T2 Diabetes – Hibernation Lite?

I ran into a couple of interesting references to bears, diabetes, and hibernation. This got me (and others) wondering about the connection. While most of the folks speculated that bear metabolism might give clues to “curing” our “disease” of diabetes, I instead wondered if this might just be a pointer to very unused metabolic pathways in humans and a kind of “hibernation lite”.

Humans are Euarchontoglires, some members of which hibernate.



Euarchontoglires (synonymous with Supraprimates) is a clade and a superorder of mammals, the living members of which belong to one of the five following groups: rodents, lagomorphs, treeshrews, colugos and primates.

There’s a reason bunnies and lab rats are useful for medical testing, they are our distant cousins. Squirrels are in there too along with beavers in the rodent group. Many of these animals have facultative hibernation or winter torpor states.

Now evolution tends to be a a pack-rat for metabolism. It doesn’t just toss out a system wholesale because it isn’t needed at the moment. Usually it finds a way to just adjust the trigger mechanism to shut it off. For this reason, you can do interesting things with various animals. The most extreme one I read about decades ago (so no references that I know of now) has to do with “chicken teeth”. Some enterprising biologist took a sample of chicken gum tissue and transplanted it “somewhere else” on their body. There, removed from the local hormones of the mouth and jaw, it formed teeth. Yes, chicken teeth. See, when they evolved from dinosaurs and developed the beak, they didn’t just drop all tooth genes; only shut off the actual formation of teeth step in the location of the mouth.

Now this raises an interesting question: Did all those Euarchontoglires which have some sort of hibernation evolve it separately, or was it an inherited primitive that some of us have turned off? We don’t know, but we DO know that if you inject the hibernation trigger molecule into lab rats they go into hibernation, so at least some of the Euarchontoglires ‘had it and lost it’; and that argues for a more wide spread set of genes for it.

But that’s all off in the Rodents & related lines, not Primates. do ANY Primates hibernate? If so, that would argue the original ‘metabolic skill’ ought to be widely shared in the whole group, not just a rodent thing.


First discovery of a hibernating primate outside Madagascar

December 3, 2015
University of Veterinary Medicine — Vienna
Up to now, three species of lemurs on Madagascar were the only primates known to hibernate. Researchers at Vetmeduni Vienna in Austria, now show for the first time that another primate species that lives in Vietnam, Cambodia, Laos and China, the pygmy slow loris, also uses hibernation to save energy. The results were published in Scientific Reports this week.

So Lemurs and Loris both hibernate. Not exactly chimps and baboons, but spread from Madagascar to Asia…

While not proof, it does argue for a common metabolic system throughout the lot of us. Some biochem examination (and / or genetic examination of the system) ought to show degree of common source vs independent evolution.

Presuming it’s more likely a bit of common source… (and having some vague memory of someone inducing a hibernation like state in several animals and maybe even people with a sulphur gas /compound some years back causing a ‘stir’ about us being able to hibernate too, or some such) The most likely conclusion is that we either have the full blown metabolic paths in us, or somewhat disused and perhaps slightly broken by uncorrected mutations set of such metabolic paths (and states).

The Paper Chase

So OK, up front, the “paper” that caused the rush of folks after bear hibernation as diabetes state was withdrawn. The reason was ONE of several researches had fudged some data that showed up in 2 graphs. The sponsors and the other authors are re-doing the paper without him and stand by the conclusions. Time, one hopes, will sort it out. In the mean time I’m presuming that there is some “there there” on the basic biochem of finding diabetic markers in hibernating bears.


Retraction Watch

Retraction of grizzly bear-diabetes study follows departure of Amgen scientist for data manipulation

The retracted paper made the cover of the August 2014 issue of the journal. (Cell -EMSmith)

A study that looked to hibernating bears to understand the mechanisms behind diabetes has been retracted because an author based at the biotech company Amgen “manipulated specific experimental data” in two figures.

Gee, “manipulated specific experimental data” is called “adjustment & correction” in “Climate Science”, maybe he needs to start studying bears as climate proxies ;-)

LOTS of links in this quote in the original…

According to the The Wall Street Journal, Amgen discovered the manipulation while reviewing the data following publication of the paper,”Grizzly bears exhibit augmented insulin sensitivity while obese prior to a reversible insulin resistance during hibernation.” Published in Cell Metabolism last year, the paper has been cited 8 times, according to Thomson Scientific’s Web of Knowledge.

A press release from the journal last year — coverage in Science and Nature followed — explained the purpose of the study:

While diabetes rates are on the rise and are having serious effects on millions of people’s health, researchers studying grizzly bears have now discovered a natural state of diabetes that serves a real biological purpose and is also reversible. Investigators reporting in the August 5 issue of the Cell Press journal Cell Metabolism note that grizzly bears are obese but not diabetic in the fall, become diabetic only weeks later in hibernation, and then somehow become “cured” of diabetes when they wake up in the spring. The research reveals how natural biology, through evolutionary experimentation, can teach us new things about how animals naturally cope with conditions that would cause disease in humans.

And here’s the retraction note, which details the study’s problems:

This article has been retracted at the request of the authors.

Amgen requested the retraction as an outcome of an internal review where it was determined that one of the Amgen authors had manipulated specific experimental data presented in Figures 1 and 3. Because of data manipulation, this author is no longer employed by Amgen. The authors at Washington State University and University of Idaho are confident that the physiological data generated for this manuscript are accurate and representative of the true metabolic responses of these grizzly bears and are currently repeating the mechanistic portions of the study. Amgen deeply regrets this circumstance and extends their sincere apologies to the scientific community.

