Monday, November 21, 2011

Adipotide and the Bad Fat

Just a brief respite from mitochondria:

Adipotide is a drug which targets the blood vessels supplying adipose tissue. It causes impressive fat loss by killing fat cells. Anon posted these two links on the last post.

There are other processes which can produce adipocyte destruction. We've discussed both acquired and congenital lipodystrophes in the past. They produce whole body fat loss with progressively deteriorating glucose tolerance because fatty acids have no adipocytes to enter, so end up accumulating in all tissues, producing pathological insulin resistance and diabetes. This is basic physiology and exactly what you would expect.

Adipotide is different. It produces fat loss with improving metabolic conditions and decreased hunger. How come a dead adipocyte is good from Adipotide and bad from auto immune attack?

Alex emailed me the full text. Here is the snippet from the email conversation which was my initial take on what might be happening:

"How does the drug get any improvement? You'd need to see the data and how they generated it but if the drug preferentially targets abdominal fat there would be an improvement in systemic insulin resistance until enough total [whole body] fat cells were lost for the overall for deterioration in insulin sensitivity due to muscle lipid accumulation to precipitate diabetes.

Of course during lipolysis you would have FFA release acting like an obese fat cell becoming insulin resistant and sending FFAs systemically to most non CNS mitochondria... Reduced need for food and increased ATP for activity from the metabolic flexibility perspective..."

Look here: Surgical removal of visceral fat improves peripheral insulin sensitivity (there's a lot I could write about this paper but no time). This paper looks OK, other papers by this group are very dubious.

Visceral fat seems quite important, here's an early brief review.

And here is the only quote we need from the Adipotide paper (thank you Alex for the full text):

"MRI and DEXA imaging confirmed that weight loss in the rhesus monkeys occurred primarily because of visceral fat loss."

Now, that's all hunky dory. What is the question we need to ask? Actually, there are a few:

Why is visceral fat Bad Fat? Why do we make it? If we get rid of the Bad Fat, will health be Good for ever? Did we evolve Bad Fat to kill ourselves? Is there a survival benefit from Bad Fat if we continue to drink >30% of our calories from fructose based drinks? Would having our omentum removed do good or bad things long term if we continue to mainline fructose? Would we need to get rid of our Bad Fat if we poured the Fanta down the urinal rather than down our throats?

I rather like Bad Fat. It opens all sorts of avenues of thought. There's so much about it that fits together but no more time to blog at the moment.



majkinetor said...

With adipode and other 'similar' techniques like cavitation, is there any concern with all that fat being released in the plasma from massive adipose death ? I know that females doing cavitation are advised to run for 45 minutes after it to 'clean up', along with low caloric diet.

So, one colegue asked me about an opinion on cavitation recently and although I felt its not 'natural' since humans typically do not get lots of dead cells releasing fat in the plasma just like that, I couldn't point to any particular problem with it in few acute sessions apart from well known yo-yo outcome known for all such techniques. In GCBC there are pages about the yo-yo thing happening with hibernating animals after their fat is removed in the lab.

Wouldn't all such procedures, no matter the agent that caused it, produce this same phenomena in most people ?

On the safety side, I guess cavitation might even be the safest option then...

blogblog said...

Or you could go on a VLC diet.

I have lost 7kg in three weeks by keeping carbs below 5g/day. My appetite would be now be described as non-existent and I now barely eat 500Cal/day. I have a lot of energy and am sleeping perfectly. My IBD has gone into remission.

My feeling is that some of us (particularly northern Europeans) have essentually zero carbohydrate tolerance and need to stick to meat and butter.

blogblog said...

one of my sisters had liposuction on her thighs about 20 years ago. She simply put on fat in other areas such as her upper arms instead.

Ned Kock said...

One of the receptors that the drug binds to has an interesting name - prohibitin.

bopes said...

If there is some kind of teeter-totter relationship between visceral fat and peripheral insulin sensivity, and if it took evolution like a zillion years to work that out, I'd think twice before destroying one half of it by removing visceral fat cells through surgery or drugs.

Travis Culp said...

The problem (in the modern context) with visceral adipocytes is their much higher transmembrane flux of FFAs, which dumps loads of them onto the liver via the portal vein. The liver then packages them up as VLDL-TGs and sends them on their merry way. These TGs (again, in the modern, sedentary context) travel around but find no home in muscle mitochondria and become oxidized (due to our greater oxidative stress) and proceed down the road toward foam cells, plaques etc. That's on top of the hepatic insulin resistance that is brought about by the presence of the FFAs.

Take home point? If you're going to fuel yourself as though you're an athlete, get off your ass and act like one. There's nothing dangerous about glucose (or even fructose from whole fruit) for a truly active person. If you exercise vicariously through characters in video games and on television, then by all means restrict carbohydrate intake.

Regarding the surgical/drug-induced adipocyte apoptosis: because obesity usually results in quite significant adipocyte hyperplasia, to the tune of billions of cells, (you can't exactly store an extra 1-200 pounds of fat with hypertrophy in your default set) the post-obese have quite a problem with having so many more adipocytes than the never-obese. I would guess that 20 pounds of fat for them acts quite a bit differently compared to 20 pounds on the never-obese. My guess is that if you have 20 pounds of fat stretched out to many times as many adipocytes, the overall leptin secretion is markedly reduced since they're all insufficiently full to cross a secretion threshold. We do see reduced leptin secretion in the post-obese, so this may be true.

Arby said...

My thoughts exactly. On TAD Adipocytes expand until their larger size forces FFA's out into circulation despite the effects of insulin. Then the person reaches a point of equilibrium.

On a post obese LC dieter, a drug such as this might be a helpful way to reset to a lower equilibrium, and the insulin resistance side effects should be irrelevant.

bopes said...

Is there an optimal number of visceral fat cells?

mnature said...

Is fat bad? Reminds me of the cholesterol debate. Cholesterol was bad. Very, very bad. Then, only some cholesterol was very, very bad, and other cholesterol was very, very good.

Then I think about weight. So many people that are just too heavy. An obesity epidemic. Can't find a good definition of obesity, other than being a certain percent over ideal weight. Can't find a good definition or analysis of ideal weight. Oh, there are tables, many fine pretty tables, showing ideal weight depending on a few factors.

And then, finally, the sobering fact that people are living longer and healthier than ever before. Facts are the enemy of truth, because the truth is that being obese makes you sickly, and you die young . . . and we know that because, well, because everyone knows that.

Bottom line: How do we know what an ideal weight is? How do we know that fat is unhealthy? How do we know that not being fat is healthy? Are we making up facts, or are there real studies of real people (as opposed to mice, rats or rabbits)?

