A question for Gabe

[Cora]

Gabe,
I was wondering if there's any science behind the notion of increased weight gain with stress. I was at maintenance weight for a t=year without any difficulty. Then my stress level went through the roof. My weight has been steadily climbing for the last 6 months despite increasing exercise and increased vigilance with my diet (not perfect, but really trying hard to stick with 30 - 40 carbs per day). My LBM has increased by about 5 lbs, but that still leaves 10 lbs of real increase. What do you think. Could increased cortisone production from the stress be causing this? :confused:

[Gabriel Guzman]

Cora, you're not the only one that has experienced the detrimental effects of stress. I myself wasn't too convinced of the link between stress and weight gain, but more learning and new evidence have made me change my views in that regard as I've also experienced something similar during the past 2 years. That doesn't mean there's nothing we can do, though.

There are some studies that suggest that an increase in cortisol (not cortisone) is associated with increased adiposity, particularly in the abdominal area.

I reveiwed a minuscript back in 2005 that showed evidence that adiposity could be increased in mice under glucocorticoid stimulation. The manuscript was rejected because other problems but it did catch my attention that the animals significantly increased their abdominal fat under glucocorticoid stimulation. Whether that also happens in humans is still a matter of controversy, even though you already have products in the market that aim to lower, or at least control cortisol levels in order to decrease adiposity. The study caught my attention because it resembles something that is sometimes seen in individuals that tend to gain weight while under glucocorticoid treatment for epilepsia. According to some people, since stress increases cortisol levels, then the rationale is that if you control your cortisol levels (note that not necessarily your stressors), then you control and decrease your abdominal adiposity.

Another, more intriguing and detail discussion of how stress can affect adiposity was presented by Mike Eades in his two-parter blog "Fat and Happy (http://www.proteinpower.com/drmike/archives/2005/07/you_might_find.html)" and "Fat and Happy II (http://www.proteinpower.com/drmike/archives/2005/07/i_found_several.html)".

Basically, what has been shown in animals (including humans) is that when we are under stress we seem to sick 'sugary' foods (i.e. confort food), which may come with or without fat. If they come with fat, obviously we get a 'double-wammy', not only from excess carbohydrates but also from the combined effect of higher insulin levels going around all the time and increase fat accumulation in the fat cells both because of increased synthesis and increased internalization.

I commented to those two blogs but unfortunately the comments don't show anymore. So, I'll do my best to see if I can summarize.

I used to not put much stock into the link between cortisol and weight gain, and still don't but, as somebody who likes to learn, I'm also willing to relinquish previous positions on certain subjects in view of, precisely, new learning.

This is how I understand it; when we're under stress, just as it happens with other animals that have been studied, we seem to prefer 'comfort foods' (i.e. foods containing sugar and fat). The consumption of these foods increases our caloric efficiency (i.e., we gain weight on fewer calories), and gain fat in our abdominal area. This situation, as pointed out by Mike Eades, may be augmented by elevated insulin levels resulting from an increase in sugary foods.

In the study that prompted Mike's blog about it, the researchers noted something significant: in the presence of insulin, the increased abdominal fat sends a signal somehow (maybe through an as-of-yet undiscovered hormone or peptide?) to the hypothalamus to cut back on the release of corticotropin-releasing factor (CRF), which is responsible for the release of cortisol. Thus, when we're under stress, we tend to eat confort foods that will feedback to stop the stimulus that makes us feel stressed, but with a price... more caloric efficiency and more abdominal fat. Here is where I commented back then.

The researcher's field was 'brain'; my field back then was 'adipocytes'. So, for me it was rather immediate that the 'yet undiscovered hormone or peptide' was none other than leptin, which is a hormone produced by the adipose tissue. The more adipose tissue you have, the more leptin you make. Leptin is also responsible for part of the control of appetite as it also acts in the brain. When people lose adipose mass in a very dramatic way, their levels of leptin also drop sending a signal that triggers food consumption so fat mass can be restore and so leptin levels. Once leptin levels are restored, the hormone acts in the brain to control food intake. The problem is that obese individuals have more than enough leptin but it doesn't seem to work to control appetite and food intake. The reasons are debatable and are out of the scope of your question but suffice to say that fatty acids that can 'trap' leptin so it cannot go to the brain, may be responsible for the lack of effect of higher levels of the hormone in obese individuals.

