Ray Peat - Cortisol and Diabetes

"Oxidation of sugar is metabolically efficient in many ways, including sparing oxygen consumption. It produces more carbon dioxide than oxidizing fat does, and carbon dioxide has many protective functions, including increasing Krebs cycle activity and inhibiting toxic damage to proteins. The glycation of proteins occurs under stress, when less carbon dioxide is being produced, and the proteins are normally protected by carbon dioxide."


I won’t go into this too much, as this was the topic in a recent blog post on sugar and carbon dioxide, but I do believe, especially considering my own experience with both a very high carbohydrate and a very high fat diet, that for things like vasodilation and athletic performance and recovery – a carbohydrate-based diet is vastly superior. Even something as simple as breathing through my nostrils is easier on a carbohydrate-based diet. While it is possible that there is no “best” form of fuel for the human body, nearly all top athletes in the world eat predominantly carbohydrates to increase speed, performance, recovery, and so on. It’s very possible there is a “best” form of fuel for the human body, and that glucose is it.

"When sugar (or starch) is turned into fat, the fats will be either saturated, or in the series derived from omega -9 monounsaturated fatty acids. When sugar isn't available in the diet, stored glycogen will provide some glucose (usually for a few hours, up to a day), but as that is depleted, protein will be metabolized to provide sugar. If protein is eaten without carbohydrate, it will stimulate insulin secretion, lowering blood sugar and activating the stress response, leading to the secretion of adrenalin, cortisol, growth hormone, prolactin, and other hormones. The adrenalin will mobilize glycogen from the liver, and (along with other hormones) will mobilize fatty acids, mainly from fat cells. Cortisol will activate the conversion of protein to amino acids, and then to fat and sugar, for use as energy. (If the diet doesn't contain enough protein to maintain the essential organs, especially the heart, lungs, and brain, they are supplied with protein from the skeletal muscles. Because of the amino acid composition of the muscle proteins, their destruction stimulates the formation of additional cortisol, to accelerate the movement of amino acids from the less important tissues to the essential ones.)"

It’s certainly interesting to note in the first sentence of this passage that any fat that is manufactured in the body is saturated or monounsaturated – mostly palmitic acid and Mead acid. In fact, Peat strongly believes that eating lots of carbohydrates, even if they are converted to fat as in fructose being converted to palmitic acid in the liver, is highly beneficial. Palmitic acid displaces omega 6 (linoleic acid), and is one of the tools in Peat’s toolbox for purging the body of excess polyunsaturated fat.

The rest of the passage is all a pretty accurate portrayal as far as I’m concerned, and is the reason why low-carbohydrate diets can be so metabolically destructive if continued long-term. Simply put, a lack of glucose subjects the body to an increased amount of pro-aging, pro-stress hormones. That’s not to say, as JT has alluded to in the comments in the past (despite the fact that he ended up with severe adrenal fatigue after prolonged carbohydrate restriction) that it’s impossible for you personally to not improve your health on a low to moderate carbohydrate diet. It may be very possible that producing a little more adrenaline and cortisol may help balance out an individual’s physiology – where others need to produce less and derive more of their energy from carbohydrate consumption.

But that is just a theory. Experiment for yourself, but watch out for increased pain, irritability/anxiety, cold fingers and toes, loss of appetite, and other negative signs that can occur when you consume a high ratio of protein to carbohydrate at a meal.

"The diabetic condition is similar in many ways to stress, inflammation, and aging, for example in the chronic elevation of free fatty acids, and in various mediators of inflammation, such as tumor necrosis factor (TNF)."

I used to believe, like Joseph Mercola and other low-carb zealots, in the Obeaster bunny. You know the story, you eat too many carbohydrates, this stimulates insulin, and if you keep at this long enough the obeaster bunny will come and bring you a basket with lots of sugar (high blood sugar/insulin resistance, metabolic syndrome, type 2 diabetes). Yeah, I like that idea. The Obeaster basket. Perhaps if we started calling “Syndrome X” the “Obeaster Basket” people would finally catch on.

But then I encountered a more accurate depiction of what’s really going on – inflammation and cortisol (from psychological stress, sleep loss, chronic infection, chemical contamination, and any number of other things that can trigger the identical hormonal chain reaction) cause a chronic elevation of free fatty acids, which cause insulin resistance and interfere with glucose clearance. I came to the same conclusion as Peat long before I looked closely at his work, only to discover that he saw it the exact same way (but in much greater and elegant detail) and has for decades. The irony is that to keep cortisol down, it requires frequent carbohydrate feedings – what most diabetics have been led to believe by guys like Mercola as being the CAUSE of diabetes. Many of these “alternative renegades” are swimming in the complete wrong direction. Carbohydrate restriction should be reserved only for those who do not produce sufficient insulin, and even in that case it might still be better to eat lots of carbohydrates and take a larger insulin dose.

"Rather than the sustained hyperglycemia which is measured for determining the glycemic index, I think the “diabetogenic” or “carcinogenic” action of starch has to do with the stress reaction that follows the intense stimulation of insulin release. This is most easily seen after a large amount of protein is eaten. Insulin is secreted in response to the amino acids, and besides stimulating cells to take up the amino acids and convert them into protein, the insulin also lowers the blood sugar. This decrease in blood sugar stimulates the formation of many hormones, including cortisol, and under the influence of cortisol both sugar and fat are produced by the breakdown of proteins, including those already forming the tissues of the body. At the same time, adrenalin and several other hormones are causing free fatty acids to appear in the blood."