Travis Culp said...

mnature: Get some visceral adiposity going for a few decades and report back (if you're still in the land of the living). A healthy skepticism is great, but sometimes conventional medicine actually is dead on. Imagine that.

blogblog said...

people are not living longer and healthier lives. The increase in life expectancy is almost entirely due to reduced child mortality and the availability of antibiotics.

ItsTheWooo said...


Liposuction is useful in post obesity care, because as travis points out, adipocyte hyperplasia is just as much of a problem as is hypertrophy. targeted liposuction of obesity prone body areas can help normalize fat distribution.

I had skin removal + liposuction and the end result is, in spite of a lower total body fat in KGs:

1) I have less signs of starvation (i.e. my leptin levels are higher, as my fat cells are larger)
2) My body appears more balanced; my upper arms and face are no longer emaciated, even though my body fat in kgs is less than it was before surgeries

For a person who hopes to lose weight with liposuction... you are far more likely to end up diabetic or with IGT... but for a person who has tons of deflated post obese fat cells, then liposuction can be quite useful to normalize the body and replicate a pre-obese physiological condition.

ItsTheWooo said...

This is quite interesting. It seems that a reasonable medical therapy for obesity and diabetes, would be a drug that targets and kills visceral fat tissue... assuming side effects were tolerable and did not include cancer/making your arms fall off.

I think we will find that the accumulation of visceral fat, at least in human beings, is often the symptom of glucose intolerance of peripheral tissue, white adipocytes. If your fat tissue is at its genetic capacity, and insulin is trying its very best to process all this sugar and FFA lingering about, the next step is depositing it in organs, and visceral fat.

The harm of visceral fat suggests that organs have the capacity to store some fat, and this is physiologically normal, and probably contributes to health of the organ (e.g. a very very tiny amount of fat in the organs)... the problem is when insulin resistance in your body fat, and skeletal muscles, is so much on high blast that the fat content of your viscera becomes abnormally elevated. This suggests truly desperate levels of glucose tolerance and insulin sensitivity. It suggests that the fat tissue is either absent, extremely IR, and/or at its genetic capacity to replicate and expand.
When this occurs, it's sort of like when a person in debt has borrowed from the LAST PERSON that trusts him.... after that act of desperation, he is SOL because he has exhausted all his resources, total social dysfunction (homelessness/crime) may result after.

Seeing lots of fat in your visceral organs is a similar situation from an endocrinological/metabolic perspective, and suggest truly desperate levels of insulin sensitivity and glucose tolerance. Insulin resistance/capacity to process and handle nutrients is truly at max. Diabetes then onsets. Visceral fat does this not because visceral fat is evil, but because having significant visceral fat is merely a sign that there is literally NO WHERE to put or use glucose and fat. The inflammation produced from visceral fat, is the expected result of your visceral organs being like "holy crap, why on earth do we have fat? Lets send out inflammatory cytokines to stop this and prevent further fat deposition ASAP, we really shouldn't be having fat deposited in us like this, and the inflammatory products we make will prevent any further fat accumulation."

ItsTheWooo said...

(pt 2)
See yer organs don't know about diabetes and autoimmune destruction of white adipocytes, and it doesn't know about severe insulin resistance. All it knows is "too much fat being deposited = send chemicals that stop the deposition of fat". This then results, purely unintentionally, in even more severe IR and a far worse prognosis.

Sometimes the homeostatic mechanisms built into our physiology can actually cause profound life threatening illness, if they are triggered abnormally.

For example, a burn patient will experience PROFOUND vasodialation as a result of heat trauma. They will go into shock and cardiovascular collapse from this. One of the first things done for people who have been exposed to fire and burns is to start fluid replacement, because they go into shock.

Vasodilation upon heat exposure (and constriction upon cold stress) is an absolutely physiologically adaptive response. The body never intended to be exposed to burns and severe heat stress - cardiovascular collapse is merely an unintentional side effect of this otherwise adaptive physiological mechanism.

People who try to kill themselves by slitting wrists stereotypically do so in a steamy bath, precisely because the heat will prevent their blood vessels from constricting and clotting. If you want to die of blood and fluid loss, immersion in a hot bath helps nicely.

High stress responses, physiologially, lead to heart attacks, precisely because the stress response promotes vasoconstriction and clotting, and encourages breakdown of tissues for rapid energy. This contributes to modern disorders like diabetes, heart disease/attacks, and high blood pressure. We evolved this stress response to help us to live through being mauled by a bear, or for male animals to survive conflict and competition (males easily develop stress induced ailments like high bp and heart disease, because the male endocrine system boosts the stress reactivity/responsiveness of the body).

Rambling tangent!

Anyway. When we observe that during global metabolic disorder, to the point that the body is so desperate to store nutrition SOMEWHERE, that it ends up in your liver and viscera, don't be surprised when this results in tons and tons of chemicals being made which are trying to stop that process. The organ is functioning at the level of the organ; homeostasis can only occur when there is no gross abnormality in any organ or system. When the organ, subjected to dysfunction (hey, stop shoving tons of fat on me, WTF are you doing?) then releases cytokines to promote resistance to insulin and fat disposition, the organ is only trying to save itself. IT doesn't know this will kill it sooner, it's just an organ, and it is operating as it was genetically formed with the instructions programmed.

John said...

Slightly off-topic: VDRKO mice have very low fat (including visceral) and very high EE.

Since nutritionists recommend grains, and dermatologists recommend never going outside, we might as well work on a way to ablate VDR to cure obesity and visceral fat.

bopes said...

BTW, I did a bit of googling on my question above about about the optimal number of visceral fat cells. Now, I could be wrong, but I think the correct answer may be 42.


Arby said...

What about adipocyte apoptosis induce by Leptin?

Or by vitamin A?

Does anyone have an update on these lines of research?

John said...


Both the lean and obese vitamin A mice had much less fat than controls, with the title being kind of misleading. Vitamin A usually induces UCP1, which seems to "override" its inhibitory effect on leptin, since there is obviously an observed overall fat reduction.

Here shows retinoic acid causing white adipose to take on properties of brown...

...Retinoic acid in general increases ketosis and fatty acid oxidation (hence body fat reduction) without increasing plasma FFAs.

Would ROS increase retinoic acid?

Anek Dodl said...


I love it when you "talk" like this!

The question I'm always looking for an answer to is why I easily lost a ton of weight (2 lbs a week minimum) when I first went low carb (size 8 to size 4), reversed by eating yogurt as my weight was getting dangerously low (103lb at 5'5"), and now can only lose minimally (4 lbs) by eliminating cheese/yogurt. I've read this is not an uncommon problem going LC.

Any idea why this happens?

John said...

...oh, and RA increases t3 uptake...?

