?How does it lower your cholesterol?

Just wondering how having a low carb lifestyle lowers cholesterol. I
have heard many stories of this and I just wanted to know exactly how
that works.

Just wondering how having a low carb lifestyle lowers cholesterol. I
have heard many stories of this and I just wanted to know exactly how
that works.

AFAIK

- by weight loss (the most important part I think)
- by reducing transfats intake (reduces oxidised LDL)
- by reducing glycemic load (reduces triglycerids, which AFAIK leads to
increasing HDL and reducing liver synthetised LDL).
- by increasing good fat intake (if you care, of course
- by increasing antioxidant intake (if you are not JC who thinks that
vegetables are not necessary

Mirek

P.S.: So far, my TC increased

"Mirek Fidler" wrote in message
...
Just wondering how having a low carb lifestyle lowers cholesterol. I
have heard many stories of this and I just wanted to know exactly how
that works.

AFAIK

- by weight loss (the most important part I think)
- by reducing transfats intake (reduces oxidised LDL)
- by reducing glycemic load (reduces triglycerids, which AFAIK leads to
increasing HDL and reducing liver synthetised LDL).
- by increasing good fat intake (if you care, of course
- by increasing antioxidant intake (if you are not JC who thinks that
vegetables are not necessary

Mirek

P.S.: So far, my TC increased

This sounds about right. Some combination of the diet/exercise/weight loss
really improved my cholesterol levels.

Here's why low carbing can lower blood sugar. Explanation courtesy of Dr.
Bernstein's book, Dr. Bernstein's Diabetes Solution.

When you have high blood sugars glucose bonds to proteins in the blood
stream. After 24 hours, these bond can solidify and become permanent. This
is called "glycation." One of the proteins glucose bonds to is the protein
part of a blood fat (lipid) molecule. This is the part of the lipid that
docks with cell receptors. Once this protein becomes glycated, the cells
that hook up to it in order to remove cholesterol from the blood stream can
no longer recognize it, so the cholesterol isn't removed and builds up.

When you lower your carbs very significantly, your blood sugar normalizes,
glycation goes way, way down and hence your body is more able to remove the
cholesterol from the blood.

It is worth noting that if your cholesterol goes down via low carbing, it
may be a hint that you are running higher blood sugars than is healthy for
you. I discuss this in my article
http://www.geocities.com/jenny_the_bean/risk.htm

-- Jenny - Low Carbing for 4 years. At goal for weight. Type 2 diabetes,
hba1c 5.2.
Cut the carbs to respond to my email address!

Low carb facts and figures, my weight-loss photos, tips, recipes,
strategies for dealing with diabetes and more at
http://www.geocities.com/jenny_the_bean/

Looking for help controlling your blood sugar?
Visit http://www.alt-support-diabetes.org/...0Diagnosed.htm



"*AmBeR*" wrote in message
om...
Just wondering how having a low carb lifestyle lowers cholesterol. I
have heard many stories of this and I just wanted to know exactly how
that works.

"*AmBeR*" wrote in message
om...
Just wondering how having a low carb lifestyle lowers cholesterol. I
have heard many stories of this and I just wanted to know exactly how
that works.

I'm not sure, but I think the cholesterol you eat is not as nasty as the
cholesterol the body would make to replace it, if you didn't eat
cholesterol.

Also, I think that just being much less obese somehow causes cholesterol
levels to be lower.

"Cubit" wrote in message
. com...
"*AmBeR*" wrote in message
om...
Just wondering how having a low carb lifestyle lowers cholesterol. I
have heard many stories of this and I just wanted to know exactly how
that works.

I'm not sure, but I think the cholesterol you eat is not as nasty as the
cholesterol the body would make to replace it, if you didn't eat
cholesterol.

Also, I think that just being much less obese somehow causes cholesterol
levels to be lower.


I am not sure, but this is how I think it works.....
Cholesterol is a form of a fat, yes?
When we eat no or low carbs, the body is then forced to burn fat for fuel.
Less fat to end up floating around the bloodstream?

