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  #886   ^
Old Sun, May-06-18, 09:33
GRB5111's Avatar
GRB5111 GRB5111 is offline
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Good analysis on this dynamic. There's a point when increasing protein:fat ratio transitions the energy source from fat to glucose (due to increased GNG) triggering an insulin release lowering blood glucose. While we now know that increasing protein in one following a LC compared to a SAD approach has less of an impact on insulin release while maintaining a high glucagon response, moving to a higher ratio of protein to fat is going to upset this balance at some point. I'm happy to see that Jimmy jumps on challenges at the drop of a hat, but this is a complex issue with many variables at play, so assuming a root cause for a perceived "hypo" must be interpreted carefully.
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  #887   ^
Old Sun, May-06-18, 09:55
teaser's Avatar
teaser teaser is offline
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Quote:
Pancreatic alpha-cell function in idiopathic reactive hypoglycemia.
Ahmadpour S1, Kabadi UM.
Author information
Abstract
Idiopathic reactive hypoglycemia (IRH) is a well-documented but overdiagnosed syndrome. The presence of transient hypoglycemia and enhanced insulin secretion and/or increased insulin sensitivity before the onset of IRH is well documented. However, the data regarding glucagon secretion are sparse. Therefore, this study assessed glucagon and insulin responses to (1) oral ingestion of 100 g glucose oral glucose tolerance test (OGTT) and (2) a 100-g protein meal after an overnight fast in a randomized sequence at intervals of 7 to 10 days in five subjects with previously well-documented IRH and six normal subjects. Basal plasma glucose and insulin levels were not significantly different in both groups. However, basal glucagon was significantly higher (P < .025) in IRH subjects (347 +/- 83 ng/L) compared with normals (135 +/- 20 ng/L). In IRH subjects during the OGTT, hypoglycemia (2.7 +/- 0.11 mmol/L) occurred at 150 +/- 16 minutes and was preceded by a markedly higher (P < .01) peak glucose concentration (11.7 +/- 0.6 mmol/L) at 36 +/- 6 minutes in comparison to normals (8.8 +/- 0.4 mmol/L), indicating the presence of impaired glucose tolerance in these subjects. Similarly, the plasma insulin increase was significantly higher (P < .01) but delayed in IRH subjects compared with normals. In contrast, glucagon suppression was not significantly different in both groups, although glucagon failed to increase following hypoglycemia in IRH. During a protein meal, plasma glucose declined in both groups, with a significantly (P < .05) greater decrease in IRH subjects (-0.8 +/- 0.2 mmol/L) compared with normals (0.5 +/- 0.1 mmol/L). However, the glucagon increase was significantly (P < .01) blunted in IRH subjects (61% +/- 15%) in comparison to normals (152% +/- 39%). Thus, basal hyperglucagonemia with normal glucose concentration may suggest the presence of a hyposensitivity of the glucagon receptor in IRH. Moreover, the lack of appropriate suppression during the OGTT despite marked hyperglycemia, the lack of an increase at the onset of hypoglycemia, and the inhibited response to a protein meal in IRH subjects compared with normals denote altered glucagon secretion in IRH. Therefore, it is likely that glucagon receptor downregulation and impaired glucagon sensitivity and secretion may contribute to postprandial hypoglycemia in IRH.


I saw this abstract yesterday, it does sound a lot like what Jimmy describes. Wonky glucagon is really all it takes.
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  #888   ^
Old Sun, May-06-18, 21:21
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GRB5111 GRB5111 is offline
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Plan: Very LC, Higher Protein
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Yes, wonky as a blunted glucagon response in those with IRH coupled with a greater, but later insulin response. That would tend to make one feel pretty crappy at some point.
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  #889   ^
Old Tue, May-08-18, 06:09
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teaser teaser is offline
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https://www.sciencedaily.com/releas...80503142852.htm

Quote:
Fasting boosts stem cells' regenerative capacity
A drug treatment that mimics fasting can also provide the same benefit, study finds

As people age, their intestinal stem cells begin to lose their ability to regenerate. These stem cells are the source for all new intestinal cells, so this decline can make it more difficult to recover from gastrointestinal infections or other conditions that affect the intestine.

This age-related loss of stem cell function can be reversed by a 24-hour fast, according to a new study from MIT biologists. The researchers found that fasting dramatically improves stem cells' ability to regenerate, in both aged and young mice.