I once ate lots of beef liver for a week. I then sprinted and got a bad cramp in biceps and lat--not sure if it was related or improper warm-up or whatever as I was fine the next day.

nancan said...

It would be great if there was an easy, cost effective test for distribution of fat in one's body. I would love to have known how much visceral vs external fat I lost.

blogblog said...

102 lbs at 5'5" is not a dangerously low weight by any stretch of the imagination (It is around the same BMI as most Japanese women). In fact it would be have been considered completely normal before WW2.

We are now so used to obesity that we think a healthy weight is anorexia.

Anek Dodl said...


I'm back to a size 8 (BMI 23) and wouldn't mind being a size 6 or size 4 again (BMI 17), but it just doesn't seem possible as I've only lost 4 lbs giving up cheese/yogurt which are usually very fattening for me (casein?).

I'm encouraged by your VLC results. I'm sure when I first went LC I kept my carbs as low as possible only because I thought I didn't really need them so that may be the reason I lost weight so rapidly. My conflict is my reversal of RA following Dr. Ayers' advice on Cooling Inflammation which basically stresses diversity of diet for optimum health.

I think I may just throw caution to the wind (yet again!) and quit eating veggies altogether or something drastic (like Peter).

Meat and butter I could stick to, maybe even 500cal/day. What carbs do you eat for 5g/day?

Arby said...

Thanks for the answers John. Interesting links too. I couldn't parse ROS?

Am I correct in my assumption? Does adipocyte volume have anything to do with FFA availability to the body? Or is 12 billion half empty adipocytes the same as 6 billion full ones?

Anek Dodl said...


Forgot to respond to your comment:

When I was a teenager many, many years ago, I weighed around 103 lb and my doctor told me not to go below 100 or it would be dangerous for my health so that's always been my ruler.

John said...


...Reactive oxygen species. I'm wondering if "oxidative stress" increases retinoic acid in the way it does with other things like uric acid-to-allantoin, but of course we don't have that catalyst, so I don't know if it's a good comparison. I would guess this is all involved in "antioxidants" too.

I don't really know about the adipocytes.

Travis Culp said...

Mary: Body fat levels that are too low generally trigger some kind of hypothalamic intervention, whether it be a reduced body temperature, loss of libido, amenorrhea etc. You can however simulate that state without actually being in it via a problem in leptin signalling or for the former, with carbohydrate restriction, which lowers T3.

If you start triggering hypothalamic failsafes, it's probably a good idea to change direction, but if you have no measurable or perceptible problem at a particular weight, it's probably (but not necessarily) fine.

Regarding your specific question, there's likely some difference now in what you eat or do or some different factor that has changed your metabolic rate etc. I doubt it's due to a different reaction to yogurt.

Anek Dodl said...

@Travis Culp

Thanks - I think you hit the nail on the head with triggering a hypothalamic failsafe as I was losing weight very fast (until I had no fat to sit on - uncomfortable) so I'm glad I chose to change direction. At size 8, I don't feel fat, but I just wanted an explanation as to how it could have been so different a mere 2 years ago. I will be satisfied with what I've got now.

In writing about it here, I think it was the fact that no carb seemed even more reasonable than low carb at the time so if something was a carb I couldn't see making the effort to chew it (sort of like Peter haha).

Thanks again for finally clearing this up for me.

blogblog said...

5g carbs = 100ml cream + 25g berries

ItsTheWooo said...

@blogblog Asians are of a slighter build than caucasians and other ethnicities.

I am 5'5 and when I weighed 104 pounds, I was repulsively thin. Mind you, this is also before any skin surgeries, so you can imagine how emaciated I was (I probably actually weighed ~90 given that a lot of the weight was skin).
People would stare at me in the street, and not in a good way... in a "is that a cancer patient? " kind of way. Something interesting happens when you become extremely thin... men completely stop looking at you, but women look at you with repulsion/disgust (In my experiencing having been emaciated, women are fascinated by emaciation, probably due to fashion magazine influence. Men just ignore you totally.)
A few times, people just assumed I had anorexia nervosa, and once a woman asked me to speak to her daughter about the dangers of eating disorders. Yea. That's how bad I looked I suppose.

I was so thin that my feet would hurt because they were boney. I was so thin that sitting hurt. I was so thin that in the cold of winter, it felt like I would die...a cold that begets paralysis, your heart leaps and you feel your heart might stop, it can barely keep up with the stress of cold. These were miserable times and I was deeply depressed.

Take note, After having multple rounds of skin removal surgiers, and gaining a lot of weight, I now weigh 115-120, and at this weight I still wear a size zero and am considered quite thin by everyone I meet. I am no longer underweight, but I am at the low tier of what is considered healthy thin. I am much, much bigger than I was then.

Frankly, it is absurd to say that 102 pounds is a "normal" weight for a 5'5 female. Perhaps for some women this is a healthy weight, but THE MAJORITY of women will find this weight to be very underweight. Asian people have small builds. I am not an asian. 102lbs would leave me looking like a frightening wreck.

ItsTheWooo said...

Your info / interest in vitamin A is fascinating. I will have to add this to the list of the hundreds of things I need to read/blog about. I suspect this may be important.

I've heard that people find it more difficult to lose weight the second time around... I never had to worry / deal with this. However, given the weight range I have fluctuated for the past 7+ years (which has been, approximately, 105 to 125) I have never observed any progressive difficulty with losing weight. I have continued to find weight loss to be just as easy at it was, if anything, I find it gets easier to lose weight the more I repair my glucose tolerance with supplements and adhere to low carb / glucose/ insulin control.

I think some of hte problems people may have when they low carb yo-yo is that they are worsening their glucose tolerance by repeatedly dieting , and then letting go of their eating . It's shown that a drop in leptin sets the body up for higher maximum weights via altering how adipocytes are regulated - in short, a drop in leptin (starvation, or dieting) encourages hyperplasia of adipose tissue when insulin excessively rises again (refeeding/going off the diet).

Another possible issue that people just do not low carb "as well" the second time around, because they know recipes and treat foods, and they wind up simply eating too many carbs as compared the the first round of weight loss. If, the first time coming into this you ate nothing but eggs, mayo, celery, butter, and steak... but the next round you are eating egg and cream cheese splenda and berry meals, I would expect weight loss to be more rapid and easier the first time because you are eating less carbs and your insulin levels/ FFA availability from adipocytes is better.

Both of these effects may be occurring, but I simply do not believe in any real "golden shot" phenomenon. I think yo-yo dieting ruins glucose tolerance and promotes progressive fattening for endocrinological reasons, but the key is to NOT. YOYO. DIET. If you can't stick to what you are doing, DONT DO IT. This is why I hate fasts and people who go on crash diets they have no intention of maintaining in any form. WHy are you doing something you are bound to fail with? The body will only get more stress sensitive, insulin resistant, and fatter in the long run.

