The FastDay Forum

I have been fasting for a few months now, but have recently noticed a couple of changes and would be interested to hear views on what's going on.

First of all, just to set the scene, I don't fast for weight loss; in my case it is for the preventative health benefits (I'm particularly keen to avoid Alzheimer's Disease, which is in my family). For that reason, I've been sticking to one fast day a week not two, and diverging from the 500 calorie recommendation after fasting by eating as much as I want to after breaking the fast. This is because I believe the health benefits to be related to the state your body goes into while fasting rather than the calorie restriction itself. I measure how I am doing by looking at the rate of ketones in my urine, using the cheap 'dipsticks' you can easily buy (I get 'Ketostix' online).

So, the first thing I've found is that fasting is getting much, much easier. Yesterday, for example, I did almost 22 hours on water only with only one real hunger pang early in the morning. I think it is partly because my brain and body have both got used to the routine we are in, and have learnt that they won't be getting any food on Saturdays!

But the other really interesting thing is that I now enter 'ketosis' faster each week. When I started fasting it would normally take me 16 hours to register any ketones, but now it is taking just 12 or 13 hours (I think on average it takes people a lot longer - I've heard 48 hours, but I don't know how far into ketosis that is).

I'm very interested in these two changes, and am wondering if there is any connection. For example, is the earlier ketone production helping to 'fuel' my body, thus making the fast easier?

Any thoughts welcome!

[carorees]

Yes, once you enter ketosis you don't get hunger pangs they say. True ketosis happens when all your glycogen stores are used up. You can store 1000 to 2000 cal as glycogen, the amount depends on the size of your liver and muscles. Things that can speed up entry into ketosis are low carb diet before the fast and exercise during the fast.

I think that some ketones are produced before the glycogen runs out completely as some glucose is needed by the body.

People who are used to constant carb availability are often "metabolically inflexible" meaning they can't switch into fat burning easily, due to high insulin levels. Fasting lowers insulin and allows the switch into ketosis. I think that the more we fast the easier this switch becomes and perhaps happens sooner allowing more glycogen to be preserved to supply the small amounts of glucose required by some tissues. This helps to prevent protein loss.

I would be quite interested to get some of those ketostix myself. I tend to feel a bit peckish at breakfast time...probably habit, and then again mid afternoon. I am wondering if the mid afternoon hunger is a sign that the glycogen is running low and I'm about to switch to fat burning. I find doing some high intensity exercise gets rid of the hunger pangs, possibly because it forces the switch to fat burning.

Anyway, should have said at the start: welcome to the forum!

The glycogen in the muscles is only available to those muscles so it's only the liver glycogen that needs to be considered.

I'm not sure what switches ketone production on - if the liver can maintain blood sugar by gluconeogenesis the brain doesn't need the ketones ?

Mag, I have pondered on this subject many times and have thought that the opposite is more likely to be true. My view is that the more we fast the better we become at sparing our glycogen and increasing fat metabolism, and with the sparing of the glycogen the longer it will take to go in to ketosis. As a result the "brain benefits" may require a longer period of fasting as we get more adapted to fasting. I guess a full study would give the best answer. Your observations may be down to changes in your diet before your fasting day and or exercise, eg your glycogen stores are lower than normal before going in to the fast so you go in to ketosis sooner. I always like to exercise on a fast day too to (maybe?) speed up the process of going in to ketosis by burning up more muscle and liver glycogen.

A few more thoughts/observations on fat burning and ketosis. I don't think glycogen stores are ever totally used up, even in ketosis there is still some glucose production vis gluconeogenesis. With fat burning in general, I don't think we are ever burning either glucose/CHO or fat, it's always a mix of the two, plus some protein. There isn't a cut off point where you stop burning CHO and switch on fat burning, rather there's a ratio of CHO to fat burning. Many factors will affect the ratio eg depending on when you last ate, the composition of your last meal, how fit you are etc etc. After 2-4 hours of fasting the average person will be burning roughly 2/3 fat and 1/3 CHO. This is reflected by the respiratory exchange ratio (RER) or respiratory quotient (RQ) figure. The longer you fast the lower your RER value will fall and the more fat you will be burning. The online consensus seems to be that a resting RER for a sedentary person is around 0.8, a value of 0.7 indicates that the body is predominantly burning fat and a value of 1 predominantly CHO. We are always somewhere betwen 0.7 and 1 unless we're going hell for leather on a high intensity exercise burst/sprinting when the value can exceed 1.

[carorees]

Mag, I have pondered on this subject many times and have thought that the opposite is more likely to be true.

Skippy, I'm confused by your arguments. What you cite below supports an earlier shift to ketosis.

My view is that the more we fast the better we become at sparing our glycogen and increasing fat metabolism, and with the sparing of the glycogen the longer it will take to go in to ketosis.

Increasing fat metabolism IS ketosis. I wonder if you are confusing ketosis (normal fat metabolism) with ketacidosis (happens in diabetes only), so the better we are at sparing glycogen the SHORTER time it takes to enter ketosis.

As a result the "brain benefits" may require a longer period of fasting as we get more adapted to fasting.

Shorter not longer

Your observations may be down to changes in your diet before your fasting day and or exercise, eg your glycogen stores are lower than normal before going in to the fast so you go in to ketosis sooner. I always like to exercise on a fast day too to (maybe?) speed up the process of going in to ketosis by burning up more muscle and liver glycogen.

