10 replies to this topic

[reason]

It is suspected that some fraction of the benefits of calorie restriction for health and longevity are keyed to the hunger response in some way - i.e. that being hungry more often is necessary to gain the full effects. There's not all that much work on this so far as I'm aware, however. You might look at one study suggesting increased levels of ghrelin, the hunger hormone, are linked to an improved immune system response, for example. Studies investigating the contribution of hunger to the benefits of calorie restriction would have to run by manipulating the hunger response separately from calorie intake to try to isolate its effects.

Here is one recently published example of such a study. It is unfortunately focused only on aspects of Alzheimer's disease rather than on longevity, but it is still intriguing. The reduced inflammation is a sign that the researchers might be on the right track:

It has been shown that caloric restriction (CR) delays aging and possibly delays the development of Alzheimer's disease (AD). We conjecture that the mechanism may involve interoceptive cues, rather than reduced energy intake per se. We determined that hunger alone, induced by a ghrelin agonist, reduces AD pathology and improves cognition in [a] mouse model of AD.

Long-term treatment with a ghrelin agonist was sufficient to improve the performance in the water maze. The treatment also reduced levels of amyloid beta (Aβ) and inflammation (microglial activation) at 6 months of age compared to the control group, similar to the effect of CR. Thus, a hunger-inducing drug attenuates AD pathology, in the absence of CR, and the neuroendocrine aspects of hunger also prevent age-related cognitive decline.

Link: http://dx.doi.org/10...al.pone.0060437

<br> <br>View the full article

[DR01D]

From an evolutionary standpoint it makes sense that hunger might be beneficial to health. Outside of the modern world it's something that almost every animal faces on a daily basis.

I try to go to bed a little bit hungry every night.

On Tuesdays and Thursdays I eat all of my calories by lunch and skip dinner. I'm a little hungrier on those evenings. I think when my kids move out of the house I'll eat this way every day.

Over the long term I hope this pays off. I suppose I'll never know for sure but it makes sense and it's easy to do.

Edited by DR01D, 04 April 2013 - 01:33 PM.

[JohnD60]

I try to go to bed a little bit hungry every night.
.

complete speculation by me here.... it would seem to me that doing this on a regular basis would result in desensitization and a coresponding reduction in the desired hormone response. Just a thought.

[DR01D]

complete speculation by me here.... it would seem to me that doing this on a regular basis would result in desensitization and a coresponding reduction in the desired hormone response. Just a thought.

That's possible. I'll never know for sure if going to bed a little bit hungry does anything.

But at least it's easy.

Edited by DR01D, 05 April 2013 - 01:30 PM.

[misterE]

If you lower the calorie-density of the diet, you can practice CR without ever being hungry.

[Matt]

@misterE From my own experience, you can do CR without feeling much hunger. During the early years when my diet was quite different, and I was consuming more protein, I would rarely ever feel hungry. After going vegetarian, but more so after becoming 'mostly' vegan, I do experience daily hunger (mostly morning before breakfast, before meals and in the evening for 20 minutes or so). I actually don't mind the hunger all that much, it doesn't feel bad, if anything I feel much more alert because of it. To me, it also signals that I am in a CR'd state. I actually feel better on a low protein diet (approx 10% of my calories). I also aim keep methionine pretty low as well. I changed the way I do CR based on the results out of WUSTL showing we need to consume less protein to significantly lower our IGF1 levels. There's plenty of evidence now to suggest that insulin/igf1 signalling is very important in aging from experiments on tiny organisms to humans.

[misterE]

we need to consume less protein to significantly lower our IGF1 levels. There's plenty of evidence now to suggest that insulin/igf1 signalling is very important in aging from experiments on tiny organisms to humans.

OK interesting points… I use to think that also, but think of this: insulin-resistance is well known to cause accelerated ageing, with insulin-resistance you actually have low levels of IGF-1 and less insulin-signaling. You would think that if lower levels of IGF-1 and less insulin-signaling is healthy and prolongs life… why then aren’t diabetics living long healthy lives?

[theconomist]

we need to consume less protein to significantly lower our IGF1 levels. There's plenty of evidence now to suggest that insulin/igf1 signalling is very important in aging from experiments on tiny organisms to humans.