--
Evelyn

(To reply to me personally, remove sox)

(*AmBeR*) wrote:

Just wondering how having a low carb lifestyle lowers cholesterol. I
have heard many stories of this and I just wanted to know exactly how
that works.

It isn't well understood and there is such widespread bias against
low-carb diets in the medical and research communities that few have
bothered to study it in the last 135 years since low-carb diets have
been in existence.

I can tell you my brother went on Induction for most of 5 months and
lost 40 lbs. At the start his doctor proclaimed that Atkins was
"bull****" the moment my brother mentioned it to him. The doctor
immediately put him on a month of cholesterol medication because he
was eating too much fat & cholesterol & his numbers were high(had been
for a while). By the 4th month he had not returned to the medication,
his numbers were down and his doctor simply told him "keep doing what
you are doing". (how does crow taste?)

The other problem is the bias that modern medical and research have
created in the public with little accuracy. Many might remember back
when all fats were bad. Then some fats were declared good even healthy
and saturated were the evils of the day. Now a specific transfat is
the evil doer. One might look back and realize that the information in
the past was misleaading at the least. Fats aren't simply bad for you,
but our culture has been bombarded with this over simplified message
for decades. Undoing that damage will take decades.

It wasn't until the last month of research that I found out that the
body MANUFACTURES cholesterol! As a troubleshooter my mind instantly
realized this was a critical fact in understanding anything about
cholesterol--how much does the body make compared to consumption? if
you eat no cholesterol what level do you maintain(fasting level)? why
does the body make it? it must either have a purpose or be a
byproduct? if a byproduct, what is the cause? What do I eat that
causes the body to make it? If it is a waste byproduct how is my body
designed to get rid of it? If it has a purpose, what controls how much
i make? Without all these answers everybody is just shooting in the
dark. I found only one page that said that 80% of the body's
cholesterol is made not consumed. If accurate, that means
low-cholesterol diets are bull****! since if you went totally
cholesterol free you'd only reduce your numbers by 20%.

If you are concerned don't have your bolld tested for the first six
weeks on the diet. Atkins says the results are very erratic for the
first month+ on the diet. You coudl find it scary high or artificially
low. At the two month point you may want to get another blood test. By
then your body will have settled into a more stable pattern as will
your eating habits. First few weeks I ate more eggs. Now less, simply
because eggs at breakfast every morning can get boring. I've reverted
to mostly skipping breakfast which was normal my entire life.
DiGiTAL_ViNYL (no email)
350/331/200
Atkins since 1/12/2004

This was interesting. It gets to the technical bits at the end.


http://www.redflagsweekly.com/
WHY THE ATKINS DIET IS HEALTHY

By RFD Columnist Malcolm Kendrick MbChB, MRCGP

(email - )

I was idly watching a programme on the Atkins diet last night which, to my
surprise, was reasonably balanced. Yes folks, the Atkins diet has crossed the
pond to reach the United Kingdom. Although, in reality, all it is doing is
returning. After all we invented it nearly one hundred and fifty years ago.

A man called Banting promoted a diet pretty much indistinguishable from that of
Atkins in 1863. In fact, the verb to ‘bant’ is used in Sweden as a term for
going on a diet

To find out more about the Banting diet (now known as the Atkins diet) go here

Anyway, reasonably balanced or not, on this programme there was still an
unquestioned view that, even if the Atkins diet did help with weight loss, it
was still damaging to health. It would cause kidney disease, and osteoporosis
and heart disease. Various professors of nutrition were wheeled out to condemn
the Atkins diet as dangerous nonsense.

Ignoring the kidney disease and the osteoporosis for now, the nutritional
professors made the usual statements. For example, ‘It is known that
saturated fat increases the level of blood cholesterol and causes CHD.’ They
didn’t quote any evidence for this. As far as they were concerned it is just
a known fact.

Well, what is the evidence that a diet high in saturated fat raises your
cholesterol level? Where does it come from? The Framingham Study? That world
famous study that is quoted by medical experts around the world.

