Chris Kresser and Chris Masterjohn discuss cholesterol in 3 podcast episodes the third episode here there first two are linked in the comments. You can find more at Chris Materjohn's blog at the Weston A Price Foundation website is also a great source regarding cholesterol He also writes the blog "The Daily Lipid" which is a great source of information.

My fuzzy recollection on the theory is that high carb = inflammatory = body raises triglycerides to counteract. Low carb = anti-inflammatory = less triglycerides.

I don't recall if that theory panned out, or it was some other mechanism.

I don't believe triglycerides are formed in the blood, I thought it was in the liver.

As I understand it triglycerides (triacylglycerols) are formed in the liver and adipose tissue (fat cells). When the body uses stored fat as an energy source the triglycerides are broken back down into glycerol and fatty acids and then are released into the bloodstream to be used as fuel. In their triglyceride structure they are too large to pass through the cell walls.

What I personally don't understand is where or how the glycerol is produced, but I have read in various places that glycerol 3-phosphate is produced by burning glucose. This I understand as the reason for reducing carbohydrate, that less glycerol 3-phosphate is produced and thus fewer triglycerides are then formed and stored.

This is why in my head (and it is most likely wrong) a person could do one or the other. That being either eating a high-fat/low-carb diet or a high-carb/low-fat diet. A high-fat/high-carb diet is going to set things up for large scale triglyceride formation and storage, where as the other two will reduce this. I am still trying to find someone to tell me if this is a load of rubbish or actually the case.

I think this is why high-carb/low-fat vegetarians stay slim, simply there are fewer free fatty-acids present. And with high-fat/low-carb people there are fewer glycerol 3-phosphate/glycerols present.

Like I said I could be completely mistaken here, so please take it as merely a guess from the information I have attained so far.

Glycerol is basically half a glucose molecule. Two triglycerides give 6 fatty acids and 1 glucose (okay the glycerol has to be converted, but the math still holds).

When you eat high carb, you will have excess glucose that has to go somewhere. The body doesn't like high blood glucose levels. It will first replenish glycogen. But if you are not very active there may not be any room to store much glycogen in liver or muscle. Secondly, the ratio of glucose to fat burned by various tissues will increase slightly. Third, excess glucose goes to the liver and fat cells to be converted to triglycerides for longer term storage. This is why high carb diets create more triglycerides than low carb diets.

And for a discussion of what happens when you eat fat, I will quote wikipedia:

"Triglycerides, as major components of very-low-density lipoprotein (VLDL) and chylomicrons, play an important role in metabolism as energy sources and transporters of dietary fat. They contain more than twice as much energy (9 kcal/g or 38 kJ/g ) as carbohydrates and proteins. In the intestine, triglycerides are split into monoacylglycerol and free fatty acids in a process called lipolysis, with the secretion of lipases and bile, which are subsequently moved to absorptive enterocytes, cells lining the intestines. The triglycerides are rebuilt in the enterocytes from their fragments and packaged together with cholesterol and proteins to form chylomicrons. These are excreted from the cells and collected by the lymph system and transported to the large vessels near the heart before being mixed into the blood. Various tissues can capture the chylomicrons, releasing the triglycerides to be used as a source of energy. Fat and liver cells can synthesize and store triglycerides. When the body requires fatty acids as an energy source, the hormone glucagon signals the breakdown of the triglycerides by hormone-sensitive lipase to release free fatty acids. As the brain cannot utilize fatty acids as an energy source (unless converted to a ketone), the glycerol component of triglycerides can be converted into glucose, via glycolysis by conversion into Dihydroxyacetone phosphate and then into Glyceraldehyde 3-phosphate, for brain fuel when it is broken down. Fat cells may also be broken down for that reason, if the brain's needs ever outweigh the body's.

"Triglycerides cannot pass through cell membranes freely. Special enzymes on the walls of blood vessels called lipoprotein lipases must break down triglycerides into free fatty acids and glycerol. Fatty acids can then be taken up by cells via the fatty acid transporter (FAT)."

Without as many carbs, more fat will be burned as a ratio of glucose/fat. Triglycerides will come mostly from dietary and body fat. So as long as you don't eat supranormal amounts of fat the overall Trig number should come down.