Again, I’m not sure where he gets the idea that starch is a pro-cancer and pro-diabetes substance in and of itself. An insulin spike in the absence of carbohydrate as happens when you consume protein by itself probably shouldn’t be compared to an insulin spike from starch, which is accompanied by lots of carbohydrates to keep the blood sugar from falling. While some people very well may feel symptoms of adrenal hormone activation from eating starch, many feel this activation from eating sugar but NOT when they eat starch. Again, know what it feels like to be having a surge of adrenaline (cold fingers and toes, irritability, appetite suppression, etc.) and try to figure this out for yourself – free of mental interference from biochemical oversimplifications like the one Peat uses in the above paragraph.

"Since the work of Cushing and Houssay, it has been understood that blood sugar is controlled by antagonistic hormones: Remove the pituitary along with the pancreas, and the lack of insulin doesn't cause hyperglycemia. If something increases cortisol a little, the body can maintain normal blood sugar by secreting more insulin, but that tends to increase cortisol production. A certain degree of glycemia is produced by a particular balance between opposing hormones."

This is more of Peat’s genius shining through. Many hormones are involved in blood sugar regulation. Insulin sends blood sugar down and cortisol sends blood sugar up. Yet, low-carb authors believe that eating carbohydrates, which generally raise insulin and lower cortisol, is the cause of diabetes. Clearly there is more to the story.

The work of Cushing showed the effects of cortisol excess. The disease Cushing’s Disease, which is basically a severe manifestation of metabolic syndrome that is typically caused by taking corticosteroid medication, shows the basic impacts of cortisol excess in the human body. Abdominal obesity, PCOS, moon face, stretch marks/striae, hyperglycemia/diabetes, increased heart disease risk, high cholesterol and triglycerides – you get the picture. It is very clear.
Houssay was a Nobel Prize winner who, at one point in his career, supposedly cured diabetics with sugar and coconut oil according to Peat. I do believe that sugar could very well be a wonderful anti-diabetic tonic (assuming most cases are caused by excess cortisol exposure, which I believe they are), and not the cause of diabetes as many falsely believe. But most comparisons that I’m aware of hint that sugar tends to cause greater levels of free fatty acids in the blood than starch, which would make starch hypothetically preferable to sugar in the treatment of diabetes based on this assumption.

"Tryptophan, from dietary protein or from the catabolism of muscles, is turned into serotonin which activates the pituitary stress hormones, increasing cortisol, and intensifying catabolism, which releases more tryptophan. It suppresses thyroid function, which leads to an increased need for the stress hormones. Serotonin impairs glucose oxidation, and contributes to many of the problems associated with diabetes."

Here Peat thinks that tryptophan might have a role in hyperglycemia, and I have a hunch that all of Peat’s villainous amino acids (tryptophan, methionine, cysteine) may be a very big factor in the grand scheme of things. I know personally that reducing animal protein consumption provides the greatest immediate improvement in overt inflammatory issues I’ve struggled with since my early teens (back pain, pain in lower calf muscles similar to shin splints, asthma). These problems seemed to come to a peak during my milk diet experiment, in which I consumed nearly 200 grams of dairy protein per day (dairy protein is one of the richest sources of tryptophan). And, it’s worth mentioning that virtually every book published on reversing type 2 diabetes or claiming to have dramatic success with the disease is by a vegetarian zealot (Fuhrman, McDougall, Barnard, Whitaker, etc.).

"“Diabetes” is often the diagnosis, when excess cortisol is the problem. The hormones have traditionally not been measured before diagnosing diabetes and prescribing insulin or other chemical to lower the blood sugar. Some of the worst effects of “diabetes,” including retinal damage, are caused or exacerbated by insulin itself."

Every diabetic on earth should know that cortisol can and often is a root cause of insulin resistant diabetes. Unfortunately, cortisol tests are very unreliable and do not test intracellular cortisol – something authors Shawn Talbott and Jon Gabriel have both mentioned being more significant than the amount of cortisol showing up in blood or saliva. Malcolm Kendrick reports that those with high baseline cortisol will have low cortisol levels in response to stressors – similar to how those with high baseline insulin will generally have a low insulin response to food. Like I said, unreliable. But the evidence against cortisol is too strong to seek for an alternate prime suspect in the causation of most cases of diabetes.

Of course, the root causes are very individual if cortisol is the chief culprit – as hundreds of diet, lifestyle, hereditary, and psychological factors can cause hypercortisolism. A very individual investigation is the only way to flush out the root cause(s), but in the meantime one can probably make great improvements by focusing on diet and lifestyle modification that is anti-stress and anti-inflammatory (such as getting lots of sleep, staying well-hydrated, increasing meal frequency, eating plenty of calories, minimizing omega 6 consumption, eating plenty of carbohydrates at each sitting, and decreasing animal protein in the diet).

"Antiserotonin drugs can sometimes alleviate stress and normalize blood sugar. Simply eating sucrose was recently discovered to restrain the stress hormone system (“A new perspective on glucocorticoid feedback: relation to stress, carbohydrate feeding and feeling better,” J Neuroendocrinol 13(9), 2001, KD Laugero)."