"In Framingham, Massachusetts, the more saturated fat one ate, the more
cholesterol one ate, the more calories one ate, the lower people's serum
cholesterol...� Dr William Castelli 1992 (Director of the Framingham study)

So the evidence obviously didn’t come from Framingham. What about studies in
children? These poor vulnerable imps, where the damage is first being done?
Just to get a bit of genetic diversity into the equation, let’s look at
Chinese children first.

‘Children in the intervention group were fed with low-cholesterol and
low-saturated fatty acid diet, and the control group with normal diet. The
duration of intervention was three months. Compared with the control group,
serum cholesterol levels of children under intervention were not significantly
changed. Total cholesterol: 4.64 (186dg/ml) vs 4.68 (188dg/ml) mmol/L LDL: 2.66
(107dg/ml) vs 2.62 (106dg/ml).’ Zhu WL et al Zhonghua Liu Xing Bing Xue Za
Zhi. 2003 Sep

Then children in the UK:

‘Unexpectedly, significant inverse associations were found between the
dietary content of saturated fatty acids on the one hand and the serum
concentrations of cholesterol… on the other.’ Samuelson G et al Br J Nutr
Mar 2001

The reality is that, in many different studies, it has been shown that the more
saturated fat you eat, the lower your cholesterol - although the difference is
not that great. Of potentially greater importance is that a high fat diet has a
more significant effect on raising HDL and lowering VLDL. Which is supposed to
be very healthy indeed.

Consider this extract from the University of Pennsylvania:

‘The Atkins Diet limits carbohydrates but permits unrestricted amounts of
protein and fat. Compared to a conventional, high-carbohydrate, low-calorie
approach… at one year, the Atkins dieters had significantly greater increases
in good cholesterol (HDL) and greater decreases in triglycerides (VLDL).’

I’m sorry that I can’t present you with anything much from PubMed (the
bible of mainstream medical research) about this. But as others may have
discovered, any paper that supports the Atkins diet has no abstract attached in
PubMed – you just get blanks. Did someone use the word censorship? Not me
your honour. I would never dream of saying such a thing.

Now, anyone who has read my scribbles before will realise that I don’t think
the level of any lipid in your blood makes the slightest difference to the rate
of CHD. But most other people do, so I think it is worth explaining why a high
fat diet will automatically raise HDL and lower triglycerides.

A fact, by the way, that seems to have created stunned surprise amongst many
researchers when results from the Atkins diet were published. Which just shows
that they need to go back and read their textbooks again.

In order to understand why a high fat diet should, and does, raise HDL levels
and lower VLDL levels (and may also lower LDL levels), you need to understand a
bit about fat and sugar metabolism and the role of lipoproteins in your blood.
Starting here.

When you eat fat it is absorbed by the gut and stuffed into very large
lipoprotein known as a chylomicron. The fat in a chylomicron is almost all
stored in the form of three fat molecules attached to a glycerol molecule, a
structure known as a triglyceride. Three fats and a glycerol = tri-glyceride.
By the way, cholesterol also sits in chylomicrons as a co-passenger. (Anything
insoluble in water/blood, such as cholesterol, has to be carried around in a
lipoprotein)Chylomicrons are then released into the bloodstream and travel
through the body losing chunks of triglyceride all the while as they pass fat
cells. (Fat cells attack chylomicrons with a ‘lipase’ enzyme, chopping bits
off). As this happens chylomicrons shrink, turning into Very Low Density
Lipoproteins (VLDLs), which are otherwise known as…
‘triglycerides.’ How confusing is that?

In fact, the nomenclature in this area must be the most confusing in all of
medicine.

LDL is known as ‘bad’ cholesterol
HDL is called ‘good’ cholesterol
VLDLs are named triglycerides…
It’s little wonder that most people haven’t the faintest idea what anyone
is talking about in lipid metabolism. Chylomicrons, VLDL, HDL and LDL are all
lipoproteins. I wish that people would stop calling them things like
‘cholesterol’ and triglycerides’, and ‘good’ cholesterol and
‘bad’ cholesterol. It really doesn’t aid understanding.

