly sweet (and so reduces the amount of other sugars required) but it counts as fibre rather than sugar on the label.  This combined with the fact it can be advertised as a prebiotic makes the food sound healthier.  An example of a food that uses inulin in this way is Bakers Delight’s Hi-Fibre Lo-GI White Bread.

Yoghurt manufacturers like Vaalia like to use it because it allows them to lower the fat content (on the label at least) without affecting the ‘mouth feel’.  Inulin has a mouth feel similar to fat, so if it is included as a fat substitute they can use less sugar to compensate for the lack of fat.  This gives the marketing advantage of being able to say the product is low fat, high fibre and low(er) sugar.

Diet purveyors like Tony Ferguson use inulin because it has the useful property of masking the aftertaste of artificial sweeteners and they can also promote the product as being a healthy fibre rich prebiotic.

In summary then, fructans are choc full of fructose but our digestive systems can’t get at it directly.  Instead our gut bacteria digest it for us.  But the fatty acids created by the bacteria do eventually find their way into our bloodstream.  And some of the latest research (see the August 2008 edition of Pancreas Journal – there’s a nice little stocking filler for Christmas) says that fatty acids released in this way may not trigger an appetite suppressing response (unlike normal dietary fat, which does).

This means that we could just be skinning the cat another way.  Whether bacteria fill our arteries with fatty acids (when we digest fructans) or our liver does the job (when we digest fructose) is probably beside the point if neither of them trigger a hormonal response that suppresses our appetite.

I’m not happy that we know enough about fructans (and in particular inulin) to be certain that their effect on our bodies is not just as bad as pure fructose.

I’ll be avoiding foods that contain them.  This doesn’t mean I’ll be avoiding onion and asparagus.  I figure we are adapted to eat fructans in the small quantities contained in those foods (just as we are adapted to eat whole fruit).  But I will be avoiding bread, yoghurt and anything else that includes Chicory, Inulin, Fructo-oligosaccharide or FOS on the label as an added ingredient.

Low Fat Diet = Heart Disease?

By | Big Fat Lies, Sugar | 2 Comments

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

Fructose and Babies

By | Sugar | 2 Comments

A very interesting piece of research has just been published in Obesity on suckling rats.  Just in case you haven’t picked your copy from the News-agent, I thought I’d mention it here.

Now I know that a bunch (herd?) of suckling rats is quite different from from breast-feeding humans.  For starters we have two less legs (and quite a few less breasts).  But in the past, rat experiments involving fructose have produced identical results to subsequent human trials, so this research should not be dismissed out of hand.

The rat pups were divided into four groups:

  1. The Control group were left in peace to suckle from their mother’s teat;
  2. The Formula  group were given yummy rat milk substitute;
  3. The Fructose group were given the same as the Formula group but had some fructose mixed in.
  4. The Galactose group were also given the same as the Formula group but they got some extra galactose.

At three weeks, the pups were weaned and put on to a normal rat food diet until they turned eight weeks old (about 5 years old in human terms).  At that point the researchers changed the rat food for half the Control group by ensuring that they received 65% of their calories from fructose.  This continued until the study ended after 12 weeks.  By then the rats were the equivalent of eight years old.  So some rats were just fed fructose for the first three weeks of their lives (while suckling) and then given a normal diet and they were compared to rats that had a normal diet until they were the equivalent of 5 years old when they were switched to a high fructose diet.

The rats that started life with fructose added to their formula were fatter than all of the other groups right through to the end of the study.  Remember these rats were on healthy diets from weaning onwards and had no exposure to fructose beyond the suckling period.  They were even fatter than the poor rats that were put on a 65% fructose diet (which is a lot even by our fructose infused standards).

Worse than that, the group fed fructose during suckling also had the worst results for insulin resistance and muscular fatty acid uptake.  These last two are sure signs of insulin resistance in humans (and rats) which ultimately leads to Type II diabetes.

The study concludes that “Consuming fructose during suckling may result in lifelong changes in body weight, insulin secretion, and fatty acid transport involving CD36 in muscle and ultimately promote insulin resistance.”  Suckling equates to the breast-feeding period in humans.  If these results translate to us, it suggests that a child receiving fructose during the first year of its life may be programmed from day one for obesity and Type II Diabetes.

This study builds on a much earlier study done by the New Jersey Medical School (in 1997) which I mentioned in Sweet Poison.  They noticed that suckling rats exhibit an immunity to fructose.  But in the that study, the researchers were also able to make the pups take up more of the fructose by introducing it earlier in their diets (during suckling), thereby effectively destroying what little protection they had against the stuff.

Now all of this would be merely interesting (at least for rat aficionados) were it not for the fact that some humans do feed babies fructose during the breast feeding period.  As far as we know, breast milk does not contain fructose but some of the substitutes for it definitely do.  Many Soy formulas (about 20% of the US market) contain sucrose (which is 50% fructose) instead of lactose (which contains no fructose).

And these new results back up a 2005 study by the Children’s Hospital of Philadelphia involving 653 formula fed babies (after they had grown up) which concluded that:

“In formula-fed infants, weight gain during the first week of life may be a critical determinant for the development of obesity several decades later. These results contribute to the understanding of chronic disease programming and suggest new approaches to obesity prevention.”

I know this latest study is just a bunch of fat rats but it doesn’t look good for formula fed babies if the formula contains fructose or if breastfeeding is being supplemented with fruit juices or other sources of fructose.