A SUGARY TALE - Part One

[Guest guest]

A SUGARY TALE

(First article in a series on 'type II diabetes')

By Red Flags Columnist, Dr. Malcolm Kendrick

( email - malcolm@... )

For the last thirty years, give or take, people with type II diabetes have

been instructed to eat a low fat high carbohydrate diet. Why? Because it is

'known' that a high fat diet causes heart disease. It is also known that

people with type II diabetes have a greatly increased chance of dying of

heart disease (true). Ergo, type II diabetics should not eat fat.

And so, most people with type II diabetes now slavishly follow a diet that

is, in all likelihood, doing them considerable damage, based on a misguided

belief that fat in the diet is harmful. In reality, the last thing that

someone with type II diabetes should do is eat a high carbohydrate diet.

I know that, for most people, this sounds utterly counter-intuitive. But I

would like to take you on a journey into the world of type II diabetes, one

that I have travelled over the last two years. It's a bit of a winding path,

primarily because a lot of misinformation needs to be unwound before it is

possible to re-start with a clear slate.

I hope that, at the end of this journey, you will understand what type II

diabetes actually is. In truth, I hope you will understand that there is no

such disease as type II diabetes, that there is no such thing as insulin

resistance, and that almost everything you think you know about this area

is, not so much wrong, as tangled up in a big mess.

The start

I became interested in type II diabetes as a result of my fascination with

heart disease. I knew that there was a strong connection between the two,

and so I realised that I had better find out more about type II diabetes.

What it was exactly, what caused it, that sort of thing.

At first sight the disease process itself seemed very simple. As you get

fatter, the body, in an attempt to fight back, becomes more resistant to the

effects of insulin. At one level this makes sense. The main function of

insulin is to switch on various food storage mechanisms in the body, so if

you can block these actions you can, presumably, fight against weight gain.

The downside, of course, is that sugar levels go up, as sugar is trapped in

the blood.

Like many others I nodded sagely when resistin - a direct antagonist to

insulin released by fat cells - was discovered. It seemed that a simple

negative feedback loop was in operation with the body battling against

excess food storage through 'insulin resistance.' By golly, it all made

sense.

Then, one day, I thought about it a bit more, and started mentally picking

at something that looked like a small flaw, a loop in the jumper if you

like. After a bit more picking the entire jumper suddenly fell apart in my

hands, and I realised that what had looked like a fine upper body garment

was, in fact, just a set of disconnected loops made to look like a jumper.

As I gazed at the metaphorical unravelled ball of wool lying at my

metaphorical feet, I knew that the simple model linking obesity to insulin

resistance and type II diabetes made no sense at all.

So I had to gather up my thinking and start again, from the beginning -

which is a very good place to start. And I began by looking more deeply into

obesity, and what effects it should have on insulin release and insulin

sensitivity.

At its most simple level obesity can be thought of in the following way. If

energy input is greater than energy output you will put on weight.

Therefore, to lose weight you can reduce input, or increase output. Which

may seem like a statement of the obvious.

What may be less obvious is that insulin has absolutely no effect on either

of these things. Insulin does not (except perhaps in the most minor fashion)

reduce hunger, or block food absorption. Nor does it increase the metabolic

rate. Nor does it stimulate you to go out and take exercise. Nor can it

force the body to excrete energy - the body has no system for excreting

energy anyway.

Therefore, if you become resistant to the effects of insulin, and levels

rise, what exactly happens to prevent weight gain? Nothing much would seem

to be the answer. All of the food you eat will still be absorbed, and once

absorbed it has to be stored somewhere.

At this point it is probably worth running through the energy storage

systems in the body, before returning to the main argument.

There are, basically, three forms of stored energy, and three places they

can be stored.

Energy can be stored as

Glucose/glycogen (glycogen is a whole bunch of glucose molecules stuck

together - think of it as concentrated glucose)

Triglycerides (Three fat molecules attached to a glycerol. Glycerol is a

half of a glucose molecule)

Protein (Not really an energy store unless you are starving, in which case

protein is broken down into amino acids, transported to the liver and

converted to glucose)

Energy can be stored in:

Muscle. Muscle can store about two thousand calories of fat and one thousand

calories of glycogen (and a lot of protein obviously)

Liver. The liver can store about five hundred calories of fat and the same

amount of glycogen

Adipose tissue. Adipose tissue can store hundreds of thousands of calories

of fat/triglyceride

And that's it. There are no other forms of energy (of any significance), and

nowhere else to store it.

If, as you get fatter, muscle, liver and adipose tissue become resistant to

the effects of insulin, where does the excess energy go?

Well, as you have probably worked out, there is nowhere else for it to go

but adipose tissue. You can't squeeze more energy into the muscles or the

liver, they can't take it (not quite true, you can end up with a fatty

liver, but this still represents a minute amount of the total energy store).

The brain kidneys and lungs cannot store energy. It doesn't go into bones,

and it certainly can't disappear into thin air.

Thus, whilst insulin resistance does make it more difficult (if that's the

right word) to store excess energy as fat, it will still happen anyway,

because there is no alternative. So what, exactly, is the point of that?

