Re: Mattson's Mice

[Guest guest]

--- In , " Rodney " <perspect1111@y...>

wrote:

> .................... For insulin: the CR group was 68% lower;

fasting was 79% lower;

> third group 50% lower (strange, because they ate the same as the

> controls and were fed every day?????).

This last finding may be an especially interesting result. The third

group had 50% lower insulin than the control group despite the fact

they ate the same amount and were not fasted!!!

The only inference I can see that might be drawn from this is that

the control group had food available all day and nibbled throughout

the day. The third group ate all their food at once when it was

presented to them in the morning. Then they ate nothing the rest of

the day because there was nothing to eat.

If this is the correct inference, then those who advocate lots of

small meals throughout the day are totally 'out to lunch'!

Rodney.

[Guest guest]

--- In , " Rodney " <perspect1111@y...>

wrote:

> As you can see from these numbers fasting results in a greater

> decline in glucose and insulin than CR, but it apparently causes a

> rise in the other two markers measured.

> Perhaps someone here can explain to us the

> importance/significance/relevance of IGF-1 and beta-

hydroxybutyrate?

> Please?

Thx, Rodney, for wading through that report! I'd also be interested

in the info re: IGF-1 and beta-hydroxybutyrate. I've decided to

become my own guinia pig and fast for 24 hours every Wed. Last

Wednesday, I ate my last meal at 4:00pm and didn't eat again until

Thursday after 4:00pm.

No reason for my doing a weekly fast except I wanted to see the

effects. This highly UN-scientific of course. LOL

Laurie

[Guest guest]

The significance of the higher IGF-1 and beta-HB in the fasting mice, in

comparison to the CR mice is debatable. Some believe low IGF-1 may be an

important component of the life extending and cancer reducing properties of

CR; however, this is a somewhat debatable point.

" Mounting evidence from rodents indicates that decreased GH and IGF-1 levels

results in longer life-span, indicating that GH supplementation could

accelerate aging. "

http://snipurl.com/63n1

In humans, IGF-1 has been correlated to increased risk of prostate and colon

cancer.

" IGF-1 and cancer

IGF-1 is known to stimulate the growth of both normal and cancerous

cells(2,5). In 1990 researchers at Stanford University reported that IGF-1

promotes the growth of prostate cells(2). This was followed by the discovery

that IGF-1 accelerates the growth of breast cancer cells(6-8). In 1995

researchers at the National Institutes of Health reported that IGF-1 plays a

central role in the progression of many childhood cancers and in the growth

of tumours in breast cancer, small cell lung cancer, melanoma, and cancers

of the pancreas and prostate(9). In September 1997 an international team of

researchers reported the first epidemiological evidence that high IGF-1

concentrations are closely linked to an increased risk of prostate

cancer(10). Other researchers provided evidence of IGF-1's link to breast

and colon cancers(10,11). "

http://snipurl.com/63mz

Beta-HG is a ketone body, associated with ketosis- and ketosis can be

induced by fasting. The metabolic effects of ketones may be beneficial to

several organ systems, the nervous system most notably.

>From: " Rodney " <perspect1111@...>

>Reply-

>

>Subject: [ ] Mattson's Mice

>Date: Fri, 30 Apr 2004 02:03:45 -0000

>

>Hi folks:

>

>For those who cannot face wading through the technical jargon in

>Mattson's mouse study, here is my summary of the findings most

>relevant to us here. (If anyone thinks what I write here is not

>entirely accurate, please correct it. I am certainly no kind of

>expert in this stuff, as you will already have figured out ; ^ )))

>Thanks.)

>

>They measured four biomarkers of mice on various different dietary

>schemes. (I ASSUME that it is better in the case of each of these

>biomarkers for the number to be lower. Someone please correct if

>mistaken). The four markers were fasting glucose; fasting insulin;

>IGF-1; and beta-hydroxybutyrate.

>

>The calorie-restricted mice were fed 40% less than the others. All

>the other three groups of mice ate pretty much the same quantity!

>One was eating ad-lib - the control group; another was eating as much

>as they wanted but only given food on alternate days (i.e. fasting);

>the third group was fed the same quantity as the fasting group, but

>they were fed daily. I will refer to this last group as 'the third

>group'. (Having this group enabled the researchers to distinguish

>between the effects of the quantity consumed by the fasting group and

>the effects of the fasting factor separately). The fasting group ate

>the same amount as the control group because they ate twice as much

>on the days they were given food.

>

>Now here are some biomarker numbers for the three non-control groups

>compared with the ad-lib control group. It is notable that the CR

>mice show reductions for all four markers. The fasting group and its

>associated 'third group' showed declines for two markers, BUT

>INCREASES FOR THE OTHER TWO:

>

>For fasting glucose: the CR group was 29% lower than the ad-lib

>control mice; the fasting group was 35% lower (even though they ate

>much more than the CR mice); the third group was ONLY 5% lower.

>Fasting has a very big influence on fasting glucose apparently.

>

>For insulin: the CR group was 68% lower; fasting was 79% lower;

>third group 50% lower (strange, because they ate the same as the

>controls and were fed every day?????).

>

>For IGF-1: CR was 16% lower; fasting 16% HIGHER; third group, 15%

>HIGHER.

>

>For beta-hydroxybutyrate: CR, 46% lower; fasting 95% HIGHER; third

>group, 20% HIGHER.

>

>As you can see from these numbers fasting results in a greater

>decline in glucose and insulin than CR, but it apparently causes a

>rise in the other two markers measured.

>

>Perhaps someone here can explain to us the

>importance/significance/relevance of IGF-1 and beta-hydroxybutyrate?

>Please?

>

>Rodney.

>

>

>

>

>