where does dietary fat go?

Crisseyda

This question has been floating around in my head for a while. I have come to partial answer, and I was wondering if you all had any resources to better explain the physiology.

1. Glucose is water-soluble, and high levels in the blood are detrimental. So the body signals the alarm, releases insulin, and stores that stuff away pretty quick.

2. Fat is not water-soluble and can only be transported in the blood in little packets: chylomicrons, LDL, HDL, etc. High levels of fat in the blood are not harmful. The dietary fat is circulated through the body, processed by the liver a few times, circulated again. When insulin levels are low, it is preferentially directed to muscle tissues (and away from storage tissue); when insulin levels are high, it is preferentially directed to adipose tissue (and away from muscle tissue).

So... my theory is that on a ketogenic diet, when insulin levels stay low, the fat just sort of hangs out in the blood and waits for the muscles and other tissues to use it. My question is: how many hours? How long can it hang out there?

To me, this also partially explains the appetite suppression on a ketogenic diet. The food just lasts longer in the bloodstream. It's available for a longer period as a source of energy.

LINIA

Don't know why, but agree am certainly a lot less hungry--- it's nice to be able to ignore cookies and ice cream. KETO must be how we are meant to eat.

wabmester

Volek did a study you might like. Fat levels in the blood are actually lower on a high-fat diet compared to a high-carb diet.

https://news.osu.edu/news/2014/11/21/study-doubling-saturated-fat-in-the-diet-does-not-increase-saturated-fat-in-blood/

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0113605

The results show that dietary and plasma saturated fat are not related....

So circulating fat doesn't seem to suppress hunger. In fact, one of the markers of metabolic syndrome is high circulating fat.

Crisseyda

@wabmester

I'm talking about levels of fat during the postprandial period. When the doc draws your lipid panel, you've got to fast for 12 hrs prior, or it's not accurate. Glucose is cleared out much faster then fat (especially in the presence of low insulin levels, where the fat is not directed to adipose tissue).

Metabolic syndrome is characterized by insulin resistance, which means high insulin levels. In the case of metabolic syndrome the free fatty acids are chronically elevated. It's like the system is backed up at all levels and the fat has nowhere to go. The excess insulin is both promoting the liver to create new fat (from sugar), while at the same time blocking that fat from muscles and directing it to stored fat.

In a normal person, you would rarely see high triglycerides and high glucose elevated at the same time for an extended period because insulin would put them both away; however, in someone who ate a low carb meal, free fatty acids would be increased as they are available for the body to use them as a source of fuel. I feel like the main point is that fat as a fuel is more effective than carbohydrate because the body can only tolerate a certain amount of glucose in the bloodstream (just a few grams) before it tries to rectify the situation and turn that glucose into fat. Fat, however, is not inflammatory--however, in the presence of inflammation certain types of fat are more easily oxidized (but that's another discussion entirely).

Great study btw.

wabmester

You bring up some good points. Let's start with insulin and glucose.

First, insulin affects more than glucose. It also drives fat into adipose tissue, for example.

Taubes and Ludwig suggest that high-carb meals cause an increase in hunger. Insulin overshoots and drives sugar so low that you can end up with hypoglycemia a few hours after a meal. It also drives fat into adipose, making that energy unavailable. Their theory was that this causes you to become more hungry on a high-carb diet.

So in their world, LCHF doesn't have a magical satiety effect. It allows us to have a NORMAL response, and the high-carb response is ABNORMAL.

Of course, it's a lot more complicated than that. For example, if we're insulin resistant, then as you note, both circulating glucose and fat levels are always high, so we should never get hungry! But we do.

Leptin has a role. It's supposed to down-regulate hunger when we have plenty of STORED fat, but it fails for many overweight people. Why? Perhaps we become leptin resistant, and low-carb somehow improves leptin sensitivity.

Then you have to consider the GI tract. It secretes several hormones that regulate appetite. One of the main differences between high-carb and low-carb is digestion times. The longer digestion takes, the more "full" we are. Protein may be especially satiating partly for that reason.

Finally, the brain has a role. Processed foods, especially, are engineered to drive the brain nuts in terms of hunger and craving. So simply eliminating processed foods helps a ton in terms of appetite control, and most people dump processed foods when they go low carb.

It's also thought that ketones have a role. Perhaps they are directly sensed by the brain as "plenty of available energy" and drive appetite lower.

GaleHawkins

Just to stay in a state of nutritional ketosis insures a clean diet I found really without effort since I made eating for better health my only WOE goal. Not sure what fixed my cravings and health in general but 30 days into this WOE starting Oct 2014 fixed my craving then my health issues.