As I hope is now obvious, once you start thinking about it, it becomes clear

that insulin resistance can do nothing to prevent obesity (this was my loop

in the jumper). Which means that insulin resistance does not represent an

adaptation, or negative feedback loop, designed to prevent obesity. Or, if

it is, then it is the most stupid feedback loop discovered. Because it can't

work.

In short, there is no way that obesity, or a raised BMI, can be linked in

any simple fashion to type II diabetes.

Yet, and yet, when you study this area there seems little doubt that an

increasing BMI does appear to be the most important risk factor for

developing insulin resistant diabetes - type II diabetes. For example, women

with a BMI of more than thirty five have a ninety times increased risk of

developing type II diabetes, versus women with a BMI less than twenty five.

On the other hand, if you have a BMI of about twenty two (slim), you have

almost no chance of developing type II diabetes.

If these were the only pieces of data that you had, then it would seem

reasonable to suggest that obesity is the cause of type II diabetes.

However, there are plenty of other data that don't fit so neatly, if at all.

However, by the time these bits of data emerged the mainstream had made its

mind up. Obesity causes diabetes. And so, rather than open up the area for

another look, all contradictory data has been made to fit, which has created

a confused mess.

So, what is the contradictory data, exactly. The first problem, which is not

exactly contradictory, is that most obese people do not suffer from

diabetes. Which suggests that obesity is not sufficient to cause diabetes.

We do not have a simple causal relationship. You may not think that this is

a huge problem, some people are just more susceptible than others - hold

that thought.

A much more fundamental problem is that you can find non-obese populations

who have high rates of insulin resistance. Emigrant Asian Indians, for

example, have a frighteningly high rate of type II diabetes although they

are much less obese, on average, than the surrounding Caucasian populations.

This is also true for emigrant Japanese in Brazil and the USA, Australian

Aboriginals, and Native Americans - and others too numerous to mention.

So, although it is true that obese people are much more likely to get type

II diabetes than thin people. It is also true that most obese people do not

have type II diabetes, and you can also find several non-obese populations

suffering from very high rates of type II diabetes. Which means that obesity

is neither sufficient, nor even necessary, for type II diabetes to develop.

And, if you keep looking, the association between obesity and diabetes

fragments even further. For example, if you remove more than twenty five

pounds of fat through liposuction this has no impact whatsoever on sugar

levels/insulin resistance. On the other hand if you lose twenty five pounds

on a diet, this will almost completely reverse insulin resistance (at least

temporarily). Um?

And looking at the Japanese again, we find that Sumo wrestlers - who have

BMIs that put them in the super-obese category - have no signs of insulin

resistance at all. I could go on, but that's enough contradictions for now.

So how would you go about fitting all of these facts together? In general,

when you find direct contradictions to your central hypothesis you have two

choices.

Choice one is to develop an ad-hoc hypothesis to explain each contradiction.

Choice two is to rip up the model and start again. The mainstream research

community decided to go down the ad-hoc hypothesis route.

For example.

Question: Why do emigrant Asian Indians have such a high rate of type II

diabetes (up to 60% in some studies), despite having much lower BMIs than

Caucasians.

Answer: They are genetically susceptible to developing type II diabetes;

therefore we need to re-define obesity in this population. Let's lower the

'obese' BMI to twenty five instead of thirty. (In this way, they fit back

into the hypothesis)

Genetics always provides a good catch all explanation for almost any

contradiction. If you find an obese group with low rates of type II diabetes

they are 'genetically protected', if you find a group with high rates of

type II diabetes despite being non-obese they are 'genetically susceptible'.

Ergo, when you find that Australian Aboriginals have an even higher rate of

type II diabetes, with an even lower average BMI than Emigrant Asian

Indians, you can lower the BMI that defines obesity in this population to

around twenty two (which has happened). This is known as stretching the

hypothesis to fit the facts.

By constantly redefining obesity, you can still claim that obesity is the

underlying cause of type II diabetes in all populations. (You may recognise

this 'altering the boundaries of normal' technique from the Cholesterol

hypothesis. Keep lowering the level considered raised until everyone has a

raised level).

Oh yes, genes are most wonderful things. They can explain away contradiction

after contradiction (so long as you don't think about it too hard). It's

like playing a joker in a game of cards; you can never lose when you invoke

genetics.

Apart from genetics, there are many other ad-hoc hypotheses that are thrown

into this particular mix to explain away other contradictions. However,

rather than going through them all, one by one, I chose the opposite

approach.

I decided to rip the central hypothesis up and start again. See if I could

find another, better, hypothesis. One where the facts all fit snugly into

the hypothesis, rather than the other way round. This is always my preferred

route.

But in order to travel down this route you have to question everything, even

the things that seem written in stone.

Here are four, almost sacrilegious, questions that I asked myself.

Question one: does obesity cause diabetes?

Question two: is there such a disease as type II diabetes?

Question three: is there such a thing as insulin resistance?

Question four: Is the blood sugar level important, or is it a red

herring?

And you know what, after doing this, everything started to fall into place,

although I had to spend several months learning a great deal more about

human physiology and energy metabolism.