Leptin does, however, have a role in controlling appetite by controlling the release of CRF, so it's plausible that when we choose 'comfort food' while under stress, which makes us gain adiposity, our leptin levels also increase providing the necessary feedback so food intake can be controlled. Gaining adiposity while under stress may actually serve to generate enough fat tissue, which in turn can produce enough leptin that can act in the hypothalamus. Since there was no measurement of leptin levels in the study that Mike discussed, we can only speculate that it was in fact leptin what caused the decrease in the 'stress-related' products that induced food intake and gain of abdominal fat.

This all mean that there is science behind the notion of increased stress and increased adiposity. Cortisol is just one of the players that shows up under stress conditions but it's not the only hormone, therefore, I still take the studies showing its association with gaining abdominal obesity with a pinch of salt.

To me, the association between stress per se and abdominal adiposity is more important and suggests that it is not just cortisol what needs to be controlled but the stressors (the causes of stress being those physiological and/or psychological). Maybe there is nothing we can do about our physiological response to stress (stress--> consumption of 'comfort food' --> sense of gratification/satisfactio --> apparent reduction of stress --> price in increased abdominal adiposity), but at least we know that there is an explanation.

The fact that we seem to know now how stress may play against us in yet anohter way, also provides with a possible way to counteract at least one of its effects. Since we know that we may be drawn to choose 'confort foods' when we are under stress, then in my opinion, it is only there where we can have some control; in the 'choosing'. First, I suppose we need to recognize that we are under stress... denial doesn't lead anywhere. Second, now that we're aware that our own physiology may conspire against us when we're under stress, we must recognize that we may still have the power to choose what kind of food we will consume. This is perhaps the most difficult part, isn't it? Because it's so easy to just give in and it takes a lot of reasoning to choose a protein-rich food instead of a sugary/sugary-fat one.

People develop different strategies, including not having a single piece of 'confort food' in their pantries or learn how to make 'substitutes', which still taste like what they 'crave' but don't harm them as much. So, if we recognize that stress is slowly taking over certain areas of our lives, we better start preparing and planning a contingency plan. Perhaps we can't remove the stressors at this moment, but we can still choose what to eat when the urge shows itself.

Interestingly, we seem to be very similar to rodents regarding how our brain responds to diet and stress. This is contrary to the way we respond to diet in other organs, such as the adipose tissue, for example in which the results from rodents may not reflect what happens in humans. Nonetheless, there was a study that showed how rats responded to a diet lower in carbohydrate while higher in fat with respect to their food intake and body weight. The diet that provided less carbohydrate and more fat provoked a distinct pattern of hypothalamic hormones and neuropeptides that conrol appetite. In fact, a diet lower in carbohydrate and higher in fact provoked a decreased in anorexic neuropeptides (those that induce feeding), whereas a diet higher in carbohydrate and lower in fat provoked an increase in orexigenic peptides (those that induce feeding). In humans, studies show that an increase in protein, even when carbohydrates are not reduced significantly, results in an increase in satiety with a concommitant decrease in appetite, despite 'ad libitum' food intake.

This all suggests, at least to me, that there may still be a way out of physiologically wired fate when we're under stress if we can still make the effort of choosing what we eat, no matter how bad things are. Having protein-rich foods always at hand and particularly when we're under stress may not only help with our appetite by increasing satiety but also may induce our hypothalamus to control and/or decrease the amount of orexigenic peptides. The 'need' for something sweet, can also be taken care of by learning how to make 'alternative' 'confort foods' that provide the same gratifying sensation but won't impact our bodies as sugary foods would.

I hope I didn't make this more confusing that it is while trying to provide a possible answer!