Got that? Eating sucrose stifling the stress hormone system… Interesting that diabetics often crave sugar like a mofo, but are afraid to eat it because they are under the impression that sugar caused their diabetes. This may be a tragic mistake akin to thinking that water causes thirst, and avoiding it when you are thirsty – only to finally cave into cravings for water and beat yourself up over a lack of willpower. But there is still much controversy here. Like Rosenfelt has been so good about in the comments section of late – there is a study showing an increase in the stress system when ingesting sugar instead of fat or starch. Saying that sucrose lowers stress hormones as if it were textbook truism may be too great of a leap.

"The free fatty acids released by the stress hormones serve as supplemental fuel, and increase the consumption of oxygen and the production of heat. (This increased oxygen demand is a problem for the heart when it is forced to oxidize fatty acids. [A. Grynberg, 2001]) But if the stored fats happen to be polyunsaturated, they damage the blood vessels and the mitochondria, suppress thyroid function, and cause “glycation” of proteins. They also damage the pancreas, and impair insulin secretion.


A repeated small stress, or overstimulation of insulin secretion, gradually tends to become amplified by the effects of tryptophan and the polyunsaturated fatty acids, with these fats increasing the formation of serotonin, and serotonin increasing the liberation of the fats."

We know that the stored fats in modern humans have become increasingly polyunsaturated due to massive changes in the type of fat consumed over the past century. So at this point the conversation becomes incredibly interesting if polyunsaturated fats really do indeed have such a powerful anti-metabolic and protein-glycating effect. Author Barry Sears who has taken a similar physiological approach to understanding modern disease as Peat has, has dubbed this fat “toxic fat,” believes that storing this fat is actually protective in a sense, and that releasing it into the body via standard dieting can be very poisonous. In my experience, losing fat has been highly detrimental to health and metabolism without exception, and my primary strength has been helping people recover from losing fat, so it’s an interesting point of view. It would be funny if the increasing body fat that Americans see with advancing age was really a great protector against the Standard American Diet. I’ve argued all along that the human body is not stupid, and does the best it can with the tools it is presented with. Keep in mind that in elderly Americans, as was found in the compiled NHANES survey data, the obese (BMI 30-35) have the best mortality and morbidity statistics.

Stay tuned for our next conversation on glycation – a term frequently abused in the carbohydrate witch hunt, and much more about polyunsaturated fat’s role in diabetes.

TXNIP and Obesity Guest Post by Brock Cusick

Howdy folks, we interrupt Ray May for this highly-anticipated guest blog post by none other than Brock Cusick, frequent 180 commenter, follower since the dawn of http://www.180degreehealth.com/, and author of the blog http://cusickonnutrition.blogspot.com/.  While we can never expect any two people to have identical views, even when those two people grew up watching the movie Condorman on every single sick day, I have allowed Brock to share his views openly - discussing some new research he has come across that identifies yet another important link in the body weight regulation system of the human body.  I hope it triggers some great conversation.  I share some of the thoughts I exchanged with Brock about this in the comments section.  Anyway, thanks Brock - for the post and your inspiration.  Like the time you wrote me, "If do right, no can defense."      

The Body's Fatness Regulator Has Been Found
There are moments when a single piece of information falls into your lap and whole new vistas become clear. Many small pieces of information previously formless snap together into a working whole, and what was confusing just moments before, becomes discernible. I had one of those moments on Tuesday, the 26th of April, 2011 - and I would like to share it with you.

This post is about weight loss and diabetes, why we get fat, and how we can lose it.

Researchers at Yeshiva University’s (go Macabees!) Albert Einstein School of Medicine have identified and characterized a curious little protein (link goes to synopsis; full paper costs $30) produced in the hypothalamus (long known to be involved in body fat regulation) called thioredoxin-interacting protein (TXNIP, which I pronounce “ticks-nip”). Unsurprisingly this TXNIP has an influence on “thioredoxins”, a class of proteins found in many tissues throughout the body.

The best way to think of TXNIP is as a graduated signal - like a light on a dimmer switch going from “off” to “barely on” and all the way up to “bright as possible.” The hypothalamus senses certain things about the body’s current condition and then produces the appropriate level of TXNIP so it may instruct all of the thioredoxin-producing tissues of the body how to behave. In this way the diverse tissues of the body (which have no way of communicating directly with each other) act in unison.

Just what TXNIP signals is absolutely incredible. High TXNIP levels cause white fat cells to retain fat, brown fat cells to reduce heat production, and all of the body’s tissues to become insulin and leptin resistant, while low TXNIP levels cause white fat cells to release lipids (lipolysis), brown fat cells to produce heat (thermogenesis), and all other tissues to become insulin and leptin sensitive. In one fell swoop one protein explains obesity, Type II Diabetes and cold feet. Moreover weight gain and diabetes occurred “in the absence of any effect on feeding behavior. Oxygen consumption, respiratory quotient, physical activity, and brown fat temperature were decreased in hTXNIP-expressing mice compared with controls, suggesting that lower energy expenditure in hTXNIP-expressing mice accounted for their higher rate of body weight gain.”

To translation the geek-speak: The mice that got fat didn’t eat any more than the lean mice; their bodies just became insulin resistant, partitioning calories over to the love handles and “paying” for the calorie deficit by throttling down various metabolic activities. If that doesn’t shut up the “calories in/calories out” and “Just eat less! Have discipline!” crowd, they can no longer lay claim to being in any reality-based community.