In fasting mice, cells begin breaking down fatty acids instead of glucose, a change that stimulates the stem cells to become more regenerative. The researchers found that they could also boost regeneration with a molecule that activates the same metabolic switch. Such an intervention could potentially help older people recovering from GI infections or cancer patients undergoing chemotherapy, the researchers say.

"Fasting has many effects in the intestine, which include boosting regeneration as well as potential uses in any type of ailment that impinges on the intestine, such as infections or cancers," says Omer Yilmaz, an MIT assistant professor of biology, a member of the Koch Institute for Integrative Cancer Research, and one of the senior authors of the study. "Understanding how fasting improves overall health, including the role of adult stem cells in intestinal regeneration, in repair, and in aging, is a fundamental interest of my laboratory."

David Sabatini, an MIT professor of biology and member of the Whitehead Institute for Biomedical Research, is also a senior author of the paper, which appears in the May 3 issue of Cell Stem Cell.

"This study provided evidence that fasting induces a metabolic switch in the intestinal stem cells, from utilizing carbohydrates to burning fat," Sabatini says. "Interestingly, switching these cells to fatty acid oxidation enhanced their function significantly. Pharmacological targeting of this pathway may provide a therapeutic opportunity to improve tissue homeostasis in age-associated pathologies."

The paper's lead authors are Whitehead Institute postdoc Maria Mihaylova and Koch Institute postdoc Chia-Wei Cheng.

Boosting regeneration

For many decades, scientists have known that low caloric intake is linked with enhanced longevity in humans and other organisms. Yilmaz and his colleagues were interested in exploring how fasting exerts its effects at the molecular level, specifically in the intestine.

Intestinal stem cells are responsible for maintaining the lining of the intestine, which typically renews itself every five days. When an injury or infection occurs, stem cells are key to repairing any damage. As people age, the regenerative abilities of these intestinal stem cells decline, so it takes longer for the intestine to recover.

"Intestinal stem cells are the workhorses of the intestine that give rise to more stem cells and to all of the various differentiated cell types of the intestine. Notably, during aging, intestinal stem function declines, which impairs the ability of the intestine to repair itself after damage," Yilmaz says. "In this line of investigation, we focused on understanding how a 24-hour fast enhances the function of young and old intestinal stem cells."

After mice fasted for 24 hours, the researchers removed intestinal stem cells and grew them in a culture dish, allowing them to determine whether the cells can give rise to "mini-intestines" known as organoids.

The researchers found that stem cells from the fasting mice doubled their regenerative capacity.

"It was very obvious that fasting had this really immense effect on the ability of intestinal crypts to form more organoids, which is stem-cell-driven," Mihaylova says. "This was something that we saw in both the young mice and the aged mice, and we really wanted to understand the molecular mechanisms driving this."

Metabolic switch

Further studies, including sequencing the messenger RNA of stem cells from the mice that fasted, revealed that fasting induces cells to switch from their usual metabolism, which burns carbohydrates such as sugars, to metabolizing fatty acids. This switch occurs through the activation of transcription factors called PPARs, which turn on many genes that are involved in metabolizing fatty acids.

The researchers found that if they turned off this pathway, fasting could no longer boost regeneration. They now plan to study how this metabolic switch provokes stem cells to enhance their regenerative abilities.

They also found that they could reproduce the beneficial effects of fasting by treating mice with a molecule that mimics the effects of PPARs. "That was also very surprising," Cheng says. "Just activating one metabolic pathway is sufficient to reverse certain age phenotypes."

The findings suggest that drug treatment could stimulate regeneration without requiring patients to fast, which is difficult for most people. One group that could benefit from such treatment is cancer patients who are receiving chemotherapy, which often harms intestinal cells. It could also benefit older people who experience intestinal infections or other gastrointestinal disorders that can damage the lining of the intestine.

The researchers plan to explore the potential effectiveness of such treatments, and they also hope to study whether fasting affects regenerative abilities in stem cells in other types of tissue.


There's that fasting benefits/rejuvenates progenitor/stem cells theme once again. We have effects in neural, immune, mesenchymal stem cell populations. I'd throw in mitochondria benefits as at least rhyming with this idea.
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  #890   ^
Old Tue, May-08-18, 11:30
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NEMarvin NEMarvin is offline
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Plan: keto
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So fasting can be a good thing.... (states Captain Obvious....)