Anyway, moving on. Apart from chylomicrons, the gut also sends out VLDLs
de-novo, and the VLDLs do pretty much the same thing as chylomicrons, dropping
off triglycerides here and there (mainly into fat cells) and shrinking. Quite
what the difference is between a shrunk down chylomicron and a VLDL is, I
don’t know. (By the way, just in case you’re wondering, VLDLs also contain
cholesterol as a co-passenger. All lipoproteins have cholesterol in them)

Not all chylomicrons and VLDLs travel round dropping off triglycerides. Some go
straight to the liver where they are absorbed, broken down, and unpacked. And
their contents are used to make other things the body needs.

However, wherever they go, all of the ‘fat containing’ chylomicrons and
VLDLs produced by the gut drop off their fat load, shrink, are then absorbed
and completely disappear. So a few hours after a meal they are gone. And if you
were to measure VLDL levels a few hours after a high fat meal they would have
returned to ‘normal’. Whatever normal may be.

Thus, if you eat a high fat meal, almost all sign of it will have disappeared
in a relatively short space of time. And there will be no change in any lipid
level. Or at least not any lipid level that anyone can be bothered measuring.

However, if you eat a high carbohydrate meal, the metabolism acts in a very
different way. Carbohydrates are absorbed and transformed into sugars in the
gut, from whence they go straight into the bloodstream, same as fat. But
because sugars are soluble in water they don’t need to be carried in a
lipoprotein, so there is no immediate effect on lipid levels from a high carb
meal. You just get a sharp rise in blood sugar level.

A certain amount of the sugar will be absorbed into fat and muscle cells, and
then stored as glycogen. But if you eat a big carbohydrate meal, the fat and
muscle storage cannot cope, and the excess sugar has to be absorbed by the
liver to prevent the sugar level getting too high.


However, the liver cannot store that much sugar, so it starts to convert it
into fats, in the form of triglyceride. At which point, the liver then packs
this excess triglyceride into a VLDL and sends it out into the bloodstream -
along with some cholesterol. (Unlike with sharks, the liver in humans is not an
energy storage organ)

So you get a kind of delayed VLDL rise after eating carbohydrates. But there is
a key difference between the VLDL made by the guts, and the VLDL made by the
Liver. The VLDL made by the liver, unlike that made in the gut, shrinks into a
low density lipoprotein (LDL). The dreaded heart disease causing lipoprotein
– the one they call co-lest-erol.

Why does this happen to ‘liver manufactured VLDL’, when it doesn’t happen
to the VLDL made in the gut? Well, as liver manufactured VLDL leaves the liver,
it interacts with an HDL molecule which transfers it’s proteins to the VLDL
molecule. One of the proteins transferred is apolipoprotein B-100. And the apo
B-100 molecule is the unique LDL ‘identifier.’

On the other hand, VLDL made in the gut has apolipoprotein B-48 attached to it
and this VLDL doesn’t become an LDL molecule as it shrinks.

Now, if you are not already completely confused, I will explain what this
means.

Rewind. If you eat fat, it is absorbed from the gut, packed into chylomicrons
and ‘VLDL B-48s,’ and transported around the body and then got rid of.
Gone. So immediately after a high fat meal you will have a very high
triglyceride level, made up of VLDL B-48, but this will fall relatively
rapidly. Importantly, there can, and will be no effect on HDL or LDL levels.
And so if you measure the lipid levels in the fasting state (which is when such
things are measured) you will find nothing at
all after a high fat meal.

On the other hand, if you eat a high carbohydrate meal, the level of VLDL B-48
will not rise. But some time later, the liver will start converting excess
sugar into fat and sending this out in VLDL B-100 molecules. And this process
can go on for many hours after a meal. So the VLDL level may still be high when
you measure it.

In addition to finding a high VLDL you should also find a low HDL. Because, for
each VLDL the liver makes, an HDL hands over its proteins and disappears. So
the more VLDL the liver makes, the less HDL you will have. Cause and effect.

Also, as you may have noted. If the VLDL B-100 all ends up as LDL, the more
VLDL the liver makes, the higher the LDL level is likely to be.