The paper then goes on to identify the three factors that regulate TXNIP expression, and they are blood sugar, insulin and leptin. High blood sugar, low insulin and low leptin all cause TXNIP expression to increase, while low blood sugar (or, “healthy levels of blood sugar”), high insulin and high leptin all cause TXNIP to fall.

(What’s that, you say? Insulin spikes cause TXNIP to fall, inducing lipolysis? Yessir! I bet those Glycemic Index folks are feeling pretty silly now.)

Of the three signals the paper does not identify which input (sugar, insulin or leptin) has the strongest effect on TXNIP, but I suspect it is blood sugar - diabetics often have high insulin and leptin levels without any reversal in their symptoms. Or perhaps any one input being “out of desired range” is enough to send TXNIP up. At this point it’s an unanswered question.

Despite the uncertainty I just mentioned, this is still fantastic science and quickly leads us to what we have to do if weight loss and diabetes reversal are our goals. Anything we can do to get blood sugar low and keep it there, and anything we can do to get insulin and leptin up and keep them there, is going to work in our favor and possibly lead to weight loss. Below are the strategies I believe will trigger immediate and “effortless” weight loss-

Carbohydrates. Fiber-rich, fresh carbohydrates are the “triple threat” for weight loss (emphasis on the fiber). The fiber will ferment into short-chain fatty acids (SCFAs) in the hindgut, turbo-boosting insulin sensitivity and thus lowering blood sugar; the glucose will spike your insulin; and the calories will spike your leptin. Between these three factors TXNIP is toast. Instant leaning out. Make these the basis of your diet - fresh whole grains (brown rice, corn, oats, wheat - whatever) and potato variants with the skins on (the skin is where the fiber is). If you have the means to make fresh flour, chapati it up.

Keep protein and fat low. There’s nothing wrong with protein and fat, but they don’t boost insulin or tame blood sugar as well as carbs. Each calorie of fat or protein you eat is going to be a calorie of carbs you don’t eat before you’re stuffed for the day.

The proteins you do eat should be a mix of “normal” meat and gelatin. Fats should definitely be saturated - especially coconut oil.

Eat the Food. Never skip meals and always eat to appetite. This is about leptin, people! Leptin, leptin, leptin! This woman lost 232 lbs. over two years after switching to a regimen that never skipped meals while making no changes to the quality of her diet whatsoever. I think we can do better.

Also, if you're really craving something that's "off diet", just go for it. The stress of thinking about while you dutifully eat your potatoes just isn't worth it, and maybe you're craving it because your body knows you need some vitamin, mineral or other quality. Trust your instincts and just get back on the horse at the next meal. It's okay, I promise; I won't come over to your house and berate you for being a bad person.

No Milk. For reasons that aren’t clear to me, but many people have reported this, it is very easy to gain build muscle and lean tissues while drinking milk but damn near impossible to lose weight. Evolutionarily this makes sense - the last thing you want a nursing infant to do is lose weight. So this means that for the duration of your weight-loss effort, keep dairy to a minimum (or none at all, if you can manage). Butter (and especially ghee) is probably alright though since it lacks the proteins and sugars of milk that seem to be so anti-weight-loss.

Frequent Feeding. The TXNIP study found that any sort of fasting caused TXNIP to inexorably rise, while meals immediately quenched TXNIP production (the insulin and leptin signal). Meanwhile other studies on both humans and horses found that frequent meals kept leptin up and blood sugar low the whole day long, while infrequent meals produced wide swings in both. Don’t listen to those leangains guys - frequent little meals (FLM) is the way to go.

Anita Mills (who I linked to above in “Eat the Food”) also ate small frequent meals. Her Doctor’s advice was spot on (if incomplete) for keeping blood sugar lower and leptin higher.

Helpful note: In the last week I have already started making FLMs, and it’s quite convenient. I just make my breakfast as usual but double the amount I make and then divide it into four portions. I then eat one immediately and the other three portions go into tupperware for work. Dinner is eaten with the family normally. No sweat.

Correct Exercise. This is just as important as any dietary change. Lift weights, do bodyweight exercises, and/or Maxercise. Read Matt’s post at the previous link and his post on the PACE system by Al Sears to understand more fully the reasons why this is important, but the short version is - because it lowers cortisol and blood sugar.

Speaking of cortisol …

Lower Cortisol. Straight from Wikipedia, cortisol’s “primary function [is] to increase blood sugar”. Cortisol is bad for weight loss, mm’kay? So meditate, go for walks, do yoga - whatever. Almost anything that reduces cortisol is probably a good thing. Foods that lower cortisol, such as orange juice and ice cream, might also be helpful in moderation.

Ice Cream?? Heh heh. That’s been quite the topic du jour around here, eh? Well actually some amounts of ice cream might be good (or at least “mostly harmless”) for weight loss if you are already very insulin sensitive. Someone who is still diabetic will have increased blood sugar for hours from a bowl of ice cream (or a plate of pasta), but someone with an excellent blood sugar control should see their blood sugars return to normal fairly quickly - while also getting an insulin and leptin boost that quenches TXNIP expression. Until I hear evidence to the contrary, I’m putting this into the “Allowed in moderation” category. The basis for your diet should still be high-fiber starches though, 4 to 5 meals of the day.

