Active Low-Carber Forums
Atkins diet and low carb discussion provided free for information only, not as medical advice.
Home Plans Tips Recipes Tools Stories Studies Products
Active Low-Carber Forums
A sugar-free zone


Welcome to the Active Low-Carber Forums.
Support for Atkins diet, Protein Power, Neanderthin (Paleo Diet), CAD/CALP, Dr. Bernstein Diabetes Solution and any other healthy low-carb diet or plan, all are welcome in our lowcarb community. Forget starvation and fad diets -- join the healthy eating crowd! You may register by clicking here, it's free!

Go Back   Active Low-Carber Forums > Main Low-Carb Diets Forums & Support > Low-Carb Studies & Research / Media Watch > LC Research/Media
User Name
Password
FAQ Members Calendar Search Gallery My P.L.A.N. Survey


Reply
 
Thread Tools Display Modes
  #1   ^
Old Tue, Dec-15-15, 09:25
GRB5111's Avatar
GRB5111 GRB5111 is offline
Senior Member
Posts: 4,044
 
Plan: Very LC, Higher Protein
Stats: 227/186/185 Male 6' 0"
BF:
Progress: 98%
Location: Herndon, VA
Default Mark Mattson: IF, Health & Brain Power

Stumbled upon this Tedx talk by Mark Mattson during my searches on IF, low carb, and health:

http://tedxtalks.ted.com/video/Why-...ters-Brain-Powe

In getting some background on Mark, the more I learned, the more impressed I became:

https://en.m.wikipedia.org/wiki/Mark_Mattson

Some of this information will be familiar:

Quote:
A series of findings by Dr. Mattson during the 1990s and 2000s established links between diet and the pathogenesis of neurodegenerative disorders. He has shown that intermittent fasting can increase the resistance of neurons in the brain to dysfunction and degeneration in animal models of Alzheimer's, Parkinson's and Huntington's disease and stroke. The underlying mechanism was shown to involve increased production of neurotrophic factors and protein chaperones, suggesting an adaptive response of brain cells to the stress associated with intermittent fasting. Findings from studies of rodent models were published in the Annals of Neurology, PNAS and the Neurobiology of Disease. Findings from a study using a monkey model of Parkinson's disease were published in PNAS. Collectively, these findings provide an example of how Dr. Mattson’s basic research into the biochemistry and biology of neuronal plasticity and death has provided information that can be directly applied to improving the human condition.

Discoveries made in Dr. Mattson’s laboratory led to a new view of apoptotic biochemical cascades in the physiological regulation of synaptic plasticity and structural remodeling, and introduced the neuroscience field to the concept of “synaptic apoptosis”. He showed that, by cleaving specific glutamate receptor subunits, caspases play important roles in regulating synaptic plasticity, an entirely new and unexpected function of apoptotic proteases.

Dr. Mattson’s work has revealed mechanisms by which diabetes adversely affects hippocampal plasticity and cognitive function. In a study published in Nature Neuroscience he showed that, in both insulin-deficient rats and insulin-resistant mice, diabetes impairs hippocampus-dependent memory, perforant path synaptic plasticity and adult neurogenesis, and the adrenal steroid corticosterone contributes to these adverse effects. Changes in hippocampal plasticity and function in both models were reversed when normal physiological levels of corticosterone were maintained, suggesting that cognitive impairment in diabetes may result from glucocorticoid-mediated deficits in neurogenesis and synaptic plasticity. In a related study published in Hippocampus, Mattson showed that rats fed with a high-fat, high-glucose diet supplemented with fructose corn syrup exhibit alterations in energy and lipid metabolism similar to clinical diabetes, with elevated fasting glucose and increased cholesterol and triglycerides. Rats maintained on this diet for 8 months exhibited impaired spatial learning ability, reduced hippocampal dendritic spine density, and reduced long-term potentiation at Schaffer collateral—CA1 synapses. These changes occurred concurrently with reductions in levels of BDNF in the hippocampus. Dr. Mattson also investigated whether manipulations that enhance neurotrophin levels will also restore neuronal structure and function in diabetes. He found that running wheel activity, caloric restriction, or the combination of the two treatments increased levels of BDNF in the hippocampus of diabetic mice. Enhancement of hippocampal BDNF was accompanied by increases in dendritic spine density on the secondary and tertiary dendrites of dentate granule neurons. These studies suggest that diabetes exerts detrimental effects on hippocampal structure, and that this state can be attenuated by increasing energy expenditure and decreasing energy intake. The implications of these findings for cognitive aging are clear – dietary moderation and regular exercise will enhance cognitive function.