OK, I’m willing to stick with the physiological parts.

The original article:


Cell Metab. 2014 Aug 5;20(2):376-82. doi: 10.1016/j.cmet.2014.07.008.

Grizzly bears exhibit augmented insulin sensitivity while obese prior to a reversible insulin resistance during hibernation.

Nelson OL1, Jansen HT2, Galbreath E3, Morgenstern K4, Gehring JL5, Rigano KS5, Lee J6, Gong J6, Shaywitz AJ7, Vella CA8, Robbins CT5, Corbit KC9.
Author information

The confluence of obesity and diabetes as a worldwide epidemic necessitates the discovery of new therapies. Success in this endeavor requires translatable preclinical studies, which traditionally employ rodent models. As an alternative approach, we explored hibernation where obesity is a natural adaptation to survive months of fasting. Here we report that grizzly bears exhibit seasonal tripartite insulin responsiveness such that obese animals augment insulin sensitivity but only weeks later enter hibernation-specific insulin resistance (IR) and subsequently reinitiate responsiveness upon awakening. Preparation for hibernation is characterized by adiposity coupled to increased insulin sensitivity via modified PTEN/AKT signaling specifically in adipose tissue, suggesting a state of “healthy” obesity analogous to humans with PTEN haploinsufficiency. Collectively, we show that bears reversibly cope with homeostatic perturbations considered detrimental to humans and describe a mechanism whereby IR functions not as a late-stage metabolic adaptation to obesity, but rather a gatekeeper of the fed-fasting transition.

So ponder for just a moment. What triggers bears to gorge for hibernation? Less sunlight? Less activity? Perhaps a surge of fructose as fruit all ripens in fall? Just getting really fat enough? What has modern life brought to humans? Less sunlight. Less activity. A gigantic surge of fructose in whole swaths of “modern foods”. Getting rather fat enough… and then some.

So as we sit around in our “people caves”, not getting sunshine or activity, stuffed with fructose and gross calories, we get fat. This starts a fatter, lazier, less active cycle. Oddly, it tends NOT to start an ‘eat less’ cycle… just like the bears… Eventually it DOES seem to depress mental activity too. We eventually become more listless and “just want a nap on the couch”. (I can support this by pointing out I just woke up from my unexpected nap after a few blueberry muffins for lunch…)

Just how is this really any different from the bear cave or the squirrel curled up in a tree hole or underground? Stuffed, lethargic, in the dark.

Now when actively hibernating, the metabolism shifts. Metabolism of blood sugar is suppressed via insulin resistance and metabolism of fats is encouraged. In humans, we become “insulin resistant”, but instead of a ‘long long nap’ working off the fat stores, we keep shoving in the carbs… which have to go somewhere.

For some folks, that’s obesity. Sometimes lots of it, without an insulin issue. Still in the Fall mode, as it were. For other folks, they seem to shift to the winter mode of low metabolic rate and not forming fat. The blood sugar rises and we end up in a diabetic end of things as sugar gets, literally, pissed away. Still lethargic and still munching. Almost like we’re stuck 1/2 way into hibernation, but not getting the whole way.

This would be in agreement with the observational evidence for exercise and fasting as helpful in treating, or even ‘cures’ for T2 Diabetes. We are, essentially, putting ourselves into an artificial Spring and breaking the hibernation state.

Perhaps even the color and length of lighting matters to the trigger. This could vary by person, depending on how much of the primordial hibernation process and trigger systems existed in them.

Sabretoothed has a set of links on human light sensitivity starting about here (H/T Sabretoothed):


Earlier I’d noted the link between too much blue (too late at night) and insomnia from LED bulbs:


So who knows, perhaps running some cheap LEDs early in the morning to get jump started, running on the treadmill (real or metaphorical), then cooling down with 2700 K incandescents at night over a dinner of meat & leaves (Spring time fare) could shift a person back to a more Spring / Summer and less Fall / Winter mode…

Having put on a few pounds since functionally retiring last year, and “suddenly” having my first ever blood sugar not perfectly normal experience, I’m giving it a try. While I’m in the “normal” range, I’ve already shown I can drive it to “pre-diabetic” with a bout of lethargy and starches, yet get out of it with “meat & leaves” meals and dancercize to the TV.


So, in keeping with my “It’s my body and I’ll experiment If I want to!” theme; I’ve put two of the Dreaded Insomnia LED bulbs in my office space. I’ll be using them in the mornings especially on days I’m not outside. Shifting to the 2700 K (CFL / IC) mix in the evenings.

I’m also moving to add a lot more leaves to the diet, and have already dropped most all sugar (other than what the spouse bakes into things, like those muffins ;-)

So salads, sauerkraut, Brussels sprouts, choy, cabbages & such much more; noodles and potatoes and sugary cereals not so much. Coffee and tea black. Sugary drinks not at all. It’s springtime, after all… Think sauerkraut & wieners, not fruit tart and mashed potatoes.