Avoid Stimulants. Anything that boosts the adrenal glands is going to boost cortisol as well as adrenaline, causing high blood sugar. Sorry Mr. French-Press, you and I will just have to take a break.

Sleep. It does a body good. Sleep is so important I can’t even summarize it in one paragraph or two. Just get a much as you can. If at all possible, unplug your alarm clock and go to bed early.

And that’s it!

One last point. Let’s call this system something. In honor of the grain-based nature of this diet, the light amounts of protein and fat, the regular exercise and strict diurnal practice of sleeping a lot, I humbly suggest The Neolithic Diet. (Strictly speaking our species has been eating a carb-based diet for 500,000 years (No one tell Art De Vany!), so this diet is actually Paleo. But let’s not confuse people.)

This Neolithic Diet isn’t just theoretical. I put it into practice on April 27, 2011 and will be “live blogging” the results as they come in at my nutrition blog Chicken Soup for the Liver. If you're interested in how it works you can follow me there. Also, if you choose to try this experimental diet with me PLEASE do two things - (1) email me to let me know, and (2) take some “before” pictures. If this regimen is as successful as I hope some “before and after” shots from people other than just myself would go a long way towards convincing even more people to put this into practice. And then we’ll have really started something.

Special thanks Mark A., a 180 reader and friend, for first alerting me to this research. Super-special thanks to Matt Stone, for letting me contribute to the discussion here.
-Brock Cusick; bmcusick@gmail.com

Overfeeding Reduces Insulin Resistance?

I had to laugh as the Mayor of Hair Danny Roddy contacted me, wondering if I had heard what was being said about me at this year’s Weston A. Price Foundation conference this past weekend. I had not, but I followed his lead and snooped around on Twitter where there was a tidbit about Stephan Guyenet being asked about overfeeding reducing insulin resistance.

“Ah, you’ve been reading Matt Stone,” he said, or something along those lines. “Overfeeding does NOT decrease insulin resistance. I don’t know where he got that idea from.”

Well, I figured this was a good opportunity to share exactly where I got that idea from, and why I believe it to be so as it is defined here.

First of all, “overfeeding” is a misnomer and I should probably stop using it.  Overfeeding, in the medical literature, means giving someone a closely-monitored increase in calories above their normal, weight-maintenance requirement. When people embark upon RRARF, my program that you can read about in a Free eBook HERE, calories are not monitored. Rather, one is asked to eat at least to the satisfaction of the natural appetite and perhaps a little BEYOND appetite. I don’t say to force feed, but explicitly say to “eat as much as you can ENJOY.”

For many, this may equate to overfeeding. For others, maybe not. When eating an exclusively whole foods diet, particularly when switching out fibrous starchy foods for refined sugar and eating foods with no flavor enhancers, calorie consumption often spontaneously decreases. Although I would say that cases in which people lose weight doing RRARF is an indicator that calorie consumption decreased, I’ve also found this to be untrue – as one person in particular reported increasing calorie intake from 1,000 per day to 2,200-2,500 per day and losing 14 pounds in 2 months time. It is unpredictable, and since all the factors relevant to weight loss, calorie consumption, insulin sensitivity, and so on are not measured – no real verifiable conclusions can be made.

But I’m not Walter Willett, and I cannot have whatever I could possibly dream up to do a study on actually be sponsored and take place. I must resort to monitoring what actually happens to people when they follow this advice.

So is RRARF overfeeding? Who cares. It’s the unrealistic fiber-free fructose and corn oil-laden studies on overfeeding (a good way to develop hepatic insulin resistance like Morgan Spurlock did) that are irrelevant, not the real-life experiences and health impacts that people have who are trying the recommendations I’ve laid out in RRARF based on my own research, theories, experimentation, and personal observation.

Anyway, let’s back up a moment. I first got the idea that eating MORE food could reconcile insulin resistance while reading Schwarzbein’s books. In those books, it’s not necessarily insulin being spiked by high-calorie loads, fat interfering with glucose uptake, or carbohydrates that cause resistance to insulin. In fact, Schwarzbein goes on and on about how cortisol, elevated by things such as undereating, undersleeping, or overexercising (all things addressed as part of RRARF), can be a player in the development of metabolic syndrome. She states, explicitly for those with insulin resistance and weight problems, that they should be “eating more food, more often.”

Once again, since Schwarzbein is a practicing endocrinologist, she was actually able to see how this advice performs on basic tests such as glucose tolerance, cortisol levels, insulin levels, and so forth. Real experience and real observation with real people living in the real world.

This idea was greatly strengthened when I read Russ Farris and Per Marin’s The Potbelly Syndrome. I consider these two gentlemen to be some of the finest researchers out there. The book of course was about the hormone cortisol and contained the following passage:

“…insulin resistance leads to weight gain, but most health professionals believe that the opposite is true. If obesity does cause insulin resistance, then we would expect people who are overfed to become more insulin resistant, but that is not the case. Researchers in Indianapolis overfed six slender, active, young adults for several weeks… Five of the six subjects became LESS insulin resistant!”

This made perfect sense to me as I had been studying the wacky world of obesity research at the time, and overfeeding resulted in a drop in hunger, a rise in metabolism, and difficulty gaining more fat the more fat subjects gained. In other words, overfeeding brought about the triggering of mechanisms that made the body work hard AGAINST fat gain, and induce fat loss. Doesn’t sound like what I know of insulin resistance, which suggests that insulin resistance leads to hunger, reduced metabolism, increased propensity to store fat, and so forth.