I find that in my own N=1, that when I do fasting, even if it's just skipping one meal and doing a 18/6 or 16/8, my weight loss slows. I remember Ken I think posted something here once that there have been studies about the morbidly obese (I still fit into that category by BMI) do not respond as well to fasting and will do better once they move down to just the obese or overweight category. I have more recently wondered that if it's because when I compact my eating into one or two meals, if I do not consume enough protein because I've noticed feeling colder during fast days and following. If my protein consumption is cut anywhere from 30 to 50%, I'm thinking it could cause one or both. Ketogains folks insist even if you are IF, you need to hit your protein macros for the day.

Curious if you guys that read a lot of research studies have thoughts about either of my suppositions above?

I realize there are a lot of good reasons to Fast other than weight loss, but wondering at what point there might be counterproductive to one's primary goals?
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  #891   ^
Old Tue, May-08-18, 13:10
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teaser teaser is offline
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I guess it depends where your protein intake is to start with. I do better with a more steady ketogenic ratio, I think that sort of limits my personal comfort with fasting. A facebook page I'm on follows Dr. Fung, and they'll talk about protein backfilling, making up for the lack of protein during fasting with some extra. This hasn't really worked for me, I'll feel better during the fasting itself, but the refeed is by definition less ketogenic, and I don't find I feel as good then. Right now I'm doing a carnivore keto experiment, carbs only from heavy cream, so my protein intake can go up 20-30 grams or so without the diet being less ketogenic--I've been thinking I might do an experiment with fasting again just to see, with my protein a bit higher I'd be more comfortable with not trying to make up for the short period without protein.

If you look at calorie restriction--a group of researchers have clamped on to fasting's effects on stem cells, so they're doing study after study that shows similar effects on various stem cell populations. Fasting is sexy right now, so we see these studies. There is similar data for caloric restriction, since the two approaches have similar health/longevity effects, maybe that's not surprising. Since we've got that one little mouse study showing a life-extending effect for a ketogenic diet, I have to wonder about stem cells in that model.

In rodents, the calorie restriction model seems to depend on whether the animal's usual diet is one that would make them obese/diabetic. A question that comes up a lot is, do all these various approaches extend normal lifespan, or do they just revert things to normal? I like this image;



People who were always lean, and calorie restrict themselves to skeletal status, I suspect that's probably just as unhealthy as it looks.

There is obese and then there is weight-reduced obese. Dr. Fung concentrates on the habitual diet's effect on metabolism etc., but there are profound effects on metabolism that will vary from person to person that probably interact with the diet but have an existence of their own. My best guess is that if you respond better to eating a certain way, in weight loss, appetite and energy, then it probably really is better for you, whatever these various fasting studies say.
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  #892   ^
Old Tue, May-08-18, 16:57
GRB5111's Avatar
GRB5111 GRB5111 is offline
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Plan: Very LC, Higher Protein
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Quote:
Originally Posted by teaser
In rodents, the calorie restriction model seems to depend on whether the animal's usual diet is one that would make them obese/diabetic. A question that comes up a lot is, do all these various approaches extend normal lifespan, or do they just revert things to normal?

People who were always lean, and calorie restrict themselves to skeletal status, I suspect that's probably just as unhealthy as it looks.

Very insightful. Back to normal is the plausible state where the metabolism wants to exist.
Quote:
Originally Posted by teaser
There is obese and then there is weight-reduced obese. Dr. Fung concentrates on the habitual diet's effect on metabolism etc., but there are profound effects on metabolism that will vary from person to person that probably interact with the diet but have an existence of their own. My best guess is that if you respond better to eating a certain way, in weight loss, appetite and energy, then it probably really is better for you, whatever these various fasting studies say.