OK interesting points… I use to think that also, but think of this: insulin-resistance is well known to cause accelerated ageing, with insulin-resistance you actually have low levels of IGF-1 and less insulin-signaling. You would think that if lower levels of IGF-1 and less insulin-signaling is healthy and prolongs life… why then aren’t diabetics living long healthy lives?

I think it's due to the effects of chronic high blood sugar levels( cancer growth...) and the lifestyle that lead to diabetes which also promotes other chronic illnesses (and increased CVD risk).

Edited by theconomist, 20 September 2013 - 01:13 PM.

[nowayout]

There is a school of thought (without too much evidence beyond anecdotal so far) that ghrelin analogues like GHRPs (called growth hormone releasing peptides for their effect on the pituitary) can improve health. They are popular among some bodybuilders and HRT enthusiasts for supposedly increasing growth hormone release, as a cheap alternative to expensive rHGH. Growth hormone seems like a mixed blessing for longevity, though, so I am not sure of the ultimate benefit or harm of this.

[misterE]

Growth hormone seems like a mixed blessing for longevity, though, so I am not sure of the ultimate benefit or harm of this.

Growth-hormone (GH) is touted (and marketed) as being beneficial and such. The levels of GH rise in the body during bouts of extreme stress (like intensive exercise or fasting). One of its main roles is to promote lipolysis and inhibit muscle loss during these events; however GH doesn’t build muscle by itself. As lipolysis remains uninhibited and the levels of FFA’s increase in the circulation; they can cause the liver to become GH-resistant. The main benefit of GH is its ability to stimulate IGF-1 production. IGF-1 is the main hormone that actually builds muscle.

However, GH cannot enter the liver in the presence of elevated FFA’s. Insulin-secretion is needed for the suppression of FFA’s, which allows GH to stimulate IGF-1 production (which is beneficial in terms of metabolic-health). Once again, this doesn’t occur if you are insulin-resistant, because if you are insulin-resistant, the insulin you secrete would be unable to inhibit lipolysis. This is why elevated GH is a hallmark of diabetes.



J Endocrinol. 1988 Sep;118(3):353-64.

The role of growth hormone in diabetes mellitus.

Holly JM, Amiel SA, Sandhu RR.

Abstract

The insulin and growth hormone (GH)/insulin-like growth factor-I (IGF-I) axis are two endocrine systems that are interlinked at many levels. GH is one of the glucose counter-regulatory hormones, rising in response to hypoglycaemia, it has both intrinsic hyperglycaemic actions and causes insulin resistance. Both IGF-I and its receptor have high structural and functional homology to insulin and its receptor. Insulin can regulate IGF-I production, acting on the GH receptor or at a post-receptor site. Conversely IGF-I is thought to have a permissive effect on the pancreatic insulin response to glucose. Growth is compromised in poorly controlled diabetic children; however, a causal link with altered GH/IGF-I levels has not been proven. Insulin-dependent diabetes clearly causes derangements in the GH/IGF-I axis. In poorly controlled diabetics GH levels are invariably raised whilst normal or low levels of IGF-I are found, indicating a dissociation between the two factors. Altered IGF-binding protein levels are also found, with high levels of small binding protein and low levels of large binding protein. These derangements are probably the result of interactions at many levels although the exact mechanisms are not fully understood. Raised GH levels could result from altered hypothalamic/pituitary control or reduced feedback inhibition. The latter could, in turn, result from low IGF-I levels, reduced availability of IGF-I to relevant receptors or increased levels of inhibitors (possibly the small binding protein). Low IGF-I levels could be directly due to deficient insulin levels or simply to lack of available circulating binding protein. Alternative or altered molecular forms of circulating GH in diabetes seem unlikely on present evidence. That GH has an effect on glycaemic control is most evident from the abnormal glucose tolerance seen in acromegalics, but is also seen with physiological GH variations such as during the pubertal growth spurt. In diabetics the derangements to the GH/IGF-I axis, caused by poor metabolic control, leads to aggravation of the metabolic problems. Altered GH/IGF-I levels have been implicated in the long-term complications associated with diabetes, and whilst GH/IGF-I are not essential for the early changes involved in these complications they may still play an important role in their development, especially proliferative retinopathy.

[nowayout]

When I mentioned that the blessing of HGH could be mixed, I was referring to the association of low GH and low IGF-1 levels with longevity in some studies (independent of confounders like diabetes) which has been discussed in these forums before.