http://atkins.com/science/researchsummaries/liver.html
You might also find this article informative. Its kinda technical but explains it well.
WHY THE ATKINS DIET IS HEALTHY
By RFD Columnist Malcolm Kendrick MbChB, MRCGP
(email - malcolm~llp.org.uk )
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.
Overworked kiddney's?
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