ItsTheWooo said...

I believe adipocyte apotosis via leptin may be affected by hyperinsulinemia; leptin is only elevated in a hyperinsulinemic condition in normal individuals. Leptin and insulin help keeps adipocytes in balance - insulin makes them grow, leptin makes old ones die.

I think leptin replacement s/p obesity and insulin control is long term theraputic. I have far fewer signs of starvation after using leptin for >2 yrs, even though I haven't taken a dose in months. I suspect most of the effect is from skin removal surgery, but I wonder if leptin helped kill off a lot of old fat tissue? It stands to reason it might have.

My experience suggests that adipocyte SIZE is far more important than WEIGHT of your adipose tissue.
If you have a post obese body with billions of redundant fat cells that are very hypotrophic, straight up your body will act like it is starving to death even if your body fat % is healthy. Your face will be bones, your shoulders will be skeletal, and you will exhibit all sequellae expected of starvation (hypotlepinemia, infertility, bradycardia, hypotension, cardiovascular disorder with peripheral extremities not being perfused well, thyroid collapse, mental disability: depression/obsessive compulsive traits/excessive stress response). Basically, look at someone with anorexia, or someone who is subjected to starvation, and that's what happens when you own a LOT of hypotrophic adipocytes, as a result of caloric malnutrition (diabetes or pathological hypotrophy of adipocytes is a bit different, high glucose/insulin deficiency complicates things).

When adipocytes are larger, they release FFA more easily at any given level of insulin; the result is sugar remains elevated (chronic hypoglycemia is a problem for non-diabetic people who are starving) and your energy is far superior.

Back when I was thinner, trivial physical stress such as lifting a heavy object would leave me shaking and weak. I was like, an invalid. I no longer have these problems, and the only time i have hypoglycemia now it is carb induced.

So yes, 12billion tiny half empty adipocytes definitely release less FFA than 6billion full adipocytes. The person with 6billion full adipocytes has higher / stable blood sugar, superior energy, and far less signs of metabolic/endocrine adaptations to starvation (defined above).

The size of adipocytes determines how easily they leak FFA, weighted against insulin levels.
If a person has very high insulin (as many severely obese do), then they do not leak enough FFA even if their fat cells are huge. This is precisely why they are obese. This is why very obese people lose their appetites PROFOUNDLY upon inducting a ketogenic (insulin-suppressive) program. Thin people do not respond quite as much as a very, very fat person who had very very high insulin (which responds to carb restriction).

As someone who experienced this (the effects of owning severely hypertrophic fat cells, and overnight having insulin levels slashed)... it feels sort of like you never have to eat again. Food just no longer is even required, and you feel fine without it. Your fat cells hemorrhage FFA in the post-insulin, hypertrophic condition, and this provides your energy needs well. Fat loss and normalizing body weight is merely a symptom of what is going on at the cell , endocrine level.

However, should you raise insulin pathologically, you are right back to where you started: always hungry in spite of copious body fat tissue. The very high insulin is weighting against your generously sized adipocytes, and the result is FFA availability is not what it SHOULD be given the severity of your obesity. Blood sugar/nutrients swings from pathological insulin secretion also contribute to the hunger of obesity.

See an insulinoma patient for more info.

Anek Dodl said...

@Travis Culp

Why yogurt? At the time, I could only eat commercial goat yogurt which contained tapioca which caused the weight gain. Anything bovine caused RA flareups until I learned about Ayers' tolerance diet and repaired my immune system - to make a long story short.

Arby said...


Thanks for the explanation. I quickly dropped 70lbs on a low calorie/low carb diet, and I suspect hyperplasia is what is causing me to gain back. I'm trying to maintain with low carb (Atkins style) and ad-lib I eat 4,000 calories per day. This may match my daily metabolism, but I've gained back 16lbs in three months... It's depressing at times, but I feel better knowing why.

Atkineers post about stalls and plateaus. I suspect that there is a homeostatic process of adiposyte apoptosis that destroys the extra fat cells as your weight slowly goes down... Mine went down too quicky and I did not benefit from this. A stall ergo could just be waiting for this process to catchup.

My other theory was lipoprotein lipase running off of basal insulin. I've considered requisting herparin shots to reduce post diet LPL. But apoptosis will do the same.

I'm combining some of your GT & amino acid dopamine advice and a large dose Vitamin A suppliment. Almost ten of my friends and coworkers followed me into the LC/LC diet clinic... I feel responsible for finding a solution for them post diet.

Anek Dodl said...

@ Wooo

Thanks - I never felt or looked bad when I was 103 lbs so I suspect you were 90 lbs without the skin (frightening!).

I don't yo yo diet - I just experiment to see what works. Cheese and full fat yogurt definitely add weight probably because I like them so much that I over indulge. I eat fresh coconut instead which satisfies me and keeps my weight stable - I can't overeat it (same as meat).

Having said that, I never starve or let myself go hungry either.

I'm currently trying one whey drink a day if needed between my two meals - it's supposed to burn thru bad fat. If it's working, it's working very slowly (lol).

Yes, I was very low carb the first time - probably only had carbs in a small daily salad (for insurance). Now I aim for diversity in my diet so I'm sure I'm getting more carbs as a result.

Thanks for the great rant, I'm going to look up the "big" words to be sure I understand them correctly. I envy your finite weight control, but I don't want to upset my endocrine system again so I've decided to be happy with size 8, especially at my age.

bopes said...

Personally I’ve plateau-ed at 10-15 lbs over target weight for some time (the excess is all visceral), despite moderately low carb and routine IF-ing (coffee w/heavy cream and/or coconut oil for breakfast, no lunch, modest dinner).

Never counted before because I could not imagine this regime was excessive, either caloricaly or carb-wise. But out of frustration I recently figured out the energy breakdown of a typical day’s food intake:

Calories: 1951
Carbs: 58.44g
Protein: 100.46g
Fat: 146.31g

On that regime, weight and gut-fat maintenance is effortless, as are upward spikes from there at the prompting of almost any carb indulgence.

Anek Dodl said...


I eat berries with cream in season too, but it's easy for me to over indulge so good thing they're seasonal! My best strategy is to exercise control when shopping, if I don't buy it, I can't eat it. It's great you've put yourself in remission btw.

Anek Dodl said...


"the excess is all visceral"

How do you know it's visceral? I have the impression visceral fat is dangerous - no?

bopes said...

Mary, I meant "all in the belly".

Whether and why visceral fat is really "bad" or not is one of Peter's questions. Personally I have nothing against it. I just wish it could take a hint and move on, go find someone else's organs to hang around.