We’ll see what happens. I’m not an ideal test subject, since my “after a dinner of potatoes and limas lots of starch” sugar was only 165. High, but only by about 20 points from any “while digesting starches” reading normal. Full diabetics could be hitting a few hundred by then. Still, IF I start plating 90s after dinner, we’ll know something happened ;-)

Clearly I need to add some exercise to the pattern too. Sleepy bears lay in caves all winter. Spring Bears are out running around. Had not planned a garden this summer (the space is a mess after 2 years of neglect), but I think that “yard time” is not optional. So I need to schedule in some shovel time, it seems. Need to go rooting around for those leaves and berries, after all ;-)

Odds & Ends & Links

Some Misc. bits are collected here, including links to some other stories based on this same source paper.


How hibernating animals are helping doctors treat diabetes and Alzheimer’s

Unlocking the secrets of hibernation could help doctors solve some of medicine’s most pressing problems
One such brain pathway helps to activate hibernation in ground squirrels when a chemical called 6N-cyclohexyladenosine (CHA) attaches to a cell surface protein called the A1 adenosine receptor (A1AR). When the action of CHA on these receptors is blocked in the squirrels, Drew’s team in Fairbanks has shown that hibernation is prevented. They also have shown that giving CHA to non-hibernators, such as rats, makes them appear to hibernate too, provided they are put in a cold environment.

“This tells us that CHA might have a potential role in therapeutic hypothermia,” suggests Drew, but there’s also another factor. Natural hibernators ‘get sick’ as they enter hibernation, and then ‘cure’ themselves when they awaken. This could have profound implications for how we assess illness and the types of treatments mounted against it.
Consider the respiratory system, for instance. In the midst of an asthma attack, and in patients with chronic obstructive pulmonary disease (COPD), airways constrict, causing the lungs to over-inflate similar to an expanding balloon. Research on Syrian hamsters shows that their lungs over-inflate to prevent lung collapse as the breathing rate decreases down to two to three breaths per minute. This happens as the animal’s core body temperature drops during the onset of torpor, a kind of short-duration hibernation. Along with overinflation, a plethora of different proteins appear on the surfaces of lung cells in human COPD and asthma. This is called molecular remodelling and it happens not just in lung disease but also in hamsters entering torpor.

As the hamsters come out of torpor, the pulmonary changes reverse, as do changes occurring in other organ systems. Decreasing body temperature in hibernation is associated with a drop in heart rate. Physiologically, the change looks like what physicians call second-degree heart block. As the animal heats up, the heart rate returns to normal. By studying the mechanisms underlying the reversals in hibernators, scientists may uncover new treatment strategies for pulmonary and cardiac disease in humans.
Elsewhere, with type 2 diabetes, patients produce the hormone insulin but the insulin is not effective because sensitivity of cells to insulin is abnormally low. Because of the reduced insulin sensitivity, cells do not absorb sugar from the blood. Scientists at the University of Tennessee have shown that essentially the same thing happens in black bears as they enter hibernation; they become insulin resistant. This keeps their cells from absorbing blood sugar (glucose), which enables them to draw energy from fats that have built up in the weeks prior to hibernation. In terms of blood chemistry, hibernating bears look like diabetic humans, but on revival from hibernation the chemistry returns to normal. This suggests there must be a chemical pathway underlying insulin sensitivity that can be adjusted. If scientists can get a hold on such a pathway, they might be able reverse the same effect in diabetic people.

But perhaps, the greatest beneficiaries of hibernation research will be those suffering from degenerative conditions in the brain. Synapses are connections between nerve cells, akin to the electronic connections in a computer. Learning and creation of memory are associated with formation of new synapses in the brain. In dementia, especially in people with Alzheimer’s disease, recent memories deteriorate along with the ability to form new ones. This happens as synapses disappear. During hibernation, connections between neurons in the brain deteriorate, just as they do in Alzheimer’s, but what happens as the animals start waking up? You guessed it; synapses are restored. In fact, on revival, hibernators go through a so-called hypersynaptic state, characterised by an overabundance of connections. Subsequently, the brain settles down to its pre-hibernation connections.

Note that it also references Alzheimer’s that is looking like Type 3 Diabetes:


So what if these are less diseases and more operating machinery out of specifications?

(Has an ad-blocker nag, so I’ve copied more freely to save you the grief)

August 5 2014
An ability of grizzly bears to cope with obesity and diabetes during hibernation could provide lessons for the care of humans, say researchers.

Every autumn, the bears prepare for winter by stuffing themselves with food and becoming obese.

Weeks later during hibernation they enter a state similar to type 2 diabetes, only to “cure” themselves when they wake up in the spring.

US scientists studying the bears made the surprising discovery that when grizzlies are at their fattest they are also most sensitive to the blood sugar regulating hormone insulin.

This was achieved by shutting down the activity of a protein called PTEN in fat cells.

Also, in contrast to humans, blood insulin levels in diabetic grizzlies did not change. Instead, cells that the hormone communicates with turned their response off and back on again when it was time to stop hibernating.

Lead scientist Dr Kevin Corbit, from the US biotech company Amgen Inc, said: “Our results clearly and convincingly add to an emerging paradigm where diabetes and obesity – in contrast to the prevailing notion that the two always go hand-in-hand – may exist naturally on opposite ends of the metabolic spectrum.

“While care must be taken in extrapolating preclinical findings to the care of particular patients, we believe that these and other data do support a more comprehensive and perhaps holistic approach to caring for patients with diabetes and/or obesity.”

Cellular mechanisms leading to obesity may in fact protect certain patients from diabetes, said Dr Corbit.