[Cora]

Thanks for the extensive answer. It sounds like you're saying that there is a real reason for weight gain while under stress, but that we may be able to blunt the effect by eating more protein and watching the sweets. That's pretty much what I've been trying to do. Most likely my weight would be worse if I wasn't! :rolleyes:

[LisaS]

You mention some FA "trapping" leptin so it cannot reach the receptors.

Is there any evidence or studies showing leptin resistance in the obese? The scenario of adequate or excess leptin, obesity and the brain "not paying attention" sounds similar to the insulin resistance story ...

[Gabriel Guzman]

Thanks for the extensive answer. It sounds like you're saying that there is a real reason for weight gain while under stress, but that we may be able to blunt the effect by eating more protein and watching the sweets. That's pretty much what I've been trying to do. Most likely my weight would be worse if I wasn't! :rolleyes:

Yes, there is a real reason and understanding it may help us create a strategy to do something about it. Pesonally, I think the hardest part is to recognize when are we under stress without rationalizing it or justifying what we eat and take action to just eat something different. Perhaps the difference now is that we don't use the reason to justify our choices but actually understand the reason to make better choices.

Maybe if we'd adopt an attitude of 'small battles' every day once we recognize that there are a lot of stressors in our lives, then we could get some of that empowerment back, coming from not giving into a craving but choosing something that will help us more. I like to think that is that kind of empowerment what works as a feedback to strengthen our resolve to go through a crisis with better chances of success.

[Gabriel Guzman]

You mention some FA "trapping" leptin so it cannot reach the receptors.

Is there any evidence or studies showing leptin resistance in the obese? The scenario of adequate or excess leptin, obesity and the brain "not paying attention" sounds similar to the insulin resistance story ...

Yes, quite ample evidence of leptin resistance in obese individuals. When leptin was first thought to be the 'miracle' hormone that would help obese individuals reduce their appetite and ther fat mass, it turned out that obese individuals have more than enough circulating hormone but they just didn't respond to it. The rare cases of mutations in the ob gene which causes morbid obesity do respond to leptin treatment but when production is normal, administration of more leptin doesn't work. That promted the idea of leptin resistance occurring at various levels; the leptin receptor or in the brains and/or the transport of the hormone through the blood-brain barrier (BBB).

Since the mid 90s it has been recognized that obese humans have an encreased cerebrospinal fluid-to-serum ratio for leptin, and some obese rats who no longer respond to peripherally administered leptin can still respond to leptin given directly into the central nervous system. In 2003, a study published in the American Journal of Physiology -Endocrinology and Metabolism series, by Banks and Farrell (Am J Physiol Endocrinol Metab 285: E10–E15, 2003) shown that normal mice made obese had decreased leptin transport through the BBB. By fasting these mice, casing a modest weight loss, they were able to recover a more normal transport across the BBB. Then in 2004 (Am J Physiol Regul Integr Comp Physiol 286:R143–R150, 2004), Levin and Banks (same group), used rats selectively bred to develop diet-induced obesity (DIO) and compared them rats bred to be diet resistant (DR) on a 31% fat high-energy diet with regard to their central leptin signaling and blood-brain barrier (BBB) transport. This time, they found that transport across the BBB was normal but sensitivity to leptin was decreased in the DIO rats.

When talking about leptin resistance, there were two questions that needed to be addressed, one is if the problem is more related to simply an impaired transport across the BBB and the other is if there is an inherited diminished sensitivity when transport is normal (hence the use of normal mice that can made obese and rats that are specifically bred to be obesity prone). Apparently, both scenarios are possible according to the studies from Banks' group. They concluded that reductions in central leptin signaling and defects in leptin BBB transport can develop independently and are likely to have different underlying mechanisms. In the DIO rat, reduced central leptin sensitivity appears to be an inherent trait, whereas defective transport is an acquired one.

An important observation to me is that in the case of the normal mice, in which transport became impaired as the mice became obese, is that the impaired transport of leptin across the BBB develops in tandem with obesity and is reversible with even modest weight reduction.

