Different Modes of Dietary Restriction

[Guest guest]

Hi folks:

This is a somewhat rambling post touching on a number of issues

looking for input in response:

I have recently become curious about the benefits of every-other-day

feeding as compared with regular CRON. By 'regular' I mean eating

appreciably fewer calories than is generally considered the 'norm'

each and every day with no fasting.

First of all, 'every-other-day' feeding has sometimes been

abbreviated to the acronym 'EOD'. But I find this possibly confusing

since that could also be construed to mean 'end-of-day' feeding. So

in the interests of minimizing confusion I am instead going to

abbreviate it to ADF - 'alternate-day-feeding'. Regular CR I will

refer to as 'EDCR' ............... every day CR. When I use the

acronym 'ADF' I mean: no calories on alternate days and eat-as-much-

as-you-want on the other days. Or, put another way, eating all you

want from 8 am to midnight (16 hours), followed by consuming no

calories until 8 am 32 hours later - what might perhaps be termed

a " 16/32 " routine.

A number of mouse CR experiments were done with the animals fed only

Monday, Wednesday and Friday (MWF), perhaps principally for

logistical reasons. This is quite similar to ADF, but involves

somewhat less frequent feeding since there is a two day gap on the

weekend. Those MWF mice seem to have thrived, since they much

outlived their ad lib siblings. So one wonders whether MWF, or ADF,

might be a better approach to caloric restriction in humans than

eating every day while restricting calories 10%, 20% or 30% each day -

'EDCR'.

What is interesting about a MWF routine is that, even when weekly

caloric intake was not much reduced, some of the standard CR

biomarkers were better on MWF than on EDCR, while weight loss was

also less drastic. Presumably this means more fat is retained -

which may be important because Warren has posted here that the CR

mice which survived the longest of all were those which had somehow

kept the greatest fat reserves.

However there are (at least) two sides to this coin. The other side

is that two biomarkers behaved dramatically differently for MWF

rodents compared with EDCR animals. Both blood beta-hydroxybutyrate

and IGF-1 were a lot lower in EDCR animals compared with their ad lib

pals, but a lot higher in those on MWF. So how are these differences

reflected in comparative maximum lifespans?

I do not have any idea what the differing beta-hydroxybutyrate

numbers mean. If anyone has any thoughts it would be good to hear

them. But as regards IGF-1 this has raised an issue of which I was

previously ignorant. A couple of Google seaches using inputs

like 'IGF-1 cancer', or 'insulin cancer', indicate that there seems

to be a direct link between cancer incidence and levels of both

insulin and IGF-1. This **suggests** that higher IGF-1 would be a

disadvantage. Yet, while mice mostly die of cancer, the MWF mice

lived a lot longer than their pals which had lower IGF-1 on ad lib.

So how harmful, I wonder, can elevated IGF-1 be? Not much, perhaps?

I don't know what to make of this. If anyone has any input about

what all this might mean to humans, please enlighten us. If MWF (or

the presumably-very-similar ADF) can better preserve body weight and

fat reserves, much improve many biomarkers, and **IF** it can be done

without causing additional cancer then it might result in even better

maximum lifespans than our standard EDCR. But the higher IGF-1 looks

like it may be a fly in the ointment - and possibly the higher beta-

hydroxybutyrate too?

One explanation for the improved biomarkers despite a much less

dramatically changed weekly caloric intake might be that both EDCR

and ADF or MWF elicit a 'starvation response'. In the case of EDCR

it is a little 'starvation' every day, and in the case of ADF and MWF

more marked starvation, but only on alternate days.

[One other item on this general topic ................ one thing I

would like to change is my tendency to sleepiness in mid-afternoon.

In this regard I had had the impression that this problem might be

prompted by what I had eaten for lunch, since the symptom usually

seems to arise about an hour after lunchtime. However I recently

read that a study of muslims during Ramadan had found that they

frequenty attribute their mid-afternoon sleepiness to the lack of

food between dawn and dusk! So, so much for that theory! Has anyone

succeeded to conquering afternoon sleepness? If so please let us

know how!]

Do yer begin to see why I decided to write this? A smaller loss of

body mass would be an advantage if it could be obtained with

excellent biomarkers and no increase in cancer. Do we know of any

study in mammals that compared survival curves of animals on ADF (or

MWF) and those on EDCR?

Rodney.