Arby said...

Bopes, have you tried increasing your intake? The most suprising thing that I've discovered is that I'd been eating and aiming for my BMR for the last 12 years. Since the first foot out of bed in the morning increases my caloric use above BMR, I've been chronically starving myself!

If Taubes et al are correct, calories don't count, and restricting calories only leads to metabolic efficiency. I have personally experienced gaining fat and losing muscle mass while eating LC at my BMR + excercise. At 4k/day post diet, I'm still gaining some fat, but I'm restoring an equal amount of dry muscle mass. Once the high caloric intake reverses my low caloric symptoms, my hunger should decrease as FFA's displace dietary intake. This, of course, will require reducing adipocyte count somehow.

mnature said...

Travis, you mention getting some visceral adiposity going for a few decades and reporting back (if you're still in the land of the living). My husband and I both started developing visceral adiposity in our late 20's, early 30's. After age 50, it ramped up quickly to an obvious amount within 5 years, and then went steady-state. We are now 60+.

This visceral adiposity happened to everyone in my family (parents, grandparents), including having high cholesterol and high blood pressure. It is quite unfortunate, as everyone only lived into their 90's. If they didn't have the visceral adiposity, I suppose they would have lived to 120.

Conventional medicine is great, but sometimes healthy skepticism actually is dead on. Imagine that. And my question remains, of how to determine an ideal weight. Though perhaps I should just consider it a hypothetical question that has no real answer.

bopes said...


To switch things up a bit I thought I'd try adding protein in the mornings (eggs & bacon, mostly) a la Jack Kruse's ideas of synching energy intake with circadian rhythms, light/dark cycles, etc. Did it a few times last week but it's been tough to maintain because I'm so used to minimal breakfasts.

Arm & leg muscles seemed to notice the extra protein, though, but so far the belly does not seem phased.

Re BMR, if that's what I was previously eating to I never felt starved or lacking in energy, but I agree my metabolism does seem devilishly efficient at the moment.

bopes said...

forgot to say, Arbitrage,

4,000 calories! Gadzooks, man, my hat's off to ye. You must have a herculean metabolism or some ferocious activity levels!

Arby said...

Bopes, wow, thanks. I'm working with a doc. I used her breathing machine to measure my BMR at 2300. Fit day gives me +1,000 for not being a complete vegetable (I occasionally get out of my chair) and the heart rate monitor clocks 500 cal during 45 minutes exercise 5 days/week. 3700 cal, and I'm usually around that in intake. But I was just as surprised as you when I added it all up. My only guide is hunger and as long as I'm low-carbing at 20 g/day, I respond to it by stuffing my face until it goes away. :)

blogblog said...

most HGs don't eat before mid-afternoon. Even those hard core high-carbers on Kitiva eat only one evening meal and fast for over 23 hours a day.

bopes said...

Blogblog, it's reassuring that my experience is not inconsistent with real life HGs. Now I needn't feel bad if I ditch the a.m. protein.

I'm guessing you would say to just dial down carbs, hard core.

Makro said...

"Even those hard core high-carbers on Kitiva eat only one evening meal and fast for over 23 hours a day."

That is pretty important info to have, given that Kitavans are a fixture of nutrition discussion...

Makro said...


Also, do you have a source for the Kitavan eating patterns? Would be good reading!

ItsTheWooo said...

I've always intuitively eaten most of my calories in teh evening, a few hrs before bed. This always maximized my energy and stabilized my glucose best. Typically my intuition is always right; what my body asks for, is typically what works for maximum energy.

Seeing as insulin sensitivity is greatest in the evening, and seeing as we should be oxidizing body fat mostly and not dietary glucose mostly (unless of course you are a fattie getting fatter), I never really understood the logic behind square meals and eating ASAP in the morning. Sounds like an excellent way to induce hyperinsulinsm and sugar swings.

I also don't get the whole "stuff yourself even if you're not hungry" some dieters, particularly LC dieters, are keen on. If you aren't hungry, thats sort of a sign that your body is easily using its own tissues for energy. That's the idea, the goal, of losing weight. When you feel hungry, it is a sign that your glucose and/or FFA are not where they should be, and so you eat.

I think another reason I have had so much success is I have ignored all conventional wisdoms of dieting, as well as LC propoganda which irrationally encourages people to stuff themselves with food even if not hungry. Then people wonder why they get sugar swings and fail to lose weight... if you aren't hungry it suggests your FFA and glucose are high and your insulin / leptin is adequate. Eating can only possibly destabilize this balance.

Every time I force myself to eat, I always end up hungrier and fatter, because forcing food predictably leads to nutrition excess with reactive insulin excess.

I never knew kitavans fast most of the day. Suddenly their excellent health in spite of very high carbohydrates and calories makes sense.
Typically metabolically healthy carb eaters are peasants starving of energy, or alternatively they are eating high calories but they are also fasting most of the day, like Mr. Pablo with his 6 pack. Both are actually using a ton of body fat for energy and their insulin levels are chronically low.

Western carb eaters, eating frequent meals and presented with high calories, always become fat fat fat. Hmmm.

ItsTheWooo said...


Well if you felt well at 103 it might be an okay weight for you, but for me such a weight was ridiculously deficient. I am much bigger NOW and people still tell me I am quite thin, so I can't even imagine how thin I was. I don't remember or have an accurate self perception of that time, but I remember thinking it was odd that my shoulders were points and little things like that.

Yep, most people are far better and lower carb the first time around and this explains the not so mysterious "golden shot" thing. When we come into this we are naive and we just eat plain , very very low carb very very high fat foods. The second time we are adding carbs and fruit and all kinds of crap and we wonder why it's slower.

ItsTheWooo said...

I hate to be the barer of bad news // point out the obviuos, but if you LOST weight with a calorie restricted program, and now you are eating a tremendous bounty of 4,000 calories per day, don't you think perhaps this extreme calorie intake might be behind your weight gain? If I attempted to eat anywhere NEAR that much, low carb or not, I would be fat fat fat. There is this misconception (WHY?) that on low carb it's a good idea to eat a ton of calories, and on low carb you have "no insulin" so you can't gain fat, etc etc etc. All of it is nonsense.

Eat as little as required to not feel hungry. Stop after this point.

If your glucose/insulin is unbalanced it may help to coinsciously restrict energy. I find that this is a very quick way to drop my insulin levels, it's a cumulative effect with reducing carbs. Something interesting happens after you restrict energy - because your insulin drops, you actually feel LESS hungry and more easily use body fat for energy. Then, you don't have to "consciously" restrict energy anymore, and it is automatic and natural.

IMO it is a big mistake and scientifically invalid to eat huge calorie quantities on a low carb diet. Weight maintenance, if not body fat gain, is the absolutely logical expectation.