Marvin - teaser's response is where I would start (I've added bold to emphasize his statements in the quote). Just a couple other observations, as this is an N=1 learning opportunity for all of us. As for protein and fasting, it appears according to current research, that the benefits of fasting largely have to do with an absence of protein for a period of time. Absence of protein can trigger autophagy, which is thought to be a desirable state to achieve periodically via IF (see Mark Mattson's TED talk and other work in this area) for healing, metabolic cleansing, and achieving general well being (clarity of mind, soundness of body). After practicing IF for both short and longer periods, I have found that an occasional fast of 4 days quarterly is helpful in this case (for me and likely others). Then, there's the question about protein consumption, which is one of the more asked questions on this forum. Some keto geeks warn that unless you limit protein, you'll get "kicked out" of ketosis. After a few years, I'm starting to find this suggestion is wrong, and teaser nails it, some people do really well with higher protein consumption. Some don't. I fall into the former group, as increasing protein recently has neither "kicked me out" of ketosis nor has caused me to add weight or find it difficult to maintain. We need to recognize that everyone is different. I'm familiar with Ken's observations on fasting related to current BMI state, and he is 100% correct as well. So, what I've been doing over the approximately 5 years that I've been strict LC is experimenting with varying macros (protein and fat) to find where I fit. If my BMI or percentage of fat opposed to lean were different, it's very likely that I would need to alter my approach. These are my thoughts to your question, and I truly believe that it's a matter of self-discovery where you vary things consistently for several weeks to see how your metabolism responds. I'm not willing to put my faith in anyone's experiences until I can experience it myself. In a way, that's a freeing thought.
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  #893   ^
Old Wed, May-09-18, 05:29
teaser's Avatar
teaser teaser is offline
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https://www.cell.com/cell-stem-cell...5909(12)00167-1

Quote:
Short-Term Calorie Restriction Enhances Skeletal Muscle Stem Cell Function


Not intermittent fasting, but "short-term" calorie restriction seems to have similar effects on muscle stem cell to other stem cell lines. Bone, muscle, brain, gut, immune cells. To be fair I have to throw in fat cells, starve fat cells and some of them seem to become preadipose cells, this is good in some ways for metabolic health, but preadipose does have a greater capacity for proliferation than mature cells. I haven't actually seen anything showing this resulting in an increased adipose cell count, just something I wonder about.

Last edited by teaser : Wed, May-09-18 at 06:04.
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  #894   ^
Old Wed, May-09-18, 09:29
teaser's Avatar
teaser teaser is offline
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Plan: mostly milkfat
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https://optimisingnutrition.com/201...phic-explained/

Marty Kendall gives some argument for the Obesity-->Insulin resistance, hyperinsulinemia model vs Insulin-->Obesity. Includes this nifty graphic from Dr. Naiman;




I think there might be some room for obesity leading to central insulin resistance leading to higher insulin supporting driving obesity a bit further.

For me Insulin-->obesity doesn't depend on insulin resistance, it depends on insulin sensitivity, specifically of fat cells. Shawn Baker has low testosterone. Does this break the testosterone-->muscle connection?

Quote:
A relevant example of this is Jimmy Moore’s recent high protein experiment where he reduced his fasting insulin from 14.2 to a very respectable 8.8 mIU/mL in five days on a high protein energy restricted diet


This is interesting, I missed that lower number, only heard other bits about Jimmy's fasting insulin being around 15. Pretty low for somebody with Jimmy's level of body fat. Fairly insulin sensitive-->and I'd argue that's something that could feed into Jimmy's experience of hypoglycemia. It's effective, it doesn't work as a therapy if the side effects can't be tolerated.

Quote:
It will be interesting to see how Jimmy’s upcoming high-fat bio hack goes. I hypothesise that Jimmy’s short-term insulin level may be lower after meals, but his longer-term fasting insulin will be higher on the high-fat approach.


I'd guess the other way, but mostly from Marty's own reasoning. Jimmy's keto experiment is going to be at the same calorie level as the high protein experiment was, so unless the protein somehow drove fasting insulin down apart from the weight loss itself, further weight loss shouldn't drive fasting insulin back up. I would be totally flabbergasted if Jimmy didn't lose on 1800 calories a day of a 4:1 ketogenic diet. I'd expect some loss of lean mass, but certainly a fair amount of fat loss to go with that.
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  #895   ^
Old Fri, May-11-18, 04:09
JEY100's Avatar
JEY100 JEY100 is online now
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Satchin Panda tweeted another fasting study published on-line yesterday in Cell Metabolism. This one on Early Time Restricted Feeding, that is, an eating window 8 am to 2 pm! Good news for all here who skip dinner. I believe that is Jean, any others? My BG stays higher until I eat, think this supports Why it works, why I should move the eating window.