So, transport is a problem and so is an inherited reduced sensitivity to leptin. Since Banks' group showed that weight loss, even if modest, had a robust effect in transport across the BBB, then the next question was to identify what could impair leptin transport. In another article published in Diabetes (Diabetes 53:1253–1260, 2004) in 2004 by the same group, they identified triglycerides as an important cause of leptin resistance as mediated by impaired transport across the BBB and suggest that triglyceride-mediated leptin resistance may have evolved as an anti-anorectic mechanism during starvation. They suggested that decreasing triglycerides may potentiate the anorectic effect of leptin by enhancing leptin transport across the BBB.

Of course, all these studies show possible mechanisms that may or not occur in humans but from the mechanistic point of view, they're very valuable in terms of understanding the possible causes by which humans can become leptin resistance as they become obese.

For added complexity, both leptin and insulin act in the brain and there can be resistance to both, which only makes things worse.

[gitfiddle]

It was a lot of reading, Gabe, but it helps to believe that the persistant cravings for comfort food that sometimes stronger than I can fight are part of my body chemistry and not a weak mind. The term "small battles" is certainly descriptive of my day. :)

[Missy]

Gabe?

I have a question? Are you saying that if one seems to be leptin resistant, (ME) and insulin resistant (pre diabetic) that perhaps being put on a triglyceride lowering medicine, that could assist in this resistance and therefore find some success in losing? I've been "border line" to "high" on my blood tests, but have resisted adding more medication...perhaps I shouldn't?

I don't "lose" despite doing all of the things necessary...and I'm eager to learn all that I can to improve my chances?

Or, do I have this all wrong? Thanks for your insight, and your willingness to share!

Lynn

[Gabriel Guzman]

Gabe?

I have a question? Are you saying that if one seems to be leptin resistant, (ME) and insulin resistant (pre diabetic) that perhaps being put on a triglyceride lowering medicine, that could assist in this resistance and therefore find some success in losing? I've been "border line" to "high" on my blood tests, but have resisted adding more medication...perhaps I shouldn't?

I don't "lose" despite doing all of the things necessary...and I'm eager to learn all that I can to improve my chances?

Or, do I have this all wrong? Thanks for your insight, and your willingness to share!

Lynn

Lynn, I wish I could say 'yes' or 'no' but I think we need a better understanding about leptin and insulin before I dare to respond that way. If there is something we need to remember (and understand) regarding the interplay between insulin and leptin is this:



Leptin inhibits insulin secretion and biosynthesis
Insulin enhances leptin synthesis and secretion


Coexistence of insulin resistance and leptin resistance in common obesity and there is mechanistic evidence that helps understand and perhaps explain why this is so.

Leptin inhibits insulin secretion and biosynthesis. The leptin receptor is present in pancreatic ß cells in rodents and humans (ß cells in the pancreas are the cells that produce insulin). A number of studies that leptin reduces insulin release from rodent and human ß cells.

Insulin enhances leptin synthesis and secretion. Feeding and insulin increase the expression of the leptin gene in fat cells and It has been reported that insulin increases plasma leptin levels in normal subjects and patients with type 2 diabetes.

What this suggests is that in obesity, hyperinsulinemia may precede insulin resistance and cause enhanced leptin production from increased fat cell mass. As we've discussed before, and because hyperinsulinemia also may result in increased production of triglycerides, which in turn can impair leptin transport across the BBB, the ensuing reduced leptin sensitivity may then lead to dysregulation of the feedback loop between insulin and leptin, resulting in increased insulin release, and aggravation of hyperinsulinemia and insulin resistance.

In other words, leptin is needed to reduce (or at least modulate) insulin release but if one is leptin resistant, then there is no effect on the pancreatic ß cells and there may be overproduction of insulin, which only makes things worse by leading to hyperinsulinemia, which in turn may lead to insulin resistance. Back to the original question regarding stress and weight gain, now we know that leptin is also needed to reduce the amount of orexigenic (induce appetite) peptides as it was likely to happen with the mice in the study that Mike Eades talked about in his blog about stress and the choosing of comfort foods. And if we are leptin resistant, it will be likely that we'll be also insulin resistant.