Likewise, with underfeeding as in Ancel Keys’s The Biology of Human Starvation, underfeeding made the men ravenously hungry, store fat at an incredible rate – particularly in the abdominal region indicative of insulin resistance, without building back muscle tissue, and other signs of insulin resistance, not sensitivity. Only after binge eating on pies, pastries, and dairy products up to 7,000 calories per day and gaining a ton of body fat did they rebuild their lost muscle mass and start to spontaneously lose body fat at an amazing rate (while still continuing to gain lean mass) eating to appetite.

In other words, underfeeding made them gain belly fat eating to appetite. Overfeeding made them lose belly fat eating to appetite. It’s not really that wild of a concept, and knowing how well the human body defends against a shift away from its weight set point, it should be no surprise that gaining weight via overfeeding causes the body to become more insulin sensitive, which increases muscle building and heat production, minimizes fat storage even in the face of massive calorie intakes as was witnessed in the famous Ethan Sims overfeeding study, while decreasing appetite.

Anyway, overfeeding lowers cortisol just as underfeeding raises it. The effects of overfeeding and underfeeding mirror one another. Even a book as scientifically straightforward as Lyle McDonald’s Ultimate Diet 2.0 lays out a simple chart of hormonal changes that take place during overfeeding vs. underfeeding. Underfeeding increases cortisol. Overfeeding decreases it.

This is the presumed mechanism, considering that cortisol blocks the action of insulin and leptin for that matter which is even more significant (and probably why underfeeding causes the weight set point to rise), that makes changes in weight a negative feedback system. This was the whole point of Russ Farris and Per Marin’s book, which can be summarized as: “Hypercortisolism causes insulin resistance, dummy, not carbs or eating too much.”

Overall the best sign of improved insulin sensitivity is improved glucose clearance from the blood after eating. I was so captivated by overfeeding’s potential surprise ability to improve insulin resistance, that I tried RRARF while monitoring my blood glucose levels and found my postprandial blood glucose readings to drop by more than 25% after just 30 days. Even two baked potatoes at a 1,000+ calorie feast couldn’t send my blood sugar above 75 mg/dl by the end of it, and I gained abdominal fat in the process, which is even more out of synch with the misinterpretations of the scientific literature held by most researchers.

Of course, many of you that have gone through the rigors of testing your own blood glucose levels witnessed the same thing while eating beyond appetite of whole foods. Martin, Lisa, Sheri and her husband, and Undertow come to mind.  Sheri for example, writes:

"My temps are great going from 96.4 up to 97.8 and even 98.0 on some days. During ovulation I was 98.5-98.7. My fasting glucose started in the low 100’s and has only dropped to a consistent 93, better but I still obviously need it lower. Then my 1 hour postprandial glucose reading jumps all over from 199 at first and then on different days 140’s or 150’s. It has been in the 110’s and low 120’s lately and I get excited it’s improving but then will jump up to the 140’s again.  I sleep a million times better, have less joint pain from an autoimmune disease and didn’t have cramps during my period for the first time in years. I have gained 5 unwanted pounds but oh well. My husband has increased his temps from 95.9 to between 97.0 - 97.5 depending on the day and also sleeps a million times better. Poor thing really packed it on with a whopping .2 pound gain- not even a half a pound. His fasting glucose has stayed even at around 87. His postprandial glucose readings have gone from the 120’s and 130’s to a typical 103. We have nothing negative to say about our experience so far and are very thankful to you, Matt."

I also just received some harder data from Chris Sandel of www.seven-health.com/

You can and read about him here: http://www.seven-health.com/about-us/

I went through his extensive data, and there is no question that his glucose clearance improved during the 30 some odd days he spent doing RRARF. To get some figures, I went through his data and did some averaging. I compared the readings from the first half of his month on RRARF to the 2nd half of his month on RRARF, and took averages and compared them. Here are the changes:

Weight Increase: 0.4 kg (insignificant)

Basal body temperature increase: Very slight from 35.81 C to 35.98 C

Fasting glucose: -4.6% from 98 mg/dl to 93 mg/dl

1-Hour postprandial glucose: -10.5% from 115 mg/dl to 103 mg/dl

2-Hour postprandial glucose: -10.9% from 119 mg/dl to 106 mg/dl

It’s also of interest that his highest 2-hour postprandial reading, which I view to be the most significant, was typically higher, and sometimes much higher than his 1-hour postprandial test towards the beginning of the experiment. This is an almost sure sign of impaired glucose metabolism, but all in all his numbers are decent for an endurance athlete taking a break (which as I’ve described in the past, from my own experience, as being a tough transition).

By the end he was able to reverse that on most days, but still has a little way to go before it’s perfected.

His highest 2-hour postprandial test was on days #9 and #10 of the experiment, which is probably pretty typical. On both of those days, his 2-hour reading was 135 mg/dl.

His lowest reading was on Day 30 of the experiment at a mere 97 mg/dl – roughly the same as his fasting level at the beginning of the experiment.

So that’s that. Maybe you can’t pinpoint what I’m talking about in the medical literature. Maybe what I’m saying doesn’t make sense with everything you’ve studied or been led to believe. Maybe you view this as poorly-controlled information (which it is) and thus unscientific and irrelevant.