Therefore, if someone is on a high carbohydrate diet, they should automatically
have a raised VLDL level, a reduced HDL level and quite possibly a raised LDL
level.

Golly gee whiz. A high fat diet reduces VLDL, raises HDL and may even lower
LDL. And a high carbohydrate diet does the exact opposite. In short, the
metabolism does exactly what you would expect it to.

So you see. Atkins was right all along. Even if he didn’t appear to know why.

LCing since 12/01/03-
Me- 265/226/140
& hubby- 310/248/180

Thanks.
Excellent piece of information, there are threee points of vagueness
for me.

1) HDL, what is considered an HDL and where does it comes from. The
term HDL only figures in the explanation when describing the VLDL
B-100's absorbing existing HDLs. But there is no explanation of
where/why the HDL exists or what created them. HDLs have the B100
identifier which passes to liver creating VLDL B-100s, which will
become bad LDL. At first I thought HDLs were simply the new
fat-stuffed chylomicrons. But the presnece of B100 means that as they
reduce they would become an VLDL B100, same as liver produced VLDLs.

2) Cholesterol. Does all Chylomicrons-B48s from the gut have
cholesterol or does it depend upon diet. Does evey liver produced
VLDL-B100 have cholesterol--is it produced there by the demand of
converting sugar to fat?

3) VLDL and LDLs have cholesterol in them. VLDL are "absorbed" or used
by the liver. What happens to the cholesterol in them? Waste, clogged
arteries, recycled back into the blood stream? If every lipoprotein
has insoluble cholesterol (is that a requirement?) then there is a
concern of what happens to it when the VLDL is absorbed.


(LCer09) wrote:

This was interesting. It gets to the technical bits at the end.


http://www.redflagsweekly.com/
WHY THE ATKINS DIET IS HEALTHY

By RFD Columnist Malcolm Kendrick MbChB, MRCGP

(email - )

I was idly watching a programme on the Atkins diet last night which, to my
surprise, was reasonably balanced. Yes folks, the Atkins diet has crossed the
pond to reach the United Kingdom. Although, in reality, all it is doing is
returning. After all we invented it nearly one hundred and fifty years ago.

A man called Banting promoted a diet pretty much indistinguishable from that of
Atkins in 1863. In fact, the verb to ‘bant’ is used in Sweden as a term for
going on a diet

To find out more about the Banting diet (now known as the Atkins diet) go here

Anyway, reasonably balanced or not, on this programme there was still an
unquestioned view that, even if the Atkins diet did help with weight loss, it
was still damaging to health. It would cause kidney disease, and osteoporosis
and heart disease. Various professors of nutrition were wheeled out to condemn
the Atkins diet as dangerous nonsense.

Ignoring the kidney disease and the osteoporosis for now, the nutritional
professors made the usual statements. For example, ‘It is known that
saturated fat increases the level of blood cholesterol and causes CHD.’ They
didn’t quote any evidence for this. As far as they were concerned it is just
a known fact.

Well, what is the evidence that a diet high in saturated fat raises your
cholesterol level? Where does it come from? The Framingham Study? That world
famous study that is quoted by medical experts around the world.

"In Framingham, Massachusetts, the more saturated fat one ate, the more
cholesterol one ate, the more calories one ate, the lower people's serum
cholesterol...” Dr William Castelli 1992 (Director of the Framingham study)

So the evidence obviously didn’t come from Framingham. What about studies in
children? These poor vulnerable imps, where the damage is first being done?
Just to get a bit of genetic diversity into the equation, let’s look at
Chinese children first.