I'm not a fan of triglyceride-lower medications just as I'm not a fan of blood-glucose and cholesterol-lowering medicine simply becuase there are ways of achieving that nutritionally.

Ron Rosedale (author of The Rosedale Diet), is a big fan of leptin and his diet is designed to get people leptin sensitive, which in turn can also get them more insulin sensitive. He describes the process of becoming leptin resistance pretty much in the way the Eades describe the process of becoming insulin resistant.

In his book he writes:


Ron Rosedale, The Rosedale Diet

When a person becomes leptin resistant, it takes more and more leptin to tell the brain that it's satisfied and that you don't need more food. Therefore, it takes more and more food to feel satisfied. The brain, not hearing leptin, frantically signals for more and more fat to be stored. Since leptin is made by fat cells, you have to make more and more fat to produce enough leptin to finally get its message across to the brain to stop being hungry and stop storing fat. This creates a vicious cycle: you eat more because your brain doesn't know how to tell you to stop, and the only way you can stop is by producing more fat to make more leptin, which means that you keep getting fatter, and more insulin an leptin resistant, which ust makes you want to keep eating more.


The Eades describe insulin resistance in a similar way, only changing the players; instead of fat cells, it's all cells that need to respond to insulin.


Michael and Mary Dan Eades, Protein Power (Ed. 1996)

When cells become resistant to insulin, the receptors on their surfaces designed to resond to insulin have begun to malfunction...

...It simply means that the receptors require more insulin to make them work properly in removing sugar from the blood. Whereas before they needed just a touch to lower it, now they need a continuous supply of excess insulin to keep blood sugar within the normal range.

As time goes by, blood sugar rises higher and stays up longer after the carbohydrate meal despite the enourmous amount of insulin mustered to lower it.

...Hyperinsulinemia means simply having too much insulin in the blood, whereas insulin resistance means that the receptors no longer respond properly to insulin.


Now, with the known interplay between insulin and leptin, we can incorporate both views and have a clearer picture of what happens when hyperinsulinemia ensues due to a carbohydrate-laiden diet. Before insulin resistance, there may be an increase in fat mass (because insulin also drives fat synthesis), which increases leptin production. Hyperinsulinemia due to continuous intake of carbohydrate-laiden foods also leads to overproduction of triglycerides, which in turn impair leptin transport to the brain, which makes it difficult to reduce food intake (leptin resistance). When leptin resistance ensues, then there is no effect on the ß cells in the pancreas to reduce the amount of insulin being produce and if the diet consists of mainly carbohydrate-laiden foods, then the pancreas is not only producing more insulin but is resistant to the action of leptin, which only worsens hyperinsulinemia and eventually more insulin resistance.

That pretty much explains the problem. How about the solution?

Rosedale also writes:


Ron Rosedale, The Rosedale Diet

Certain foods feeds into this vicious cycle ty triggering a huge surge of leptin production. Carbohydrates -including breads, grains, cereals, pastas, and starchy vegetables- are the worse offenders. When you eat this foods, your leptin levels soar. These foods can create even more mischief because they are broken down into simple sugars that can be rapidly burned by the body.


That sounds too familiar to us now, only that our effort to control the intake of those foods has more to do with controlling insulin levels rather than leptin levels. Now there may be possible to do both. Although Rosdale didn't go into details of how carbohydrates increase leptin levels, with the explanations above (insulin enhances leptin synthesis and secretion), is clear that what he was referring (perhaps without he knowing that at the time he wrote his book) is actually an increase in insulin production that results in more leptin. He writes in his book that "If you are insulin resistant, you are almost always leptin resistant..." Now you probably know why.