But this is real and is really happening in the real world to real people, which, at the end of the day, is what really counts. Former extreme tater-hater 180-Katie summed it up best when she wrote to me:

“Finally, my blood sugar control is better. A lot better! I have no idea why eating starch would improve my blood sugar control like this, but it does. It could be elf magic or nanobots for all I care, it works!”

Insulin Resistance as Starvation

From the beginnings of my health nerdfest, I have always made a habit out of thinking through the eyes of the human body. In my experience, the body is a million times smarter than the mind – even my mind, which is like a holy deity of vast intellectual wisdumb.

In other words, I try to make sense of certain physical reactions and hormonal states in context of real life. Like for example, hypothyroidism, or a reduced metabolic state. That’s a classic example. You know that the body has reduced the rate at which it burns energy.

Why would it do that? Food shortage? Some other kind of shortage? It seems to me that, on a logical level, the body would only reduce the rate at which it burned though something – be it nutrients, calories, or whatever, if it perceived that it was going through supplies faster than they were being replenished. Give the body a surplus of everything it needs, and there’s no more need to conserve. Sho nuff, doing precisely that raises body temperature pretty reliably (as well as decreases insulin resistance) as you can read about in THIS FREE EBOOK.

If we look logically at insulin resistance, especially now that we’re beyond the idea that eating carbs and spiking insulin causes insulin resistance, which it doesn’t, we can see clearly how it is tied to the starvation “programs” for lack of a better description.

By starvation programs, I mean the hormonal chain of events that take place to:

1) Conserve calories (low energy levels)
2) Lower metabolism (low muscle mass, low heat production)
3) Increase appetite
4) Store more fat than fat burned (positive fat balance)

When we think of insulin resistance as part of the orchestrated effort to defend against starvation, it makes a hell of a lot more sense.

Insulin is a hormone that curbs appetite, raises metabolism and gives us energy – in large part by helping to store glucose and amino acids into muscle cells, builds muscle tissue – it triggers a rise in many growth factors such as growth hormone.

This is all counterproductive in a state of famine. In real famine, there is very little food and therefore very little insulin. But when the body is eating a lot and acting like it is starving (from lack of nutrients, chronic stress, sleep apnea, allergies, chronic inflammation?) it would make sense to block the action of insulin.

Doing so would keep metabolism suppressed, keep food energy from going into muscle cells where it might grow more muscle and raise metabolism while simultaneously triggering an increase in energy levels and capacity for muscular exercise, make sure food was diverted into fat cells for storage instead of muscle cells, keep appetite elevated, and so on.

In other words, in preparation for an upcoming famine, you wouldn’t want to have much muscle mass, much desire to exercise, have a normal body temperature, or have a small appetite. Rather, you’d want to be like a bear or squirrel in preparation for hibernation.

And yes, it is known that there is insulin resistance and obesity in hibernating animals, followed by an extreme manifestation of what you could call “hypothyroidism,” – a deep state of slowed heart rate, low body temperature, reduced respiration, halted digestion, and so forth.

So I’m proposing that insulin resistance is far more likely to be a state in the human body that is designed to be a preparatory state for hibernation/starvation/famine. 

And I think it’s important to look at hormonal changes within the human body as a coherent network that is trying to accomplish a specific task, rather than trying to figure out what part is gummed up.

Unfortunately, when your average person eats ad libitum, they store fat, particularly fat in the abdomen where it is most readily available to the vital organs – priority number 1. That is because of the deprivation endured prior naturally triggers the storage of excess body fat for better preparation the next go around.

This leads your average person to think that the deprivation period was “healthy” and eating to appetite and taking ‘er easy is “unhealthy.” The only way to keep the body from storing fat when it is actively trying to is to eliminate one of the necessary ingredients in fat gain, such as carbohydrates, protein, fat, or overall calories. This is, of course, a short-term strategy with long-term health consequences for the vast majority of people.

I maintain that the only viable long-term solution is to thoroughly convince the body that there is no need to store excess fat, and, over time, dissipate the need to store it.  But ample food is only one form of sustenance that the body requires to deactivate famine chemistry, including insulin resistance. Sleep, rest, emotional health, inflammation, allergies, infection, and more are all things worthy of addressing in a comprehensive approach to shut this chemistry down and lose weight automatically instead of through one of the many forms of starvation/diets currently promoted.

More on the concept that obesity and insulin resistance is “Starvation” in this video…

Befriending Insulin

Make no mistake, there are some insulin haters out there. They have managed to pollute the minds of good folks like you and me into thinking that insulin is like Insulin Bin Laden – a bad dude with no redeeming qualities.

Newcomers to www.180degreehealth.com are often still under the influence of low-carbism. Yeah, I know Taubes had a lot of references. I get it. I read the book multiple times as well as many of the references which provide ample refutation to the belief that carbohydrates are inherently toxic and lead to obesity and metabolic disease (like the works of T.L. Cleave and Denis Burkitt for starters).

But insulin is a beautiful thing. Insulin, for starters, helps take food energy out of our bloodstream after digestion takes place and packs it away into muscle cells. Wow! I bet that feels really good, stimulates your metabolism, improves your immune system, satisfies your appetite, and makes your muscles grow…. It does.

The problem is, most people’s bodies are NOT working correctly, and the muscle cells are resistant to insulin. This is where the problem lies, and there is no single piece of evidence the world over that suggests, in the slightest degree, that unrefined carbohydrate staples consumed by human beings over the past 10,000 years has anything to do with causing that dysfunction.