‘Children in the intervention group were fed with low-cholesterol and
low-saturated fatty acid diet, and the control group with normal diet. The
duration of intervention was three months. Compared with the control group,
serum cholesterol levels of children under intervention were not significantly
changed. Total cholesterol: 4.64 (186dg/ml) vs 4.68 (188dg/ml) mmol/L LDL: 2.66
(107dg/ml) vs 2.62 (106dg/ml).’ Zhu WL et al Zhonghua Liu Xing Bing Xue Za
Zhi. 2003 Sep

Then children in the UK:

‘Unexpectedly, significant inverse associations were found between the
dietary content of saturated fatty acids on the one hand and the serum
concentrations of cholesterol… on the other.’ Samuelson G et al Br J Nutr
Mar 2001

The reality is that, in many different studies, it has been shown that the more
saturated fat you eat, the lower your cholesterol - although the difference is
not that great. Of potentially greater importance is that a high fat diet has a
more significant effect on raising HDL and lowering VLDL. Which is supposed to
be very healthy indeed.

Consider this extract from the University of Pennsylvania:

‘The Atkins Diet limits carbohydrates but permits unrestricted amounts of
protein and fat. Compared to a conventional, high-carbohydrate, low-calorie
approach… at one year, the Atkins dieters had significantly greater increases
in good cholesterol (HDL) and greater decreases in triglycerides (VLDL).’

I’m sorry that I can’t present you with anything much from PubMed (the
bible of mainstream medical research) about this. But as others may have
discovered, any paper that supports the Atkins diet has no abstract attached in
PubMed – you just get blanks. Did someone use the word censorship? Not me
your honour. I would never dream of saying such a thing.

Now, anyone who has read my scribbles before will realise that I don’t think
the level of any lipid in your blood makes the slightest difference to the rate
of CHD. But most other people do, so I think it is worth explaining why a high
fat diet will automatically raise HDL and lower triglycerides.

A fact, by the way, that seems to have created stunned surprise amongst many
researchers when results from the Atkins diet were published. Which just shows
that they need to go back and read their textbooks again.

In order to understand why a high fat diet should, and does, raise HDL levels
and lower VLDL levels (and may also lower LDL levels), you need to understand a
bit about fat and sugar metabolism and the role of lipoproteins in your blood.
Starting here.

When you eat fat it is absorbed by the gut and stuffed into very large
lipoprotein known as a chylomicron. The fat in a chylomicron is almost all
stored in the form of three fat molecules attached to a glycerol molecule, a
structure known as a triglyceride. Three fats and a glycerol = tri-glyceride.
By the way, cholesterol also sits in chylomicrons as a co-passenger. (Anything
insoluble in water/blood, such as cholesterol, has to be carried around in a
lipoprotein)Chylomicrons are then released into the bloodstream and travel
through the body losing chunks of triglyceride all the while as they pass fat
cells. (Fat cells attack chylomicrons with a ‘lipase’ enzyme, chopping bits
off). As this happens chylomicrons shrink, turning into Very Low Density
Lipoproteins (VLDLs), which are otherwise known as…
‘triglycerides.’ How confusing is that?

In fact, the nomenclature in this area must be the most confusing in all of
medicine.

LDL is known as ‘bad’ cholesterol
HDL is called ‘good’ cholesterol
VLDLs are named triglycerides…
It’s little wonder that most people haven’t the faintest idea what anyone
is talking about in lipid metabolism. Chylomicrons, VLDL, HDL and LDL are all
lipoproteins. I wish that people would stop calling them things like
‘cholesterol’ and triglycerides’, and ‘good’ cholesterol and
‘bad’ cholesterol. It really doesn’t aid understanding.

Anyway, moving on. Apart from chylomicrons, the gut also sends out VLDLs
de-novo, and the VLDLs do pretty much the same thing as chylomicrons, dropping
off triglycerides here and there (mainly into fat cells) and shrinking. Quite
what the difference is between a shrunk down chylomicron and a VLDL is, I
don’t know. (By the way, just in case you’re wondering, VLDLs also contain
cholesterol as a co-passenger. All lipoproteins have cholesterol in them)

Not all chylomicrons and VLDLs travel round dropping off triglycerides. Some go
straight to the liver where they are absorbed, broken down, and unpacked. And
their contents are used to make other things the body needs.

However, wherever they go, all of the ‘fat containing’ chylomicrons and
VLDLs produced by the gut drop off their fat load, shrink, are then absorbed
and completely disappear. So a few hours after a meal they are gone. And if you
were to measure VLDL levels a few hours after a high fat meal they would have
returned to ‘normal’. Whatever normal may be.

