Tuesday, August 05, 2008

AGE RAGE and ALE: fasting

Jan Kwasniewski hates fasting. I'm not so sure it's as simple as this, there are some aspects which might be beneficial.

I started thinking about fasting when Dr Davis put up this post.

I'd just like to put this in to the perspective of glycoxidation. Let's look at glucose and lipid metabolism under a fast. There is no glucose uptake from the gut. The portal vein is no longer a glycation hot spot, the systemic circulation has only basal glucose too. Arterial endothelial cells are not undergoing hyperglycaemia induced apoptosis. This minimises the need for foam cell formation as there is essentially no damage needing repair.

Chylomicrons are not being produced at all, the liver is depleted of carbohydrate and so puts out a minimum of VLDLs. However many VLDLs and subsequent LDLs are actually produced, they will not be exposed to aggressive glycation conditions. If the liver does continue to produce significant levels of VLDL, they will be based either on fats synthesised from residual glycogen stores or free fatty acids derived from adipose tissue. That is, mostly saturated with some monounsaturated. So VLDLs will be deficient in PUFA and not prone to glycoxidation. PUFA supply will be limited to hepatic stores and whatever is present in adipose tissue, ie not a lot.

Bulk lipid for energy supply will be derived from adipose tissue lipolysis and be (a) mostly saturated fatty acids and (b) in free fatty acid form. You cannot glycate free fatty acids without direct free radical attack. No amino group on a FFA to form that horrible Schiff base.

From the perspective of someone who regards arteriosclerosis as a repair process gone horribly wrong, fasting has a lot to offer in the short term, with death in the long term. LC high saturated fat diets mimic fasting in several ways: There's never a lot of glucose in the portal vein and the chylomicrons based on saturated fats are pretty well glycoxidation proof. Fat gets stored as adipose tissue after each meal and is released as free fatty acids on demand. Metabolism mostly runs on free fatty acids. The big difference is that there is no (premature!) death if the diet is sustained for more than a few months!



Jeremy said...

Why do you think fasting leads to death? The intermittent fasting experiments with rats show fasting prolongs life. Are you saying this is completely wrong in humans?

Peter said...

It's a matter of duration. How long are you going to fast for???? 6m, 9m or a year? It's not pretty.


Aaron said...

What would be interesting to look at now is the total difference between the damage between:

1: fat oxidation (high oxygen environment) with low levels of AGEs

2: low glycemic carb oxidation - with the minor AGEs

and see which one really causes more damage.

JohnN said...

Reading the comment on Dr Davis post, I'm struck by the possibility of not just reversing IHD but also AD (Alzheimer's). While burning fatty acids to simulate a fasted state one also witholds CH intake to enter ketosis - forcing the brain to be more efficient in using ketones. What will happen to the beta-amyloid plaque?

Peter said...


Yes, Alzheimers, Parkinsons and Motor Neurone diseases all appear to respond to ketosis. This is in part why I see LC as more powerful than higher carb, even if both use real foods right down the line.

Amyloid plaque I regard as debris from the primary problem. It always reminds me of living in London back in the seventies when any pillarbox on the Tottenham Court Rd could carry an IRA bomb. The shrapnel would maim you, so should be avoided, but the fundametal treatment for the problem was carried out by political negotiation in Westminster and Belfast. Just giving all shoppers full metal jackets was not the prefered choice!

I see Aaron's query in the same terms. How broken you are affects how LC you need to go. Interesting if both groups started healthy and only ate real food. Would LC beat low GI if neither group had or developed insulin resistance...


JohnN said...

I would not compare LC and Low GI on the basis of AGEs alone.
With LC you have the advantage of journeying back and forth between catabolic and anabolic states with wide-ranging transcriptional possibilities. It's all about signaling and what the cells use to communicate. AGE could be one of them.

Bryan - oz4caster said...

I've been trying the 16/8 approach to weight loss. You fast for 16 hours and eat during an 8-hour period. So far I'm at 5 weeks and I've lost 7 pounds. My goal is to lose 20 pounds, so I have a ways to go yet. However, I'm beginning to think this may not be a bad way to continue eating, not just for the weight loss.

Anonymous said...

I think low-glycemic carbs are even worse, because they are high-fiber. 85% chocolate is low-glycemic carb, but I feel better without it. I had problems with fiber all my life and never made the connection. Low-carb is not as important as NO-fiber, in my experience. We need to think out side the box. Let's say that fiber is the problem and not carbs. Take away whole fruits, veggies, potato, chocolate, beans, whole grains, and all nuts/seeds. Even white rice and peeled potatoes have too much fiber to be eaten in significant amounts. They make me tired. Sourdough white bread is better. It has no fiber at all and no additives.

I get organic sourdough white bread with only three ingredients - stone ground unbleached unenriched flour, filtered water, and sea salt. A low fiber diet is a good start, but NO fiber (0g listed) is best. I'm also using small amounts of raw unheated honey, grape juice, strained citrus juices, and maple syrup. Everything that contains fiber is gone. I also use a tea strainer on the juices if there is even a trace of fiber.

Anonymous said...

Why did you suggest 150g of lard on Davis's blog, Peter? Lard is NOT a saturated fat - contrary to popular misconception. Lard is usually 48% MUFA, 40% SFA, and 12% PUFA. It has 4-6 times as much PUFA as beef fat, kidney suet, and butter. So, 150g of lard has 18g of PUFA and 150g of beef suet or ghee would have 3-6g of PUFA. A fast is a no-PUFA diet, so the goal should be zero PUFAs or as close to that as possible. Lard doesn't cut it and should be eaten in small doses, if at all. The main fats should be from large ruminant animals and tropical oils. Today's pigs are fed an awful diet and have much more PUFAs than red meat.

Peter said...

Phew, at least we all know now!

Anonymous said...

We all know what? Pigs have lots of PUFA, since they aren't able to add hydrogen to the fats like ruminants do. JK's emphasis on pork is simply cultural bias, IMO. Beef is usually fattier and definitely healthier in terms of fat proportions. I haven't seen you mention much pork in your diet. Most of your fats seem to be from cream, beef, and cocoa butter. So it's odd to see a suggestion to eat 150g of lard, when that doesn't seem to be what you eat regularly.

Andrew S said...

re: Jeremy Fox,

The IF experiments fed those rats standard rat chow. Easting less rat chow produced less Lab Rat Chow Induced Disease, thereby prolonging life. I've seen discussion of these issues elsewhere on this blog.

Any similarity in humans would be for similar reasons: IF combined with the standard Western diet might prolong life, too. Better yet would be a non-Western diet.

I'd say the rat experiments were completely wrong in their assessment of the cause of death of lab rats.