This is a misconception amongst LC dieters, but the truth is all food raises insulin, not just carbs. Carbs merely do it the most/worst. Forcing food or aiming for a high calorie number will assure your insulin stays pathologically elevated, and if you are prone to obesity, that means fat gain.

blogblog said...

Kitiva lifestyle

blogblog said...

Regular meals only arrived with the Industrial Revolution. The highly regulated factory environments meant that meals could only be eaten at certain scheduled times e.g. in the early morning before work, at midday and in the evening after work finished.

Until about 1800 the British Royal Navy had the main meal at 2pm. This was called "dinner".

Stefansson noted that the traditional Inuits usually only ate only in the evening.

Jane said...

Visceral fat may be 'bad' simply because it's associated with fatty liver.

Fatty liver appears to be caused at least partly by copper deficiency, meaning that visceral fat may be a symptom of copper deficiency.

I heard Loren Cordain has a beer belly. He eats a paleo diet, presumably. Does he have copper deficiency? Probably. It won't be straight copper deficiency, it will be secondary to manganese deficiency.

BTW, Kitavans do eat breakfast. Look up 'kitavans breakfast', and then look up 'breakfast prevents obesity'.

blogblog said...


According to you everyone has some sort of mineral deficiency. In your case I can safely assume it is a lithium deficiency.

Loren Cordain is a fat-phobic. His ideas on paleo nutrition are quite strange.

There is no independent research that shows eating breakfast is beneficial for adults. It is all funded by cereal companies.

Eating breakfast was heavily promoted by the Kellog Brothers who were vegetarian extremists. Before the 1870s most Americans skipped breakfast.

Kitivans do not eat breakfast. They eat one cooked meal each night. They are only allowed to eat during the day if they are working.

Arby said...


You may be correct. I'm not forcing calories, just eating ad lib. I don't set a goal. I am gaining weight, but the gain has slowed even as my appetite increased. Recently, overthelast few days, my appetite has decreased, impling that lipolisys is starting to work for me again. Vitamin A? Green Tea? Or better carb discipline? I don't know why.

Overeating is a natural response to calorie restriction, see the Keys starvation studies for reference. But it also helps correct some of the imbalances caused by long term calorie restriction. I don't shiver all the time now, and my normal cold tolerance is back. If I gain some weight too, I' know how to lose it now. :)

Gyan said...

As a new participant here, I have a question. My diet is traditional and inclusive i.e. I eat both butter and bread liberally.
But the modern nutritionists tell you to exclude either butter (low-fat camp) or bread (high-fat camp).

But worldwide, the carbs were eaten along with the saturated fats-in Europe, India, and tropical islands and this diet pattern was supposed to be healthy and was frequently (or generally) showed to be healthy too.

IS there a modern evidence that shows that a high-saturated fat diet is unhealthy in conjunction with liberal carbs?.

PJ said...

I would think one of the questions we want to ask, is the one you left out:

And if you kill this fat cell, will the body continue in the future to want to add that weight back on, as it does fat lost through dieting or even through liposuction?

It doesn't help to lose the fat if it's just inevitably (unless you can out-willpower a few million years of evolution) returning. In fact if it's as harmful to lose/regain a lot of weight as has been said, then it's actually more harm than help.

Doesn't make it any less fascinating of course. But for practical reasons, this is the question I find most interesting.


blogblog said...


your experiences seem familiar. I gained about 10kg in three months on VLC. Then I lost my appetite completely for about two months and lost all the weight. Then I got hungry again and began eating more but my weight stabilised.

Arby said...

@blogblog, yes, I was just reading where you commented about you and Peter both eating about 3500 cal/day. The calories-in post if that link doesn't work. At that time you weighed 75lbs less than me now. These comments are a wealth of info for us newcomers!

Arby said...


I believe that the dead adipocyte contents will be reabsorbed by surrounding tissue after apoptosis. So if you take 12 billion half empty fat cells, kill half, and are left with 6 billion full fat cells, you should be able to maintain weight or lose on a low carb diet. Your Leptin production, and free fatty acid release will be maximized.

However, if your diet is TAD, then the fat will have nowhere to go.

Prediction: FDA bans this drug after five year trial reveals that most of the participants develop T2DM. ;)

blogblog said...


these "healthy" traditional diets were nearly always combined with high levels of physical activity and enforced or voluntary calorie restriction (fasting).

However when the same these "healthy" foods are eaten in abundance and exercise is limited the result is typically very poor health. India, Crete and Okinawa are obvious examples of where "healthy" traditional diets no longer work.

blogblog said...

I live in a hot humid climate. Peter lives in a cold climate.

US Army studies in WW2 showed that calorie consumption was 4x as high in the Arctic as the tropics for an identical workload.

Jane said...


The point about fat is this. Many years ago Leslie Klevay found a highly significant correlation between the fat content of foods and their zinc-copper ratio. The paper was published in 1974, and should have demolished the idea that heart disease is caused by fat.

The problem with dairy products is their extremely high zinc-copper ratio. Similarly, the problem with meat is its extremely high iron-manganese ratio.

You told us 'My feeling is that some of us (particularly northern Europeans) have essentually zero carbohydrate tolerance and need to stick to meat and butter.'

Carbohydrate intolerance means your beta cells are not sensitive enough to glucose, and cannot produce enough insulin fast enough to avoid having to produce a lot more later on, making your blood sugar plummet. It's caused by refined carbs, which have had most of their copper and manganese removed. It cannot be cured by meat and butter, for the reasons given above.

David Isaak said...

@blogblog: "Before 1870 most Americans skipped breakfast."

I can't find any evidence for this statement, although I can find ample evidence that it is incorrect. On the other hand, I'm not sure that anyone knows what "most Americans" did before 1870.

Certainly the published information suggests large breakfasts, with eggs and meats as the centerpeice, along with baked goods. In many farm families, workers arose and did a couple of hours of chores before breakfast (and, incidentally, brought back fresh eggs and milk with them).

The Monticello website says this about Jefferson's household:

"Like many Americans in the early nineteenth century, Thomas Jefferson and his family ate only two meals a day at Monticello: breakfast, typically at eight, and dinner, in the late afternoon."

"...Several guests recorded accounts of breakfast at Monticello. Mrs. Smith wrote: 'Our breakfast table was as large as our dinner table; . . . we had tea, coffee, excellent muffins, hot wheat and corn bread, cold ham and butter.'"

Most of the evidence I can find suggests that most Americans who could afford to ate ample breakfasts based on the English style.

Perhaps the idea that most Americans "skipped breakfast" is a confusion arising from the fact that so many of them began their day's work before returning to the house to eat breakfast?