In other patients, mechanisms leading to diabetes may protect against obesity.

Humans with low levels of PTEN were likely to possess the bear-like quality of remaining highly insulin-sensitive even if obese.

“Moving forward, this more sophisticated understanding of the relationship between diabetes and obesity should enable researchers not only to develop therapies targeting these mechanisms, but also to identify the appropriate patients to whom these therapies should be targeted,” Dr Corbit added.

“Develop therapies”? Might we not just realize we’ve got the same or very similar metabolic pathways and apply the expected natural processes and triggers to “make it Spring again” for our bodies?


6 August 2014
Grizzly bears become ‘diabetic’ when they hibernate

By Philippa Skett

Some bears can have their cake and eat it too. Grizzly bears become “diabetic” during hibernation, and then recover when they awake.

Lynne Nelson at Washington State University in Pullman and her colleagues investigated insulin activity in tissue samples taken from six captive grizzly bears over the course of a year.

As the bears put on weight in preparation for the winter, they responded normally to insulin – which prevents the breakdown of fatty tissue. But during hibernation, insulin effectively stopped working. That is a symptom in people with type 2 diabetes, in which high fat levels in the blood induce insulin resistance.

OK, so get those blood fat levels down. Exercise a lot more, eat a lot less… Avoid sugars (and starches) so your metabolism must shift to fat burning.

Linked syndromes

“Diabetes and obesity may exist naturally on opposite ends of the metabolic spectrum,” says co-author Kevin Corbit of biotechnology firm Amgen in Thousand Oaks, California. “The cellular mechanisms that could be protecting people from diabetes, and the mechanisms leading to diabetes in other patients, may also be what protects them from becoming obese.”

The results suggest there is a chemical pathway involved in altering sensitivity to insulin. This pathway could hold the key for developing treatments for type 2 diabetes.

Or maybe, just maybe, they are two ends of a metabolic oscillator designed to keep us in pace with the seasonal shift of food availability. Putting on the pounds when summer and fall arrive with lots of fruits, starches and all; but burning them up during a long winter fast and the occasional critter on the BBQ.

To the extent that is true, just getting in sync with seasonal food availability and types ought to help.

Maybe it just confuses the food storage / burning switch to be stuffing ourselves to the gills year round and never being hungry chasing dinner. Perpetual Fall Feasting might just be a Very Bad Idea.

There seems to be lots of anecdotal evidence for a fasting “cure” for T2 Diabetes:


Which would be in keeping with the idea of diabetes as Hibernation Lite. So after the Fall Feasting, you need a (maybe very short) Winter Fast, and they you are again ready for the Spring “meat & leaves” while you wait for those Fall pies, roots, and fruits again…

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About E.M.Smith

A technical managerial sort interested in things from Stonehenge to computer science. My present "hot buttons' are the mythology of Climate Change and ancient metrology; but things change...
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42 Responses to T2 Diabetes – Hibernation Lite?

  1. Larry Ledwick says:

    Lots of related dig here items under the topic of Intermittent Fasting for weight loss, where as you go on a fast (no significant carbohydrate intake), your body shifts metabolism to fat where the majority of you caloric needs are satisfied with fat metabolism, AND your body increases HGH (human growth hormone) to spare protein so the body does not consume its muscle mass for energy. As little as 50 grams of carbohydrate intake will “turn off” this metabolic shift, and the hunger reflex returns and the body starts trying to use muscle glycogen and blood sugar for energy. In the fasting state only the brain uses significant sugar intake, and some of its energy requirements get shifted to alternate metabolic paths like use of ketones.


    Click to access jcinvest00482-0014.pdf

    Similarly SAD syndrome (seasonal affective disorder) is probably part of that pre-hibernation process. It is triggered by reduced light exposure (treated with light therapy)
    symptoms include:
    Tiredness or low energy
    Appetite changes, especially a craving for foods high in carbohydrates
    Weight gain
    Problems getting along with other people (bears get cranky and protective of food sources when over feeding prior to hibernation)

    My personal suspicion is:
    That SAD is indicative of the seasonal pre-hibernation light exposure trigger for preparing for hibernation. Once my light exposure drops below a certain level (near Thanksgiving) all I want to do is eat candy and later sleep, metabolism slows down and by January or so I go several weeks without feeling fully conscious unless I can get out and intentionally expose myself to bright sun light. (to combat it during the late November, December, January, early February period I need to make a constant effort to expose myself to full sun light or bright incandescent light every day – so called light therapy)

    The fasting response is, I believe the immediate precursor to true hibernation (crawl into a cave and don’t eat anything), body metabolism shifts to fat burning and brain metabolism shifts away from glucose to getting a large fraction of its energy from ketones, while HGH increases to prevent muscle atrophy. Protein requirements for essential muscle tissue is probably met by catabolism of less critical tissues like skin tissue as body mass decreases and the excess skin is not needed.

  2. Larry Ledwick says:

    This image shows the rapid increase in HGH production with even a few hours of fasting.

    PNG image

  3. E.M.Smith says:


    I’ve had a long habit of first meal being lunch sometimes. Some (most) days, dinner ends at 6 PM, next meal is 10 AM or sometimes noon… 16 to 18 hours of fasting … wonder if that has the same effect on HGH?