A few more thoughts/observations on fat burning and ketosis. I don't think glycogen stores are ever totally used up, even in ketosis there is still some glucose production vis gluconeogenesis. With fat burning in general, I don't think we are ever burning either glucose/CHO or fat, it's always a mix of the two, plus some protein. There isn't a cut off point where you stop burning CHO and switch on fat burning, rather there's a ratio of CHO to fat burning. Many factors will affect the ratio eg depending on when you last ate, the composition of your last meal, how fit you are etc etc. After 2-4 hours of fasting the average person will be burning roughly 2/3 fat and 1/3 CHO. This is reflected by the respiratory exchange ratio (RER) or respiratory quotient (RQ) figure. The longer you fast the lower your RER value will fall and the more fat you will be burning. The online consensus seems to be that a resting RER for a sedentary person is around 0.8, a value of 0.7 indicates that the body is predominantly burning fat and a value of 1 predominantly CHO. We are always somewhere betwen 0.7 and 1 unless we're going hell for leather on a high intensity exercise burst/sprinting when the value can exceed 1.

This is all good stuff and makes perfect sense.

The ketones in urine do show that we are fat burning but don't show what proportion. I think that the issue of metabolic inflexibility is behind the "side-effects" people get on starting fasting. It would be interesting to test urine for ketones in people suffering side effects and those who are not (or longitudinally, in someone starting the diet, for several weeks).

To toss some numbers in my RQ was 0.75 after an overnight fast measured at about 10am. With an assumed 15% protein that puts me at 11% CHO and 74% fat burning - not a mile off what I eat.

My blood ketones are usually 0.0 - 0.2 mmol with 2.8 my highest after 30 mins of interval running.

...using the cheap 'dipsticks' you can easily buy (I get 'Ketostix' online)

In the interests of science I have just ordered some - £6.20 for 50 inc p&p on eBay.

Caroline, my understanding of ketosis is wrong, you'll be telling me that the earth is round next. I had always thought that ketosis only kicked in when liver glycogen was almost exhausted and was not always part of fat oxidation. Apologies Mag for my in accurate reply.
Going back to my point re RER values and that we always burning a mix of fat and carbs, then we must always be producing ketones to an extent. The volume will change depending on how fat adapted we are and how depleted liver glycogen is. With that in mind and the fact that it takes 48hrs to convert to ketones as the primary fuel for the brain/cns, I wonder what kind of positive cognitive effects we get, if any, thru 5:2ing? Mattson's research in this area so far has not included humans 5:2ing.

Phil how are you measuring your RQ, you have access to a lab?
Also seems strange that your highest observed ketone count was after what sounds like an anaerobic session?

I had an RQ measurement done in a lab, yes. The high count was with a run at 1300 with nothing to eat after breakfast. 400 calories or so which I guess takes out most of the available glycogen and leaves the brain demanding ketones.

Free fatty acids are the default energy supply from adipose tissue to muscles etc, aren't they ?

ETA reading matter...
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1193348/
http://www.ncbi.nlm.nih.gov/pubmed/2656155

[carorees]

From wikipedia
Ketone bodies are three water-soluble compounds that are produced as by-products when fatty acids are broken down for energy in the liver. Two of the three are used as a source of energy in the heart and brain while the third (acetone) is a waste product excreted from the body. In the brain, they are a vital source of energy during fasting.

When glycogen stores are not available in the cells, fat (triacylglycerol) is cleaved to provide 3 fatty acid chains and 1 glycerol molecule in a process known as lipolysis. Most of the body is able to use fatty acids as an alternative source of energy in a process called beta-oxidation. One of the products of beta-oxidation is acetyl-CoA, which can be further used in the citric acid cycle. During prolonged fasting or starvation, acetyl-CoA in the liver is used to produce ketone bodies instead, leading to a state of ketosis.

During starvation or a long physical training session, the body starts using fatty acids instead of glucose. The brain cannot use long-chain fatty acids for energy because they are completely albumin-bound and cannot cross the blood–brain barrier. Not all medium-chain fatty acids are bound to albumin. The unbound medium-chain fatty acids are soluble in the blood and can cross the blood–brain barrier.[3] The ketone bodies produced in the liver can also cross the blood–brain barrier. In the brain, these ketone bodies are then incorporated into acetyl-CoA and used in the citric acid cycle.

In normal individuals, there is a constant production of ketone bodies by the liver and their utilization by extrahepatic tissues. The concentration of ketone bodies in blood is maintained around 1 mg/dl. Their excretion in urine is very low and undetectable by routine urine tests (Rothera's test).

When the rate of synthesis of ketone bodies exceeds the rate of utilization, their concentration in blood increases; this is known as ketonemia. This is followed by ketonuria – excretion of ketone bodies in urine. The overall picture of ketonemia and ketonuria is commonly referred as ketosis. Smell of acetone in breath is a common feature in ketosis.

Skippy...note that some ketone production is always going on but it is not detectable in urine.

"These studies indicate that, in man, FFA availability is a major determinant of rates of KB production; insulin does not appear to influence ketogenesis rates by a direct hepatic effect, and glucagon can further augment KB production when FFA concentrations are increased but only in the setting of insulin deficiency."

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC370361/

[carorees]

Study from 1983!!!

More recent work showing a link between metabolic inflexibility and insulin resistance:
www.ncbi.nlm.nih.gov/pubmed/21701566
http://www.ncbi.nlm.nih.gov/pubmed/21959346

Study from 1983!!!

so what ? Gravity was explained a long time ago too.

At least it has something to say about ketones, which I thought was relevant to the topic.

[carorees]

True indeed, but you have to check there have been no more recent studies before quoting older ones. Perhaps you did, in which case, apologies.

Putting that aside, the study focuses on the effect of insulin as a direct inhibitor of ketogenesis, whereas it may be an indirect effect. As it shows that FFAs are the main influence we have to ask what prevents FFA release from adipose stores? I think it's insulin.

It's all so complicated isn't it?