He's an active scientist who is making meaningful strides in health research that perpetuates the theme of food and its regulation as a superior prescription.

http://www.sciencedirect.com/scienc...550413113005032

Quote:
Among the major effects of fasting relevant to aging and diseases are changes in the levels of IGF-1, IGFBP1, glucose, and insulin. Fasting for 3 or more days causes a 30% or more decrease in circulating insulin and glucose, as well as rapid decline in the levels of IGF-1, the major growth factor in mammals, which together with insulin is associated with accelerated aging and cancer (Fontana et al., 2010). In humans, 5 days of fasting causes an over 50% decrease in IGF-1 and a 5-fold or higher increase in one of the principal IGF-1-inhibiting proteins, IGFBP1 (Thissen et al., 1994a). This effect of fasting on IGF-1 is mostly due to protein restriction, and particularly to the restriction of essential amino acids, but is also supported by calorie restriction since the decrease in insulin levels during fasting promotes reduction in IGF-1 (Thissen et al., 1994a). Notably, in humans, chronic calorie restriction does not lead to a decrease in IGF-1 unless combined with protein restriction (Fontana et al., 2008).

I highlighted the portion in bold, as it brought to mind some of our threads that discussed IF and calorie restriction. I've often wondered what kind of role protein might play, and might its absence be the key during IF and the resulting positive impacts on insulin, BG, and cellular repair. While protein is essential, its periodic absence appears to be an enabling factor in metabolic healing.
Reply With Quote
Sponsored Links
  #2   ^
Old Tue, Dec-15-15, 21:21
Nicekitty's Avatar
Nicekitty Nicekitty is offline
Senior Member
Posts: 469
 
Plan: Banting
Stats: 150/132/132 Female 5'7"
BF:
Progress: 100%
Location: PNW
Default

Very interesting, I wonder why the restriction of essential amino acids would reduce IGF-1. Would a fat fast be almost as effective in dropping glucose, insulin and IGF-1?


Quote:
The implications of these findings for cognitive aging are clear – dietary moderation and regular exercise will enhance cognitive function.
How about not eat a diet of fat and glucose, supplemented with high-fructose corn syrup? Were they trying to replicate the SAD?, because this sounds like a good approximation.
Reply With Quote
  #3   ^
Old Wed, Dec-16-15, 14:21
Squarecube's Avatar
Squarecube Squarecube is offline
Senior Member
Posts: 877
 
Plan: atkins/paleo/IF
Stats: 186.5/159.0/160 Male 5' 11"
BF:
Progress: 104%
Location: NYC
Default

Very nice TED talk. I'm speed reading the 1911 Upton Sinclair book right now that was mentioned.

https://books.google.com/books?id=j...epage&q&f=false

Oddly I've just started a three day fast after several weeks of 24 hours tuesday and Thursday jobs. I duno, I find it very difficult to limit my calories to 500 when doing these short fasts. Sinclair says fasting is easier after 2- 3 days and he would never do short fasts as the hunger gets in the way.
Reply With Quote
  #4   ^
Old Wed, Dec-16-15, 14:34
GRB5111's Avatar
GRB5111 GRB5111 is offline
Senior Member
Posts: 4,044
 
Plan: Very LC, Higher Protein
Stats: 227/186/185 Male 6' 0"
BF:
Progress: 98%
Location: Herndon, VA
Default

Agree on the short fast observation. I find that a 3-day or longer fast is easier, as I have no hunger after the first day, and on day 3 feel that I could go much longer if I wanted. At some point early in the new year, I'll try a 5-day fast.

Thanks for the link. I'm into the book now.
Reply With Quote
  #5   ^
Old Wed, Dec-16-15, 17:25
GRB5111's Avatar
GRB5111 GRB5111 is offline
Senior Member
Posts: 4,044
 
Plan: Very LC, Higher Protein
Stats: 227/186/185 Male 6' 0"
BF:
Progress: 98%
Location: Herndon, VA
Default

Quote:
Originally Posted by Nicekitty
Very interesting, I wonder why the restriction of essential amino acids would reduce IGF-1. Would a fat fast be almost as effective in dropping glucose, insulin and IGF-1?