    Maybe I’ll try a one day a week fasting system… Never liked Monday much… could just try sleeping through it :-)

  4. Larry Ledwick says:

    Yes it does, that is one of the key features of fasting for body builders not only do they lose weight but it dramatically increases HGH to retain muscle mass even though they are losing weight.

  5. Larry Ledwick says:

    That is also suspected of being the mechanism which causes restricted diets to reduce aging effects.

  6. M Simon says:

    There is quite a bit out there about the connection of diabetes to the endocannabinoid system.


  7. cdquarles says:

    Wait a minute. Some 30/40 years ago, I thought, it was clear that insulin and insulin like peptide hormones (somatomedin and others) were known to be gate keepers of the fed to fasting transition and back. WTH????

  8. M Simon says:


    Camels do a LOT of fasting. Perhaps they would be good subjects for further research.

  9. E.M.Smith says:

    A day or two back, on some other posting ( I’ve lost where I commented, but if I were less lazy could find it…) I’d mentioned Fig Leaves as a diabetes treatment and did a blood test after eating a dinner of “Au Gratin Potatoes with Ham Bits” and Lima Beans. (I.e. very heavy on the starches). IIRC, my reading was about 165 and “only” about 20 points above the more “normal” 140 when digesting.

    Well, last night (24 hours after the tea) for dinner it was Noodles / Alfredo and Asparagus with buttered bread. Glucose about an hour later (mid digestion) was 135. So was that from the fig leaf tea? I’ll likely need to repeat the tests to rule out random walk issues.

    Now, I mention this since TODAY I’m having a bit of “run to the potty” for much softer than usual stool. Not wet, mind you, just more pudding like than normal… The general impression (i.e. mild irritation lower bowl) is that I’m reacting to something. Was THAT the tea? Or just “some bug”? Or did I eat something that doesn’t agree with me (as I do more often than I’d like… corn gets everywhere)? Again, I’ll need to do a re-test of the fig leaf to see. My strongest suspicion is just that “some bug” is the issue. Spouse has had a cold, we were traveling, etc. etc.

    Now, for one MORE data point. Today I decided to do a ‘coffee fast’ until dinner. At about 1 PM (i.e. just after when I’d normally have lunch / brunch) I’m at 105 and starting to feel hungry… Not bad yet, just pondering a ham sandwich ;-)

    So toting all that up, what do I think?

    First off, a short fast sure drops MY blood glucose fast.

    Second, I’m not very far from “normal” even on a bad day. HOWEVER, a load of direct sugar or fructose pops me up into the “over 200 you are declared diabetic” range. IMHO just because I absorb a butt load of sugar in a hurry and faster than I can process it on to fats or burn it.

    Third, even eating high starch meals, I’m in the normal-more-or-less range.

    Forth, blood glucose can change a lot with just diet. Before signing up for a “chronic disease and medication” diagnosis for life, it’s likely worth it to just try a primitive and meat oriented diet for a while… Toss in a few fasts now and then, and I’d expect a lot of folks to be found more “normal” than “sicko”.

    I’m planning to continue this particular fast until about 4 PM, then have some more or less normal kind of meal (though maybe larger than usual… ;-) and see what happens. It might just be that “one big meal a day” is fine with me. The spouse gets weak and hungry if she misses even one meal. I’m OK with skipping a few and just get a bit hungry, but not much else. I’m known to have a long digestive tract (so more ‘leaf eater’ oriented than ‘meat eater’) and about a 36 hour digestive cycle, so last night’s dinner is ‘still with me’… as is yesterdays lunch… i.e. YMMV with your digestive length.

    NOTE: I’m not a doctor and don’t even play one on the internet. I have never been diagnosed with any blood sugar disorder, so all of this might have zero relevance to anyone who DOES have a blood sugar disorder. I know that in a few ways my physiology is a bit off the average, so YMMV. (Things like that long digestion, long colon, robustness to too much, too little, or most any kind of food mix – from full vegan to 100% meat, etc.) In short, I’m just playing about with MY response to blood sugar, and you need do look at how yours works, not mine. This is just my experimental diary, not advice.

    I’m thinking of either trying a daily “fast until dinner” or a “why eat on Monday, it already sucks” fasting regimen. If anyone has opinions of what might be more interesting, speak up. (Stating why, and “to watch you suffer” is not a good reason why ;-)

  10. p.g.sharrow says:

    Back in the “old days” when I was young and lived in a ranching/farming community. The custom was a light breakfast, then 5 hours work. The main meal was dinner about 12:30 – 1:00 and then a nap. After that chores and finish the days work. Supper was snacking on leftovers in the evening.
    I tend to fast to afternoon then snack, as trying to work on a full stomach sucks. A full belly requires a nap! so that requires the main meal in the early evening. Not the best solution but, I rarely go to bed before.11:00pm and rise by 6:00am.
    Sugar and simple starches are disruptive so I try to avoid them. Hard to do with modern food supplies…pg

  11. Larry Ledwick says:

    One observation about “feeling weak and hungry” if missing a meal.
    I used to experience that but it only happens when I am on a high carbohydrate diet.

    If you are living on soda pop for example you have those sugar crashes when you run out of fuel so are forced into a grazer mode of eating where you have to eat regularly.

    Enzymes are trainable ( SAID Specific Adaption to Imposed Demands). When I was running regularly long distances my body got better at mobilizing fats for fuel and even if I have a high sugar diet for a day, or two, I no longer have those sugar crashes (or get headaches from not eating).