So, Lynn, re-taking your question:



"...if one seems to be leptin resistant, (ME) and insulin resistant (pre diabetic) that perhaps being put on a triglyceride lowering medicine, that could assist in this resistance and therefore find some success in losing?"

I think that lowering either insulin or leptin can help. However, and I can't stress this enough, changes in insulin and/or leptin sensitivity happen even before weight loss is evident. Since I'm not a big fan of triglyceride-lowering medications, I can't speak favorably about them. What I do know, and has been shown in a number of studies, is that carbohydrate control has a dramatic impact in triglyceride levels. I've seen reports in which the changes in both, blood sugar and triglyceride levels occur so soon that people taking medications for either (or both) need to be monitored carefully to adjust their dose (which is pretty much the recommendation people should follow before making dietary changes anyway). Such changes occurred before significant weight loss was recorded.

If carbohydrate control is so effective in lowering triglycerides, then is plausible to think that the effect in both, leptin and insulin will be the same: restoring sensitivity to both. On one hand, carbohydrate control acts by lowering insulin levels, decreasing hyperinsulinemia, which in turn improves insulin sensitivity and lowers triglyceride levels. On the other hand, lower triglyceride levels may restore leptin transport across the BBB and help out with control with food intake besides acting on the pancreas to modulate insulin release.

Going back to the original topic of stress and weight gain and with all this information, we might as well make our best effort to stick to a carbohydrate controlled plan (of course with adequate protein intake) while we are under stress. It could be our best chance to make it through in the best way possible, even if eliminating the stressors is out of our control.

[Missy]

Since this discussion, I went and bought both Mastering Leptin, and Dr. Rosedale's book. Currently, I'm in the middle of Dr. Rosedales...and I'm learning quite alot about the benefits of lowering your leptin resistance.

I gathered that Dr. Rosedale and the Eades where partner's at one time?

[Gabriel Guzman]

Yes, they were partners a long time ago.

By the way, as I was commenting with somebody else... after you've read Protein Power, you find out that the "Rosdale Diet" doesn't add anything particularly new but it does reinforce that carbohydrate control works by providing the optimal metabolic scenario for changes to take place. As it turns out, and given the interplay between insulin and leptin (discussed before on this thread), carbohydrate control seems to work as a 'double-wammy' as it helps achieving insulin control and improves leptin sensitivity.

[laughingW]

Ok I'm a little late coming in here but Gabe, I wondered what you think of this little writeup from Richards about stress, leptin, insulin:

(original thread from T-Tapp forums,
http://forum.t-tapp.com/topic.asp?TOPIC_ID=43755&SearchTerms=stress



Richards book, (in part) pg 160: Stress causes a rise in blood sugar; this is a hyperglycemic state. This means there is a higher than normal amount of blood sugar so that a person can either run away or go into battle….Hyperglycemia causes the body to run hot…..one way to cool off a hot hyperglycemic reaction is to eat food. The higher the concentration of the calories, the faster the stress reaction will cool off….The reason this works is because eating food causes a rise in insulin…..The fastest way to raise insulin is to eat fats and carbohydrates in combination (aka chocolate)….The rise in insulin causes a depression of glucagons, turning off the liver’s ability to make excess sugar…this settles down the hyperglycemic response to stress sometimes in a matter of minutes…..when stress is more intense or has gone on for a long time and the hyperglycemia is more sever, then dense fatty/salty junk foods sound better than sweets….This is why people stress eat….Regular stress eating is a fast track to Leptin, Insulin, and Adrenaline resistance. Pg 161 Find alternatives to stress eating…do something physically active, go for a walk…jumping jacks….this has the effect of putting the high blood sugar to use, at which point the cravings for food will cease…..

[Missy]

I had long period of chronic stress in my life, not just regular life stress...and I can tell you the LAST thing I could think of doing to alleviate it was exercise...:rolleyes: It was MUCH easier to "duck and cover" and head straight for food...especially regular soda. That leptin book really brought it all into focus for me.

