I think it is becoming clear that the collection of problems known as metabolic syndrome appear to centre around liver pathology. I accidentally ended up in these posts via iron overload and MODY1 of all things. Anyway, here's an introduction to the strange world of alcohol research in lab rats.
First I've got to apologise for these next few posts. They are mostly based around rats, fed by surgically implanted gastric canulae, with bizarre diets formulated to be fed as a liquid by constant rate infusion 23 out of 24h a day. Don't ask me why the rats got an hour off! I have to admit that I personally think lab rats are more like humans than many other observers do, but that may be because I've had so many of them as pets over the years. These rats do a number of things which are supposed to be impossible and a number which are just interesting.
Before we go to alcohol, lets just look at saturated fat and weight gain. These diets are isolacoric to the nth degree. There is no need to correct for caloric intake. They all got the same, 23/7. So we are not talking appetite here, just calories in vs calories out. All diets were 45% fat with protein and carbs also held constant. The table doesn't specifiy but you can be certain that the carbohydrate will be glucose or a glucose precursor. If you are looking at alcoholic cirrhosis you're not going to feed fructose!
Table 1 gives you the diet composition. That 45% of calories from fat was either pure corn oil or had increasing amounts replaced by a mix of beef and MCT fats. The highest saturated fat group had 30% of calories from saturated fat and 15% from corn oil.
Table 3 gives you the weight gain. Just look at the control groups: "Eat" corn oil as your sole source of fat and you gain 5.5g/d. Replace some of that corn oil with 10% of calories from saturated fat and there is a similar weight gain but go to 20% of calories as saturated fat and weight gain drops to 4.9g/d and go to 30% of calories from saturated fat and weight gain is 3.8g/d.
Under isocaloric conditions, simply switching from something quite like butter or coconut oil to "heart healthy" sunflower oil will make you FAT. Of course if you are used to eating butter and someone cooked your eggs in yellow boot polish you might lose weight because you would spit the "food" out on the floor anyway!
The rats got no choice. Corn oil fattens relative to a beef/coconut fat mixture.
Now it's worth looking at the effect of alcohol on liver pathology. This is best shown in Figure 2.
Without alcohol the lipid composition of the diet has no effect on liver pathology (small black bars). Replace carbohydrate with ethanol and the lipid source of the diet determines you liver pathology. Corn oil is catastrophic. By the time you are eating 30% of your calories as saturated fat and only 15% as corn oil your liver is almost OK. I leave it to anyone's eye to follow the trend and think about a diet which has 45% of it's calories as saturated fat and none as corn oil.
To me the message is clear. In the presence of ethanol the determinant of your liver pathology is the amount of corn oil you "drink". Fish oil does the same, the next few posts all use fish oil.
If anyone thinks that fructose is different to alcohol in it's effect on the liver, you're wrong!
I think the Food Standards Agency in the UK must have some sort of shares in liver transplantation programs or hardware.
Oh, another aspect of this study; at a given level of corn oil the weight gain was always less in the alcohol group than in the control group. Alcohol calories were being substituted for carbohydrate calories. Alcohol is not insulogenic, carbohydrate is. I'd expect alcohol to be associated with less weight gain as blood insulin levels would be lower. Come back Gary Taubes. You wus right agin! Dr Jebb, it's not a closed system.