Good question, as the absence of protein is indicated as important. I read in some of his papers that protein elimination combined with caloric restriction has some benefits. I'm reading through a lot of this information. I always viewed a fast as total elimination of calories, so I never consumed anything other than water, broth, tea, coffee with no additives of fat sources or non-glucose contributing sweeteners. My thinking is that introducing any calories from fat or protein would defeat the purpose of the fast, which is to cause one's metabolism to obtain the required energy source from endogenous fat stores.
Reply With Quote
  #6   ^
Old Wed, Dec-16-15, 17:40
Zei Zei is offline
Senior Member
Posts: 1,596
 
Plan: Carb reduction in general
Stats: 230/185/180 Female 5 ft 9 in
BF:
Progress: 90%
Location: Texas
Default

I'd also be interested to know if fat fasting could bring similar benefits. The longest fast I did was 7 days and I kept waiting for that day that the intense hunger would go away like other people had said, but for me that day never came.
Reply With Quote
  #7   ^
Old Wed, Dec-16-15, 19:39
WereBear's Avatar
WereBear WereBear is offline
Senior Member
Posts: 14,682
 
Plan: EpiPaleo/Primal/LowOx
Stats: 220/130/150 Female 67
BF:
Progress: 129%
Location: USA
Default

I remember when there was all this fuss about calorie restriction... and it turns out carb restriction was just as useful. And a lot easier!
Reply With Quote
  #8   ^
Old Wed, Dec-16-15, 23:49
Turtle2003's Avatar
Turtle2003 Turtle2003 is offline
Senior Member
Posts: 1,449
 
Plan: Atkins, Newcastle
Stats: 260/221.8/165 Female 5'3"
BF:Highest weight 260
Progress: 40%
Location: Northern California
Default

Dr. Mark Matson was featured in the TV documentary "Eat, Fast, and Live Longer" with Dr. Michael Mosley. You can watch this on youtube here. It also includes a segment with Valter Longo who researches calorie restriction and fasting and their effects on aging.
Reply With Quote
  #9   ^
Old Thu, Dec-17-15, 02:26
M Levac M Levac is offline
Senior Member
Posts: 6,498
 
Plan: VLC, mostly meat
Stats: 202/200/165 Male 5' 7"
BF:
Progress: 5%
Location: Montreal, Quebec, Canada
Default

About IGF-1. GH stimulates the production of IGF-1 when GH hits the liver, where IGF-1 is produced. GH is inhibited by hyperglycemia. It follows therefore that when there's hyperglycemia, there's less GH, there's less IGF-1.

The effect seen where IGF-1 drops, it's the free IGF-1 that drops, not total IGF-1. Most of the IGF-1 is bound to some binding protein called IGFBP-x (where x is the number of this protein). This effect also comes with a concomitant increase in at least one of those binding proteins, as Rob cited in his original post here:
Quote:
In humans, 5 days of fasting causes an over 50% decrease in IGF-1 and a 5-fold or higher increase in one of the principal IGF-1-inhibiting proteins, IGFBP1 (Thissen et al., 1994a).

The correct phrasing here is: 50% decrease in free IGF-1, with a concomitant 5-fold or higher increase in one of the binding proteins (not "one of the principal IGF-1-inhibiting proteins"), IGFBP1. It is true that the binding protein renders the hormone inert or inactive (i.e. safe to keep it in the bloodstream, until received by any cell which can unbind it, so basically all cells), but it is not true that it inhibits it, in spite of what Wiki says about that. The term inhibition specifically applies to production and/or to its effect once received by cells through their receptors. For example, hyperglycemia inhibits GH production, or insulin inhibits ketogenesis, etc.

There's this idea that IGF-1 is somehow responsible for cancer growth. Not true. The primary culprits are glucose and insulin. Feinman did an experiment with cancer and KD. It has an effect on cancer growth. Maybe IGF-1 dropped, but I doubt it. Like I said, hyperglycemia inhibits GH, therefore inhibits IGF-1 downstream, therefore KD restores normal GH production, i.e. higher GH production than with hyperglycemia, therefore higher IGF-1 production. However, it's likely that KD is pretty much like fasting, so we'll get pretty much the same effect on the IGFBP-x as well. So the idea here is that in spite of an increase in IGF-1 production, we get a drop in free IGF-1 because there's more binding proteins to bind to that IGF-1.

Mind you, that's just how I understand it. I could be way off the mark on this one.
Reply With Quote
  #10   ^
Old Thu, Dec-17-15, 02:45
M Levac M Levac is offline
Senior Member
Posts: 6,498
 
Plan: VLC, mostly meat
Stats: 202/200/165 Male 5' 7"
BF:
Progress: 5%
Location: Montreal, Quebec, Canada
Default

This bit is very telling:
Quote:
Dr. Mattson’s work has revealed mechanisms by which diabetes adversely affects hippocampal plasticity and cognitive function.