https://www.cell.com/cell-metabolis...4131(18)30253-5

Quote:
Early Time-Restricted Feeding Improves Insulin Sensitivity, Blood Pressure, and Oxidative Stress Even without Weight Loss in Men with Prediabetes

Highlights
•Early time-restricted feeding (eTRF) increases insulin sensitivity
•eTRF also improves β cell function and lowers blood pressure and oxidative stress
•eTRF lowers the desire to eat in the evening, which may facilitate weight loss
•Intermittent fasting can improve health even in the absence of weight loss


Summary
Intermittent fasting (IF) improves cardiometabolic health; however, it is unknown whether these effects are due solely to weight loss. We conducted the first supervised controlled feeding trial to test whether IF has benefits independent of weight loss by feeding participants enough food to maintain their weight. Our proof-of-concept study also constitutes the first trial of early time-restricted feeding (eTRF), a form of IF that involves eating early in the day to be in alignment with circadian rhythms in metabolism. Men with prediabetes were randomized to eTRF (6-hr feeding period, with dinner before 3 p.m.) or a control schedule (12-hr feeding period) for 5 weeks and later crossed over to the other schedule. eTRF improved insulin sensitivity, β cell responsiveness, blood pressure, oxidative stress, and appetite. We demonstrate for the first time in humans that eTRF improves some aspects of cardiometabolic health and that IF’s effects are not solely due to weight loss.


Don’t have access to the study details...only my guess an earlier window would help. It did my last blood work in Feb where HbA1c finally fell to 5.2.

Last edited by JEY100 : Fri, May-11-18 at 04:18.
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  #896   ^
Old Fri, May-11-18, 05:45
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cotonpal cotonpal is online now
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Quote:
Originally Posted by JEY100
Satchin Panda tweeted another fasting study published on-line yesterday in Cell Metabolism. This one on Early Time Restricted Feeding, that is, an eating window 8 am to 2 pm! Good news for all here who skip dinner. I believe that is Jean, any others? My BG stays higher until I eat, think this supports Why it works, why I should move the eating window.

https://www.cell.com/cell-metabolis...4131(18)30253-5



Don’t have access to the study details...only my guess an earlier window would help. It did my last blood work in Feb where HbA1c finally fell to 5.2.


Yes, it's me, breakfast and latish lunch usually with no dinner. I always have to hold myself back when people suggest to others that they not eat breakfast as if this is the optimal way to accomplish whatever it is they are trying to accomplish. It may be a helpful way to eat for many people but that doesn't mean it is the "optimal" way to eat (doesn't mean it isn't either). I do the opposite and it works well. Breakfast is my biggest meal of the day. Lots of protein and fat but not too many carbs. Works for me.
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  #897   ^
Old Fri, May-11-18, 08:35
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bluesinger bluesinger is offline
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Plan: LC/CancerRecovery
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My new get-up time is 3:15am so that I get back indoors from my walk before 5am summer sunrise. Didn't know that my eating patterns had a name: eTRF. Most days I only drink after 3pm.
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  #898   ^
Old Fri, May-11-18, 08:36
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WereBear WereBear is online now
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When I do eat, I tend towards a late breakfast and early dinner, with a 4-5 hour window.
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  #899   ^
Old Fri, May-11-18, 08:51
GRB5111's Avatar
GRB5111 GRB5111 is offline
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Plan: Very LC, Higher Protein
Stats: 227/186/185 Male 6' 0"
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Quote:
Originally Posted by WereBear
When I do eat, I tend towards a late breakfast and early dinner, with a 4-5 hour window.

I do that as well; however, I could easily move my two meals per day to early and mid-day just to experience if it has any effect. With the mid-day and early evening meal protocol, my last HbA1c test in February was 4.9, so I'm fairly happy with that. It might be a good change for my next N=1 variation to move my meals to morning and early afternoon for 2-4 weeks to see if I notice anything. The biggest obstacle is that I'm often not hungry until mid-day, and I don't like eating when I'm not hungry. It would be interesting to see if I could adapt.
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  #900   ^
Old Sat, May-12-18, 04:12
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WereBear WereBear is online now
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Quote:
Originally Posted by GRB5111
The biggest obstacle is that I'm often not hungry until mid-day, and I don't like eating when I'm not hungry.


Likewise, and I didn't recover from an eating disorder to see if I can start a new one.
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