The Rosedale Diet maybe closely related and nothing new compared to what you can find in PP...other then it's very specific, whereas, the PPLP brushes with a much broader brush. Currently, I'm trying to fine tune my woe, and Dr. Rosedale's book has helped in that reguard as well as the Eades.

Perhaps it's just because right now my mind is eagerly absorbing information...and that The Eades plan has covered it, but RDD explainations finished the job for me?

Leptin is a BIG issue for me....and thanks to your explaination Gabe it headed me in the right direction. :)

[Gabriel Guzman]

Ok I'm a little late coming in here but Gabe, I wondered what you think of this little writeup from Richards about stress, leptin, insulin:

(original thread from T-Tapp forums,
http://forum.t-tapp.com/topic.asp?TOPIC_ID=43755&SearchTerms=stress



LaughingW, I think Richards' write up is very much focused on the effect of cortisol (one of the stress hormones) on glucose levels as it acts as an hyperglycemic hormone. I see things from a different, perhaps much broader perspective. Richards' reasoning is that cortisol increases glucose levels, which in turn results in hyperglycemia and that's why you eat more. By the same token, the recommendation is to actually 'eat' a sugar-fat combo so you rise your insulin levels to stop glucagon from making more glucose. In this model, cortisol directly triggers the action of glucagon to make glucose. However, cortisol on its own can stimulate the activation of specialized enzymes involved in the making of glucose and since glucagon also has the same effect, there is a tendency among some people to link cortisol and glucagon in the same action when they aren't necessarily so.

Cortisol acts both in the muscle, fat tissue and liver to accomplish one thing... increase glucose levels as a stress signal. It acts in the muscle so there are amino acids available to make glucose; it acts in the fat cells stimulating the release of fatty acids (which contain glycerol) and when glycerol is released it can be used in the liver to make glucose and of course cortisol acts in the liver to activate the enzymes involved in the process. So, even though glucagon can also produce an increase in glucose using the same machinery, the stimulus is different. Cortisol signals stress; glucagon signals hypoglycemia.

Seems to me that eating fat and carbohydrate is hardly the best way to counteract a 'stress episode'. The reason provided, in which eating causes an elevation of insulin, which in turn causes a decrease in glucagon which in turn results in a decrease of glucose doesn't really fit what happens when chronic stress in ensued.

At the beginning of this thread, we discussed the physiological changes that occur in the brain that ultimately lead to 'stress eating' and more specifically to the consumption of 'confort foods'. With that in mind, then, we can see why eating a combination of fat and sugar is not likely to help. A combination of fat and sugar is precisely 'comfort food', and even if we don't intend to, our physiolgy pretty much directs us towards that as it was shown with those mice. That means that even if we don't intend to, we would end up eating a combination of fat and sugar anyway. Indeed, the combination of fat and sugar eliminated the 'stress symptoms' in those animals and is very similar to what happens to use but with a price... gain in abdominal fat.

I'm not going to go deep into the complexities of how the action of cortisol is regulated but I will mention that certain amino acids act as a negative feedback to cortisol action. That means that when certain amino acids made available for conversion into glucose accumulate, then the action of cortisol is limited because those amino acids, now in higher amount than needed, inhibit the process. That is a clever way the body has to regulate critical processess.

So, the reason why a sugar-fat combo works is not necessarily due to the control of insulin or glucagon, but because up to a point, the action of leptin in the brain regulates the triggers of stress hormones, at least until leptin resistance ensues. There is more about this at the beginning of the thread.

The point I'm trying to make again is that while we may not be able to control what our physiology has wired us to do when we're under stress (i.e. eating combination of fat and sugar) we can still have an impact on how much our physiological response can lead to a positive or detrimental result when we eat under stress.

At the beginning of this thread, we also discussed the possible role of triglycerides as a 'leptin-trap'. Now, Cortisol acts on the fat cells to induce the release of fatty acids. When fatty acids are broken down, they temselves free molecules of glycerol which is used to make glucose in the liver. The triglycerides that remain may interfere with the transport of leptin across the blood-brain barrier resulting in leptin resistance because the hormone can't reach the brain to control food intake.