So the problem is the overcompensation that occurs when insulin is not communicating with muscle cells efficiently. The result is that the benefits of insulin are not realized by the body. It’s kinda like water. You only get the benefits of water for cellular hydration if you drink with your mouth open.

One of insulin’s wonderful qualities in preventing obesity and metabolic disease is the fact that it is a primary satiating hormone. Yeah Taubes, you heard me. The only reason in animal studies that little critters ate themselves to death when insulin was injected is because insulin lowers blood sugar – and the animals kept eating and eating and eating in order to keep from dying from hypoglycemia.

Insulin, in the ABSENCE of food, definitely isn’t satiating. It’s deadly.

But insulin, under normal circumstances, is an appetite suppressant.

Insulin is also the primary driver of muscle growth. Because it packs amino acids and glucose needed for muscle growth into muscle cells, muscle tissue cannot be added very efficiently without insulin present in sizeable quantity.

Because of this, among other actions of insulin (such as working in concert with leptin to raise metabolism, suppress appetite, increase lipolysis/fat burning, and so forth), insulin is a profound stimulator of the metabolic rate as well – which is probably why very low-carbohydrate diets, and low-calorie diets, produce huge drops in T3 – the active hormone that regulates metabolism.

Along with the drop in T3 comes drops in testosterone as well – another of the primary hormones involved in building muscle mass and decreasing body fat, which depends upon ample amounts of insulin to be stimulated.

Insulin also works on an axis with the catecholamines – which includes cortisol. When insulin goes up, adrenal activity falls. When insulin goes down, adrenal activity picks up. Keep insulin too low for too long and you run the risk of adrenal fatigue. You are also likely to increase the activity of cortisol (which, unlike carbohydrate ingestion, actually DOES cause insulin resistance) by keeping insulin levels suppressed, which increases insulin resistance, decreases testosterone, decreases fat burning, and otherwise takes you ever-closer to metabolic syndrome.

The result is more body fat and less lean muscle tissue – not to mention a slower metabolism in general, which all ties into the fact that your muscle cells are literally starving. There is no insulin to pump vital matter into cells when insulin is low, and if you return to eating lots of carbohydrates, they are very fattening until the point at which your cortisol levels fall, your metabolism rises, your insulin resistance decreases, and then… finally, your muscle cells start receiving nutrients and you feel better for once - something nearly everyone patient enough to give RRARF a full course has experienced in full. 

The point of this post is simple. You NEED insulin. Insulin can do some amazing things for you, first and foremost allow you to experience life at your full physical potential. But you have to be insulin sensitive to receive those benefits.

The ever-popular way to deal with insulin resistance by taking carbohydrates away from a person may have all kinds of benefits in the short-term. This is because chronically-high insulin levels as a result of insulin resistance (not caused by unrefined carbs) are lowered, and many other systems are able to come into balance because of this drop in insulin.

However, it is a dead end, and is not fixing the problem. Eventually, a person on a low-carb diet will run into negative symptoms of insulin deficiency, such as decreased metabolic rate, suppressed fat burning, weight regain, lowered testosterone, decreased immune function, and so forth. This takes a lot longer to take place in an overweight, insulin resistant person, and happens VERY quickly in an insulin sensitive lean person that has no business being on a low-carb diet in the first place.

Insulin resistance, most likely, is a development that takes place as an anti-starvation system in the body – preventing fat burning while also preventing energy from being packed into muscle cells where it would raise the metabolism and build calorically-expensive muscle tissue. As we’ve discussed and will continue to discuss, the human famine response exists to prevent starvation, but any chronic form of stress from sleep deprivation to anxiety to chronic inflammation or dental infection to overexercising to nutrient deficiency is capable of triggering that chain of hormonal events… a theme seen in response to all kinds of deficiencies and stressors according to the work of true health pioneers (not to discredit Suzanne Somers, Susan Powter, or my favorite Richard Simmons) such as Robert McCarrison and Hans Selye.

The best way to bring metabolic syndrome under control? Eat unrefined, nutritious foods to appetite or beyond without severe macronutrient restriction (but an emphasis on starch to increase insulin sensitivity and lower cortisol most quickly), get lots of rest and relaxation, lots of sleep, and whatever else you can do to minimize your burden of stress, inflammation, etc. – ranging from having root canals pulled to treating sleep apnea to decreasing the omega 6 polyunsaturated fat content of your diet. Read more about this strategy that I call RRARF (Rehabilitative Rest and Aggressive Re-Feeding) in THIS FREE EBOOK.

Ironically, the hyperinsulinemia epidemic that is sweeping the globe is best solved by befriending insulin and eating plenty of high-quality, nutritious, starchy carbohydrates (as well as other foods that stimulate insulin, like beef and cheese.... mmm, cheeseburger). Going to war against insulin with a low-carbohydrate or low-calorie diet may result in many victorious battles, but that war can never be won on a collective basis with that strategy… Even if a large percentage of people could follow such a diet long-term, which they cannot and never will, because most people’s bodies are too damn smart to let them get away with it for long.

For further reading, I highly recommend THIS Series of  ARTICLES written over the summer by James Krieger (badass) that highlights many of the errors in the low-carb theories about insulin that we’ve been discussing here for the last couple of years with some very new and interesting twists.