Thus, if you eat a high fat meal, almost all sign of it will have disappeared
in a relatively short space of time. And there will be no change in any lipid
level. Or at least not any lipid level that anyone can be bothered measuring.

However, if you eat a high carbohydrate meal, the metabolism acts in a very
different way. Carbohydrates are absorbed and transformed into sugars in the
gut, from whence they go straight into the bloodstream, same as fat. But
because sugars are soluble in water they don’t need to be carried in a
lipoprotein, so there is no immediate effect on lipid levels from a high carb
meal. You just get a sharp rise in blood sugar level.

A certain amount of the sugar will be absorbed into fat and muscle cells, and
then stored as glycogen. But if you eat a big carbohydrate meal, the fat and
muscle storage cannot cope, and the excess sugar has to be absorbed by the
liver to prevent the sugar level getting too high.


However, the liver cannot store that much sugar, so it starts to convert it
into fats, in the form of triglyceride. At which point, the liver then packs
this excess triglyceride into a VLDL and sends it out into the bloodstream -
along with some cholesterol. (Unlike with sharks, the liver in humans is not an
energy storage organ)

So you get a kind of delayed VLDL rise after eating carbohydrates. But there is
a key difference between the VLDL made by the guts, and the VLDL made by the
Liver. The VLDL made by the liver, unlike that made in the gut, shrinks into a
low density lipoprotein (LDL). The dreaded heart disease causing lipoprotein
– the one they call co-lest-erol.

Why does this happen to ‘liver manufactured VLDL’, when it doesn’t happen
to the VLDL made in the gut? Well, as liver manufactured VLDL leaves the liver,
it interacts with an HDL molecule which transfers it’s proteins to the VLDL
molecule. One of the proteins transferred is apolipoprotein B-100. And the apo
B-100 molecule is the unique LDL ‘identifier.’

On the other hand, VLDL made in the gut has apolipoprotein B-48 attached to it
and this VLDL doesn’t become an LDL molecule as it shrinks.

Now, if you are not already completely confused, I will explain what this
means.

Rewind. If you eat fat, it is absorbed from the gut, packed into chylomicrons
and ‘VLDL B-48s,’ and transported around the body and then got rid of.
Gone. So immediately after a high fat meal you will have a very high
triglyceride level, made up of VLDL B-48, but this will fall relatively
rapidly. Importantly, there can, and will be no effect on HDL or LDL levels.
And so if you measure the lipid levels in the fasting state (which is when such
things are measured) you will find nothing at
all after a high fat meal.

On the other hand, if you eat a high carbohydrate meal, the level of VLDL B-48
will not rise. But some time later, the liver will start converting excess
sugar into fat and sending this out in VLDL B-100 molecules. And this process
can go on for many hours after a meal. So the VLDL level may still be high when
you measure it.

In addition to finding a high VLDL you should also find a low HDL. Because, for
each VLDL the liver makes, an HDL hands over its proteins and disappears. So
the more VLDL the liver makes, the less HDL you will have. Cause and effect.

Also, as you may have noted. If the VLDL B-100 all ends up as LDL, the more
VLDL the liver makes, the higher the LDL level is likely to be.

Therefore, if someone is on a high carbohydrate diet, they should automatically
have a raised VLDL level, a reduced HDL level and quite possibly a raised LDL
level.

Golly gee whiz. A high fat diet reduces VLDL, raises HDL and may even lower
LDL. And a high carbohydrate diet does the exact opposite. In short, the
metabolism does exactly what you would expect it to.

So you see. Atkins was right all along. Even if he didn’t appear to know why.

LCing since 12/01/03-
Me- 265/226/140
& hubby- 310/248/180

DiGiTAL_ViNYL (no email)
350/328/200
Atkins since 1/12/2004

Thanks.
Excellent piece of information, there are threee points of vagueness
for me.

Whoa. I read it and thought it was interesting. I didn't write it. LOL!

LCing since 12/01/03-
Me- 265/226/140
& hubby- 310/248/180