Fat is also digested more slowly (via bile/emulsification) and enters the system more slowly (lymphatic) which probably has an effect on the overall numbers. Anyway, by eliminating a major source of Trigs, the number is bound to come down.

One point often forgotten when we talk about triglycerides is that we measure fasted triglycerides. The insulin released from glucose, the fat/triglycerides drived from fructose, the triglyceride spike from dietary fat, all of that happened hours ago (10-12 hours usually). Consider fasting blood glucose, carb consumption 12 hours ago doesn't increase it.

Nick, a lot of those ideas might make sense if fasting blood glucose and triglycerides among healthy people are correlated. But this isn't the case as low carbers tend to have slightly higher glucose and slightly lower triglycerides, while high carbers are the opposite.

There are probably two main factors: the rate of triglycerides entering the bloodstream and the rate of clearance (converted to FFAs and then burned/metabolised). The enterance is mostly related to weight and weight loss. The clearance is related to your mitochondria's capacity to burn fats (beta-oxidation).

People who have high triglycerides (unless losing weight) likely have mitochondrial dysfunction - their mitochondria aren't burning fats well. To compensate for poor fat metabolism they crave sugar constantly and we call them sugar burners (one can have a high carb diet and still be a fat burner).

When people with mitochondrial dysfunction (sugar burners) go on a low carb diet they probably will get low carb flu. This is simply because their mitochondria can't supply all the energy they need.

But after a week or so (depends on the extent of damage) something happens, our low carb dieter gets their energy back and more, low carb flu is a thing of the past. This happens because low carb diets, ketogenic diets especially increase mitochondrial biogenesis (growth of new mitochondria). Many nutrients in meat (which low carb diets are generally rich in) support mitochondrial function and some also increase mitochondrial biogenesis. Low carb flu goes once sufficient mitochondria grow to meet the demands of fat metabolism.

Once our low carb dieter stops losing weight their triglycerides will return to a healthy level. In my opinion this is the best explanation for how high carb diets don't necessarily cause obesity or metabolic damage, how low carb flu exists, how low carb diets aid in weight loss and how low carb diets reduce triglycerides. That being said if someone has good mitochondria and eats high carb their triglycerides will still be good (consider Durianrider, 700g of fructose, 7,000 calories at about 90% carb yet triglycerides of 70 mg/dl).

May I suggest my blog series:
http://carbsanity.blogspot.com/2011/05/where-do-triglycerides-come-from-part-i.html http://carbsanity.blogspot.com/2011/06/where-do-triglycerides-come-from-part.html http://carbsanity.blogspot.com/2011/08/where-do-triglycerides-come-from-part.html

The major source of fatty acids in fasting triglycerides (almost entirely in the form of VLDL) is circulating free fatty acids, NEFA. My theory on why low carbers have low circulating trigs is that either (a) the liver stores more rather than releasing them, and/or (b) the liver esterifies (3 FA's + glycerol -> TAG) less NEFA leaving higher circulating concentrations. At least during weight loss, LC fails to suppress NEFA release from fat tissue and levels are elevated chronically. So on the production side, fewer are made. Something about higher carb/lower fat intake reduces the uptake of VLDL triglycerides from circulation. Perhaps with higher NEFA, this fosters more VLDL to be cleared/ taken up by adipose tissue.

Here is another piece to your puzzle.

http://themedicalbiochemistrypage.org/lipid-synthesis.html

In short form, triglycerides are synthesized mainly at the adipocytes. Glucose is needed for the synthesis to take place. From this I take a leap of faith: if blood glucose levels are depressed - as in low carb dieting - triglyceride formation is inhibited.

The liver may be involved (though I'm still looking for that smoking gun that shows how fructose could possibly be involved in this) and dietary glycerols may be involved (there is some evidence that triglycerides are synthesized at the point digested fats and glycerol enter the bloodstream at the small intestine). But the above mechanism of free fatty acid reaction at the adipose explains the role of underfeeding carbohydrates on lowering TG's. Perhaps too conveniently.....hack away....