Now, remember what the context is here. We're not talking about a moment of stress, which could be illustrated by avoiding being ran over by a car. That's a stress signal, an emergency signal which triggers the release of hormones that induce the immediate increase of glucose levels and prepare the body for an outburst of energy. If you're trying to avoid being ran over by a car (you make split second decisions to run, jump, duck, etc.), it's unlikely that you'll actually reach for a chocolate bar to counteract that stressful moment. The context of stress eating, is not stress as in an emergency response but chronic stress, which may lead to stress eating. So, everything in its right perspective.

I don't agree with Richards' description:



…..when stress is more intense or has gone on for a long time and the hyperglycemia is more severe, then dense fatty/salty junk foods sound better than sweets….This is why people stress eat….

It's actually due to a whole array of responses in the brain, not necessarily hyperglycemia. Hyperglycemia may be just a result of the gat-sugar combo that we seem to be wired to go after when we're under chronic stress. Therefore, I maintain that it's plausible that even in the event of chronic stress, if instead of the fat-sugar combo, a protein-rich food (low in carbohydrate) is consumed, while it would still be stress-eating, the result wouldn't necessarily be detrimental (i.e. weight gain, insulin and/or leptin resistance).

This part, however,



Regular stress eating is a fast track to Leptin, Insulin, and Adrenaline resistance...


although conveys part of the message, is better explained by the reasons presented at the beginning of this thread than just cortisol levels. Because of the choice in food is the fat-sugar combo in response to chronic stress, there is a chronic increase in insulin (which leads to hyperglycemia and insulin resistance), a chronic release of triglycerides (which trap leptin and leads to impared control of food intake, wich leads to more eating and possible weight gain), which leads to more production of leptin, but since there is now leptin resistance, then there is no control on insulin production, which makes hyperinsulinemia even worse.

The solution to counteract chronic stress, seems to me, is make our best effort not to consume the sugar-fat combo. That is not physiology but planning. If it's unlikely that we'll be able to remove the stressors from our lives, at least we can remove from our pantry the foods that will worsen the situation.

[Missy]

Thank you for your explanation Gabe. I was in "chronic stress" for years....and I turned to sugar-fat food choices constantly. :rolleyes: and...it did to me as exactly as you explained. Now, I'm here to undo that damage as best I can.

Even if you KNOW you shouldn't at the time, you do it anyway, until you REALLY understand the biochemistry behind it...and I won't do that to myself again. Thanks for taking the time to help us understand as best as (I) can.

Thanks for explaining too that the RDD is basically the "Purist" style...as I just took it as really "strict"....stricter then the Eades plan...and it's essentically the SAME plan. :rolleyes: lol

[laughingW]

By the same token, the recommendation is to actually 'eat' a sugar-fat combo so you rise your insulin levels to stop glucagon from making more glucose.
That is NOT Richards' recommendation. Sorry if that quoted snippet gave that impression.

Sounds like everyone's saying the same elephant, each from a different leg.

[Gabriel Guzman]

That is NOT Richards' recommendation. Sorry if that quoted snippet gave that impression.

Sounds like everyone's saying the same elephant, each from a different leg.


Oh... I thought that his part was taken from Richard's book, p160, as it was included in the same quote by the person who wrote that post:




...The fastest way to raise insulin is to eat fats and carbohydrates in combination (aka chocolate)….The rise in insulin causes a depression of glucagons, turning off the liver’s ability to make excess sugar…this settles down the hyperglycemic response to stress sometimes in a matter of minutes…..when stress is more intense or has gone on for a long time and the hyperglycemia is more sever, then dense fatty/salty junk foods sound better than sweets….This is why people stress eat….


Hard to know if that the interpretation of the reader that quoted the book or from the book itself. In any case, it's clear that the recommendation is to eat the sugar-fat combo to coutneract stress, which in my opinion isn't likely to work in the long-run for the reasons explained before.