    Recently I started adding fats to my diet, animal fats and butter fat are short chain fats which are easy to metabolize and convert to energy. Vegetable oils/ fats are longer chain fats and not as easy to process.


    https://en.wikipedia.org/wiki/Short-chain_fatty_acid (note reference to short chain fatty acids and health of the gut)


    Seems butter is good for you, rather than something to be avoided.

    I have noticed since I started messing around with intentional fasting cycles that my hunger onset is not as sudden or as strong as it used to be. I will notice I am hungry but it is not an over whelming urge that needs immediate satisfaction, I will get around to eating soon but don’t have to grab a candy bar to keep from being shaky.

    Based on my experience some sort of a fasting cycle seems to have several net benefits.
    Perhaps one of the causes of obesity in modern society is the fact that food is always available and folks never are forced to go without satisfying their hunger for very long, which of course keeps blood sugar elevated as we are always just past eating something.

  12. Larry Ledwick says:

    I wonder if this increase in colon cancer is diet induced as folks get pathological about low fat diets.


  13. E.M.Smith says:


    Probably as much about low fibre as anything else.

    Residency time of the “poo” in the colon goes up, as does the tendency for the colon walls to weaken and bulge (slowing even more) and more bacterial growth / toxins and…

    So eat lots of veggies and fruits and “keep it moving!”…

    (Family has had colon cancer, I’m well aquatinted with the protocols et. al. I was on the every year colonoscopy plan for a few years after some polyps, now on the 5 year plan…)


    Well, I didn’t quite make it to dinner with zero food. Had one cup of blueberry yogurt (reestablishing gut bacteria if needed for ‘whatever’ was the ‘issue) and a couple of stalks of salted celery (at zero calories really… It’s very hard to make dinner fixings when you can’t snack at all ;-)

    Dinner finishes cooking in about an hour and I’m not sure I’m going to retest. Right now, at 4:15 pm, I’m at 101 glucose and still drifting downward.

    Near as I can tell, if you want lower blood glucose, just stop stuffing it in. I guess that’s too simple to make it a billable medical treatment…

  14. Larry Ledwick says:

    I suspect another culprit to colon health issues is serious lack of Vitamin D due to pathological fear of sun exposure and over use of sunscreen. I bet if you traced back when that generation started to obsess about sun exposure you would find a good correlation with early onset colon cancer problems.

  15. E.M.Smith says:


    One hour after the dinner meal ( roast turkey / onion / carrot / celery roasted vegetables, steamed chard w/butter, some boiled peanut appetizer and blueberry muffin desert) I’m at all of 106 glucose. Not high on the sugar / starch scale, but not zero either.

    It would seem that the short ‘fast’ into the afternoon builds up a ‘sugar sink’ that sucks up the digesting dinner rather nicely…

    OK, my base ‘meal protocol’ is going to be fasting (coffee, water, maybe milk allowed) until after noon “for a while”, then as much dinner as I want. Dinners to be heavier on meats and non-starch vegetables than “usual’, but not avoiding them entirely either.

    I’m likely to also give a try at “meat mornings” and see if things change much. Just zero sugars and starches until afternoon. I’ve always done better on “bacon and eggs” than on “pancakes and syrup” for breakfast (as the sugar shot tends to put me back to sleep…)

    Regardless, when you’re putting up a 106 full of dinner and well into the digestion cycle, all is well…

  16. Larry Ledwick says:

    That makes sense. If you look up the term Carbo loading, you will see that they use that to enhance glycogen stores.

    The body uses blood glucose as its first preferred fuel, if that is not adequate it withdraws glucose from its energy bank of muscle glycogen (and liver glycogen). Glycogen being an intermediate “demand deposit” type storage for excess glucose.

    As noted in the charts from my earlier post, glycogen stores get drawn down as you are in fasting mode, and are essentially exhausted by about 28 hours of fasting, or very intense exercise. The so called “wall” in marathon running typically happens after running about 18 – 20 miles. That acute energy expenditure basically uses up all available stored glycogen and the body if suddenly forced to switch to fat as its primary energy source. If the runner is not conditioned for that switch over to fat energy he crashes as his body cannot produce energy fast enough to meet demand.

    Carbo loading is a cheat on that system. They intentionally run down glycogen stores with some long runs but do not provide high carbohydrate foods to refill the glycogen storage tank. That causes the body to respond by supercharging its processes to refill glycogen stores. They do that by eating a high fat high protein very low carbohydrate diet for a couple days, then just before the race the switch to high carbo diet, like spaghetti and potatoes etc. The body over fills its normal glycogen stores as a result just before the race so when they run that next race they have a much larger reserve of stored glycogen to draw from.

    It sounds like you are documenting that process, if you have a glycogen debt, any free glucose from your most recent meal that is left over from primary energy demands first gets shunted to restoring glycogen stores. Once those are full if you still have high blood glucose it gets routed into the fat storage pipe line.

    The implication is folks who constantly snack on high carbohydrate snacks and never allow themselves to exercise enough of fast enough to draw down their glycogen stores, set themselves up to store all excess intake as fat. If on the other hand they were like the 1940’s farm hand who ate a big meal mid day but then worked hard the rest of the day, that food energy would be diverted to productive activity or topping off normal glycogen stores rather than being saved as fat.

    Seems food intake timing and activity cycles need to be included in consideration above and beyond the total calorie intake. It might be just as important to not take in large amounts of calories shortly before a period of inactivity like sleep as it is to manage total food intake.