Translation: Hyperglycemia, therefore a high-carb diet, adversely affects the brain.

That's all I need to conclude that it's not intermittent fasting or exercise that does what's done, instead it's the lack of carbs, the lack of excess insulin, and the presence of ketones that does what's done. That's all I need cuz it's very likely that all that work was done under the premise that a high-carb diet is good for us, that we need glucose for the brain, glucose is the preferred fuel, etc, etc, etc.

Is it just me or is this just wrong?:
Quote:
adaptive response of brain cells to the stress associated with intermittent fasting

If anything, stress was removed by intermittent fasting, since carbs were removed, hyperglycemia was removed, hyperinsulinemia was removed, ketones were added.

It's wondrous how even by starting with the wrong premise, the guy somehow stumbles into the right experiment.
Reply With Quote
  #11   ^
Old Thu, Dec-17-15, 08:19
GRB5111's Avatar
GRB5111 GRB5111 is offline
Senior Member
Posts: 4,044
 
Plan: Very LC, Higher Protein
Stats: 227/186/185 Male 6' 0"
BF:
Progress: 98%
Location: Herndon, VA
Default

Martin - I'm sure you're not wrong, but I'm reading it differently in regards to stress. If the base assumption here is that one's normal fuel is exogenous caloric consumption, then fasting introduces the stress required to convert a glucose-fueled metabolism to an endogenous fat fueled metabolism with the increase in ketone bodies. I can understand the use of "stress" in this case, but it's not the most clear way to describe what's happening. When stress caused by fasting results in increased ketones and reduced oxidative stress to the body and brain at the cellular level, the "stress" stimulates the metabolism to shift from glucose burning to fat burning. The word "stress" is used in two opposite ways here, and likely a better phrasing in explaining this is that the metabolism goes through an adaptive change due to fasting resulting in reduced oxidative stress and improved stress tolerance in the brain and body at a cellular level.
Reply With Quote
  #12   ^
Old Thu, Dec-17-15, 11:02
M Levac M Levac is offline
Senior Member
Posts: 6,498
 
Plan: VLC, mostly meat
Stats: 202/200/165 Male 5' 7"
BF:
Progress: 5%
Location: Montreal, Quebec, Canada
Default

Thanks, Rob. I think you put it better than he did.
Reply With Quote
  #13   ^
Old Thu, Dec-17-15, 11:59
Squarecube's Avatar
Squarecube Squarecube is offline
Senior Member
Posts: 877
 
Plan: atkins/paleo/IF
Stats: 186.5/159.0/160 Male 5' 11"
BF:
Progress: 104%
Location: NYC
Default

Quote:
Originally Posted by GRB5111
Agree on the short fast observation. I find that a 3-day or longer fast is easier, as I have no hunger after the first day, and on day 3 feel that I could go much longer if I wanted. At some point early in the new year, I'll try a 5-day fast.

Thanks for the link. I'm into the book now.


Re longer fasts, easier. I left out the huge "yeah, but." Tomorrow night I'll be with people, it's the weekend, etc.. Maybe if I start on on mondays and go thru Friday, the whole thing might work.
Reply With Quote
  #14   ^
Old Thu, Dec-17-15, 13:36
GRB5111's Avatar
GRB5111 GRB5111 is offline
Senior Member
Posts: 4,044
 
Plan: Very LC, Higher Protein
Stats: 227/186/185 Male 6' 0"
BF:
Progress: 98%
Location: Herndon, VA
Default

That's been my experience, as holidays, anniversaries, weekends are things I've got to navigate around. Starting with my last meal on a Sunday night seems to work for a few days, and I can bury myself in work during the course of the week.
Reply With Quote
  #15   ^
Old Sun, Dec-20-15, 12:39
dan_rose dan_rose is offline
Senior Member
Posts: 189
 
Plan: None, limit carbs, Omega6
Stats: 161/140/140 Male 5'10"
BF:
Progress: 100%
Location: Loughborough, UK
Default

Sort of related, here's a recent blog on the restriction of protein (specifically methionine) on aging.
Reply With Quote
Reply


Posting Rules
You may not post new threads
You may not post replies
You may not post attachments
You may not edit your posts

vB code is On
Smilies are On
[IMG] code is On
HTML code is Off



All times are GMT -6. The time now is 08:13.


Copyright © 2000-2024 Active Low-Carber Forums @ forum.lowcarber.org
Powered by: vBulletin, Copyright ©2000 - 2024, Jelsoft Enterprises Ltd.