David Isaak said...

Here's an issue that has puzzled me for many years, and I wonder how it might be related to adipocyte numbers or adipocyte hormone signalling:

It is a common experience that in losing weight (or, though less remarked upon, in gaining it) there are long "plateaus." These plateaus might be better described as "bands" since they are typically a range of poundage rather than a ceiling or a floor.

I seem to have some sort of homeostatic equilibria at certain weights. For me, these are 152-155 lbs; 164-167 lbs; 185-189 lbs. I seem to be able to stay within any of these bands indefinitely, but in losing or gaining weight, I move through the gaps between these bands with startling rapidity.

I know that other people have reported similar effects. Does anyone have insight into why this might be such a common experience?

Arby said...

Here's a theory, but I think that I'm missing something. It's all pieced togeather and I doesn't feel right.

Assuming ad lib LC dieting: as your weight decreases your adipocytes begin to empty and the excess must be killed off to restructure your FFA delivery and Leptin output. The lower Leptin probably increases appetite along with the reduced FFA lipolisys.

Because many have reported these stalls, and many get through them, we should assume that there is a mechanism for reducing adipocyte hyperplasia. IDK what it is. Leptin shouldn't explain because it is reduced. Perhaps it is a slow trigger mechanism, but with a lasting effect.

So, to narrate the process, you lose weight while FFA's are available. Then adipocyte size, appetite, Leptin, constrains the weight loss. You plateau. After a while, adipocytes begin a long lasting die off and you swiftly proceed to the next plateau as FFA lipolisys begins freely again.

Can anyone refute or refine this better?

blogblog said...
This comment has been removed by the author.
ItsTheWooo said...

Carbohydrate intolernace, or glucose intolerance, only means that one does not tolerate glucose "normally". Your description of glucose intolerance is one but several possible types of glucose intolerance. A low dopaminergic tone can also cause carbohydrate intolerance / compensatory hyperinsulinemia for totally unrelated reasons (as "beta cell insensitivity"), as can a myriad of other issues. It's safe to say the most common cause of glucose intolerance is mitochondrial level defects in energy use, it is NOT at the level of the beta cell.

ItsTheWooo said...


Perhaps 4k cal is required , but that does seem like a very high intake. Just a suggestion, you might want to at least try manipulating either the structure of your diet or your meals to see if perhaps you can reduce your calorie intake. Sometimes, I can reduce my over all cal intake merely by altering the times I eat. FOrcing myself to eat early in the day usually leads to a higher cal intake in total, because forcing food when not hungry (early on) sets me up for excessive insulin/suppression of body fat oxidation. I merely respond by building body fat and hunger increasing. I avoid eating much early in the day , ideally. I don't fast totally but I eat very little. I feel best this way.

If you have recently started green tea that may help you, I believe it is most of use to dieting/weight reduced people. The benefits are quite obvious and extreme for me. The science is quite clear that green tea is fantastic for body fat/glucose control and energy.

Overeating is definitely a natural response to cal restriction, but we obese people are a different animal than healthy thin people. In our case we tend toward hyperinsulinism, inappropriate/excessive insulin responses, with compensatory chronic overeating to fuel body fat anabolism which was produced by the inappropriate hyperinsulinism. For someone with this disorder, intelligent manipulation of calorie intake can lead to a real and sustained drop in energy consumption long term. AS stated, eating nutrition excessively when glucose and ffa are already optimal will and can produce excessive insulin, which is the heart of obesity.

If one is presently hyperinsulinemic, forcing down calories can be a good way to induct ketosis, get the body back to using body fat for energy normally, and drop the calorie demands.

blogblog said...

@David Isaak,

Certainly the published information suggests large breakfasts, with eggs and meats as the centerpeice, along with baked goods. In many farm families, workers arose and did a couple of hours of chores before breakfast (and, incidentally, brought back fresh eggs and milk with them).

Only a 1/4 of Americans lived on farms by the 1870s. The majority of farmers were living a hand to mouth existence. The groaning tables of food would been few and far between.

Eggs traditionally belonged to the farmers wife. They were usually sold for cash not eaten.

Have a look at any authentic mid 19th century clothing or Civil War uniform. You will soon discover that the typical soldier was not much larger than a modern jockey. This was due to chronic malnutrition.

Pellagra was common in the rural south until after WW2 due to a diet consisting of mainly of corn meal.

Many slaves went their entire life without ever eating red meat. They were usually kept on absolute minimum rations until puberty to save the owner money.

Like many Americans in the early nineteenth century, Thomas Jefferson and his family ate only two meals a day at Monticello: breakfast, typically at eight, and dinner, in the late afternoon.

The wealthy got up late and went to bed late. They had servants to prepare their food.

The vast majority of Americans in 1800 rose at sunrise and went to bed soon after sunset because they couldn't afford candles or whale oil.

...Several guests recorded accounts of breakfast at Monticello. Mrs. Smith wrote: 'Our breakfast table was as large as our dinner table; . . . we had tea, coffee, excellent muffins, hot wheat and corn bread, cold ham and butter.'

A single cup of tea cost more than an entire days wages for a working man in 1800. Sugar was an expensive luxury.

Most of the evidence I can find suggests that most Americans who could afford to ate ample breakfasts based on the English style.

That would have been about the wealthiest 5% of Americans.

Perhaps the idea that most Americans "skipped breakfast" is a confusion arising from the fact that so many of them began their day's work before returning to the house to eat breakfast?

The Kellogg Brothers were physicians from Battle Creek Michigan. They created cornflakes specifically to provide a quick, cheap and easy breakfast that didn't require cooking. This is because because the vast majority of Americans (lowly paid city dwellers) didn't have the time (10-12 hour working days) or money to prepare a cooked breakfast.

blogblog said...

as long as organs are eaten meat and dairy foods form an excellent diet.

Humans can store or excrete minerals as needed. Problems only occur when a chronic deficiency is present.

Northern Europeans frequently have a intolerance of all carbohydrates including sugars and starches. It doesn't matter whether they are refined or unrefined. In my own case as little as 5-10g a day of carbohydrate can cause digestive distress.

Arby said...

Large scale adipoptosis (is that a word yet?) probably doesn't make sense under the paleo paradigm. If humans only cycled between a winter weight and a summer weight, then the adipocyte set shouldn't need to be reduced under historicle circumstances. Evolution would not need to provide for adipocyte apoptosis of as much as 1/2 of all adipocytes.

On the other hand, people do succeed after stalls in weight loss on low carb when the shouldn't be able to due to adipocyte hyperplasia.

@wooo, I want to see this thing through. Many of my friends are counting on me as an example.

ItsTheWooo said...