    If you are on a boarder line surplus calorie intake diet, you could force fat production if the excess calories are consumed just prior to a long period of inactivity, where if you ate the same amount of food earlier in the day the body would be less willing to shift to difficult to withdraw fat reserves and hold more as glycogen stores and blood glucose.

  17. sabretoothed says:

    If the UV B light is low, you can’t eat carbs. If it is high you can eat carbs no problems. Why pacific island people get really fat when they move away from islands and also Africans who used to live on the equator.

    The UV B is the key, fasting helps too, but if the UV B is high you don’t need to fast

  18. sabretoothed says:

    https://www.youtube.com/watch?v=lzJfZqXsKMA If you have ultraviolet you will be strong ;)

  19. sabretoothed says:

    The funny thing is whatever Clinton says is always opposite ;) http://www.newstarget.com/2017-03-30-chelsea-clinton-warns-global-warming-causes-diabetes.html She needs sun herself otherwise she’ll end up like her sick mum ;)

  20. E.M.Smith says:


    I’d only add that all processes have a max rate. Probably can vary (slowly) over time (slowing with lethargy and lack of use).

    So don’t do much, but keep eating, the glycogen gets full. That puts it all on the fat making process. Now if your input rate exceeds what is normally a slow process (glycogen buffering the fast surges normally) you get a blood glucose spike for the duration of digestion. If constantly eating (cronic overeating) that can be most of the day….

    To fix it:

    Cut total calories to just below daily need.
    Increase activity (draining muscle and liver glycogen).
    Fast periodically (exercise glycogen pathways to build capacity)
    Eat low suger low carb meals (route calories through fat and protein pathways).

    I’ve tested each separately with beneficial result (reduced glucose reading), though each seems to have a different rate and capacity.

    FWIW during the 100ish readings I felt a lot more energetic and moved around more. I think that is supportive of the hibernation lite model. Low glucose is Spring, go hunting… In the wild, the lethargy of high glucose would self limit as you didn’t capture food. Only in the modern world can you do nothing and still over eat…

  21. E.M.Smith says:

    10 minutes of 9 PM and I’m at 111 glucose reading.

    Looks like I’ve completely flattened the normal “meal spike” by 6 hours of fasting.

    Guess the only remaining test would be the same process, but with a carb heavy meal.

    Maybe I’ll wait a few days to try that one ;-)

  22. Larry Ledwick says:

    It would be a lot easier if the human body came with an operators manual but it is fun sometimes to try to figure out the rules by self testing.

    I did lots of A B testing when I was running marathons, and recently with the intermittent fasting to try to get back to a weight that makes my knees happy.

    Mostly there now I have lost almost 25 pounds now and my knees no longer pitch a fit if I do some light jogging and running along with my daily walks.

  23. Larry Ledwick says:

    Somewhat related on the topic of nutrition and effects of minor deficiencies, an Australian study has found a relationship between Vitamin B3, certain genetic deficiency in handling Vitamin B3 and miscarriage and birth defects.


    In another 10-15 years I suspect we will see a massive increase in the mapping of minor genetic anomalies and certain disease conditions. Eventually genetic screening will become routine precautionary diagnostic tests.

    The bad news is that those same diagnostic genetic tests could lead to insurance abuses and flagging people as being high risk for certain diseases – not for treatment but to profiteer off their situation.

  24. E.M.Smith says:

    Day 2 of the relish tray and coffee brunch:

    It’s 11 am. I’m not hungry at all, having had a repeat of the celery / coffee regimen. I am finding myself “curiously energized”. Not “coffee jitters”, I’ve only had my ‘usual’ level. More like ‘waiting for Christmas’. Just can’t sit and be a lump.

    I’m hopping up off the couch or out of bed. We have a nearly 30 year old couch and it was low to begin with. Now with flatter cushions it has been like climbing up out of a low sports car to get up. Yet today instead of the “struggle from the gravity well’ I’m just “hopping up”.

    I’ve also found myself “impatient’ at how slow the clock is moving on things like cooking dinner last night. Waiting a whole minute seeming much longer… I’ve been more productive, too. Cataloged all the various disks. Audited their contents. Logged it all. Cleared / reformatted the old LVM disks ( the 1.5 TB and 2 TB small ones replaced by a 4 TB “MyBook”) and I’m presently draining another TB disk into the LVM archive. Finding it nearly “maddeningly slow”… Realize I’ve moved these TB chunks around before. It isn’t news to me how long it takes on this hardware. What is different is that it seems like a half a day already and it’s only been 2 hours that this has been underway.

    So, on day 2, it seems like the answer to having “more day in your day” is to not eat… Curious. (or, more accurately, have a relish tray and morning hot beverage, not the doughnut and no cereal).


    Yes, as genetic mapping has taken off, all sorts of things have been turned up. Including that several diseases are mitochondria related. This matters as you only get the mitochondria from the mother. So once you know it’s broken, what happens to those women who are now marked as “defective and making defective children”? Hmmmm? We will start seeing mitochondria transplants to cure their future children and eventually even them. THAT will then show that the interaction of the mitochondria with the somatic type matters and eventually after a lot of problems, they will get the matrix of which mitochondria work with what nuclear type worked out.

    Then the optimizers will move in. Want the perfect kid? mix these genes with your own…

    So, for example, if you KNOW you get ‘maternal derived migraine headaches’ and it was on you mitochondria: For guys, just marry a woman without it. For women, do you have a kid, knowing they have a 100% chance of getting it, or wait for a mitochondria transplant? Or what?

    IMHO, that will be the first area of ‘designer babies’.

  25. E.M.Smith says:

    At noon, blood glucose ix 111 again. Exactly matching the last night ending value.

    I suspect this is my equilibrium number. Any value below that being glucose supply below demand, above that supply in excess and storage being needed.

    This would match observations. When at 100 ish values, I was hungry and a bit anxious. Over 135, a bit slothful and sated. It took a day for the balance to shift from over sugared to under, but now I “feel full” and energetic with no real calories input, and blood sugar matching my post meal high of yesterday. I would guess this means I’m running on fat metabolism, have shut down glucose to fat storing enzymes and I’m using the glycogen pathways for buffering.

    Interesting… mapping the ‘specs’ for which systems get turned on and off when. Time lag seems to be about a day, but needs better characterization. I could see a “sugar rush” overwhelming glycogen storage, turning off fat metabolism, and giving a 200 spike (so LOTS of enzymes to store glucose made and all enzymes for glycogen release or fat metabolism halted), set for about 12 to 24 hours, then an hour later the sugar is gone and you get whipsawed. Maybe a hypoglycemic plunge or just insulin systems out of whack with blood levels so some other system activates (repeated activation eventually being seen as”insulin resistance”?)

    It is a very curious feeling to gave eaten two celery sticks 3 hous ago and feel full still…

  26. Larry Ledwick says:

    I have experienced the same increased energy, part of the ramp up of metabolism noted in those links. Apparently scarce food acts as a trigger for increased motivation and energy to find more food.

    Perfectly natural adaption to imposed stress if you think about it. (SAID)
    All the folks who got lethargic when food is scarce, probably died out, where those who were wired to ramp up activity were more likely to get something to eat survived.

  27. Richard Bellew says:

    Hi Chiefio — Re blood glucose levels, what method do you use for measuring them? If you already posted this and I missed it, apologies! RGB

  28. E.M.Smith says:

    @Richard Bellew:

    No worries… it was on some other thread long ago.

    I’m using a “ReliOn Confirm” device. The traditional “test strips” you stick in a meter (uses rubidium and some odd blood reaction I think) then the electronics reads the strip. Typical “poke a finger and bleed a drop into the test strip” thing.

    They stress it isn’t for diagnosis, but I figure since it IS good enough to keep people alive, it’s good enough for playing with ;-)

    Why that brand? It was on sale at Walmart for $7. Really. See, it is pink. A sort of icky not quite plum not really pink, pink. Seems people didn’t like the color and they discontinued it and wanted the shelf space back… The black one right next to it was much more expensive, but I don’t remember exactly what the price was for it. IIRC it was in the “twenty something” to $30ish range; at least most of the cheap ones were.

    Test strips are about $1 a pop, maybe a bit less. Yeah, expensive hobby ;-)

  29. cdquarles says:

    WRT the diagnosis of diabetes and obesity; recall that medicine is subject to fads. Our host, 40/50 years ago would have not been considered diabetic nor pre-diabetic. The criteria for diagnosis was a high urine sugar level (glucose). Some 30 years ago, ‘prevention’ became a thing (shortly after DRGs, if I am remembering correctly), so the push (from government) was on to find and treat people ‘before’ they got sick. Naturally, this would not reduce overall costs, just some ‘high dollar emergency’ costs (ICUs for heart attacks). Around that time, ‘obesity’s’ definition was changed from a high body fat proportion to the BMI (well, more like 20 years ago), which is a stupid index. Mass (kg)/height^2). NB that body builders and football (American style from rugby) players are all ‘obese’ by this index.

    WRT chronic diseases for life, well, we are all going to suffer the death of the body. If it isn’t trauma that gets you, and infections are a form of trauma, your body will kill itself, eventually.

  30. Richard Bellew says:

    Thanks, Chiefio, for the rapid answer. FWIW, isn’t it strange how memory works (or doesn’t). When I was writing my question above I had absolutely no recollection that I’d ever seen your previous post. As soon as I saw the word ‘pink’ in your third paragraph I remembered your post quite clearly. Very strange! RGB

  31. andysaurus says:

    A bit late into this conversation E.M. I’m not sure if I mentioned to you before the observation that both Christians and Muslims fast for an extended period (Lent and Ramadan). I don’t know about Buddhists. It’s interesting that at least two of the World’s great religions have this ‘metabolic reset’ period.

  32. E.M.Smith says:


    Interesting indeed… almost like somone who knew something was giving directions….

  33. sabretoothed says:


    Sounds like Blue light in the house :P :P :P Why people genetically from the equatorial regions get more diabetes and heart disease when they move towards the poles. You can see it clearly in Pacific Islanders and Mediterranean genetic lines

  34. E.M.Smith says:

    FWIW, both the spouse and I felt more energetic and happier in Florida.

    She has a history of low Vit D even in California (mostly in winter). There, between the lower latitude and swimming even in winter (and two pools plus hot tub where we were living) we both got more sun year round and more activity swimming.

  35. sabretoothed says:

    I think there must be variations in the VDR receptor that we cannot test for. And these are the people getting autoimmune diseases (and diabetes is one of them).

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