Interesting historical info. I do not know if it is true or not, but I trust you, and suddenly the "excellent health" of people in past centuries makes a slight bit more sense.

Though your writing seagues into the idea that all carbs cause disease, the fact is that most people were slim until about the 1970s/80s. I know, because I was a baby in the 80s, and I distinctly remember wearing adults clothing and being the only fat kid in my classes. Today, any class of very small children has tons and tons of quite fat children, obesity is now relatively normal for children. This was not at all the case when I was a small child; it was usually myself, and maybe 1 or 2 other children who were distinctly fat.

It seems that severity/rates of obesity have risen substantially circa 1970. This suggests more than carbohydrate is involved as americans were eating lots of carbs prior to 1970.

The piece that is causing this is not carbs in general, but the invention of HFCS. HFCS is metabolically equal to sucrose, the reason it is bad is that it incentives manufactureres to bloat portions sizes and to put sugar in everything. If HFCS was never invented, the obesity epidemic could not have occurred, that is my belief. It would have been economically infeasible to create monster slushies and tons of cheap baked goods which are nothing but transfat (remember that crap? lol) and sugar.

ItsTheWooo said...

I agree. Our bodies have no natural mechanism for large scale apoptosis. This is why obesity is a permanent disorder. There is no way to remain at a reduced weight and to magically become naturally thin, without medical intervention to remove superflucous adipocytes (either drugs or surgery).

We never evolved to become obese, this is purely a modern disease. We have no counterregulation against it. Our bodies evolved without knowing that chronic hyperinsulinism for years and years is even possible. Obesity itself suggests that humans prone to it do not have counterregulation against hyperinsulinemia-induced fat storage.
The only defense is artful control of insulin levels, after inducing adipocyte hypotrophy by being in energy deficit for a few months.

I understand you would like to succeed, I can understand that... but, it's just a suggestion, you might find that trying to eat a bit less can help. Is it more important to be a posterchild for a perfect paleo low carb diet, whatever that means, or is it more important to be in control of obesity and your glucose/insulin levels?

When I was very young starting LC, I often heard the propaganda that on LC you need to "force yourself to eat". I heard the propaganda that you would gain weight if you "stopped eating". I was so young and new I believed them and began frying up steaks and forcing myself to eat them, EVEN THOUGH my body was like "well I really don't want food, why are you eating now?"

This lasted a very short while until common sense kicked in . Sitting there feeling very full and nauseated , listening to my body, lead me to conclude that it is patently irrational to assume that eating food will produce weight loss. My body generates tehse signals for a reason - nausea and fullness is telling me my body does not at this moment need food.

gallier2 said...


I disagree that HFCS and sucrose are metabolized in the same way. HFCS is a racemic mix ( of fructose and glucose mono-saccharides, while sucrose is a di-saccharide which needs an enzymatic cleavage before the chiral fructose and the chiral glucose can be absorbed.
These 2 differences (chirality and mono/di form) suggest that there might be also a metabolic difference. I have searched for more info on that subject but haven't found a lot, more because it hasn't be studied at all than the effect of not being existent.

Your other point about putting that stuff everywhere because of cheapness and practicality is still valid.

annlee said...

@Wooo, Gallier2 -

At roughly the same time as the rapid increase in HFCS, we see the major shift to industrial seed oils accelerate under the "guidance" of the US government health campaign (and I believe that was slavishly followed by other governments). We may be seeing a synergistic effect of the two unnatural "foods" in vivo.

David Isaak said...


Excuse me, but your statement was "Before the 1870s most Americans skipped breakfast."

You then go on to argue

"Only a 1/4 of Americans lived on farms by the 1870s."

The data I find most readily says that the population in 1870 was 38.6 million; the farm population was 18.4 million. Half the labor force was still working in agriculture (The latter figure is from the 1870 census. It's available from the US Census Bureau, although the pdf is 154 MB.)

Note also that "agricultural laborers" were almost as large a percentage of the population as "farmers," so the percentage of people "living on farms"
I am sure that you read somewhere that only 25% of Americans lived on "farms," but that must be a very resticted definition of farm, which excludes things like, say, ranches.

Im any case, you were talking about BEFORE 1870, when the farm population was a much larger share of the total. For instance, when I talk about what was eaten at Monticello, that was well before 1870.

Prior to refrigeration and highly mechanized transport, I seriously doubt that farm families in America always sold all of their eggs and never ate them.

When de Tocqueville toured America in 1831, he wrote back home, "At first we found the absence of wine from meals a serious deprivation, and we are still baffled by the sheer quantity of food that people somehow stuff down their gullets. Besides breakfast, dinner, and tea*, with which Americans eat ham, they have very copious suppers and often a snack." (*"tea" referring to the meal rather than the substance.")

Most of the visitors to America prior to the Civil War remark on how well-fed all the people except the urabn poor are.

The height of American soldiers in the Civil War was certainly lower than it is today, but it was higher than in Europe. It is also not clear how fine a proxy this is for anything, as slaves in the plantation south were much taller than any other group (which has led some authorities to claim that slaves were treated especially well).

In GCBC, Taubes makes a pretty convincing case that we really don't have good statistics on what people ate until quite recently; and that the numbers we do have probably greatly underestimated the past consumption of eggs, meat, milk, and fresh vegetables, since these were the products most likely to be consumed locally without ever being recorded.

I also am unable to find evidence that "most" Hunter-Gatherers never eat before mid-afternoon. It certainly isn't true of the Inuit, who eat whenever they are hungry, and are also likely to snack throughout the day.

And I know people who have spent time with the Bushmen; whether they eat in the morning has to do mostly with whether they have food on hand in the morning.

Can you point me to a source that has done any kind of systematic evaluation of the meal frequency of hunter-gatherer peoples?

Jane said...


No, humans cannot 'store or excrete minerals as needed' in one important case: iron. There is no mechanism for iron excretion.

Iron overload may be the primary cause of carbohydrate intolerance.

It works like this: iron causes oxidative stress by converting excess superoxide into the very toxic hydroxyl radical. Excess superoxide comes from deficiencies of copper and manganese, which activate superoxide dismutases.

Beta cells are very sensitive to oxidative stress, like all cells that make large amounts of proteins for export, because the proteins cannot fold properly.

Unfolded/misfolded proteins are normally cleared by the UPR (unfolded protein response), and if they aren't, inflammation follows. This is what causes your inflammatory bowel disease.

Carbohydrate intolerance involves exactly the same process, happening in beta cells and many other tissues including the hypothalamus and the midbrain. Endocrine and brain cells are especially susceptible.

Arby said...

@David, Blogblog,

According to Marie Antoinette, french peasants in the 18th century ate a lot of cake.

I don't think I follow the end conclusion/inference here. Is it worth all this debate over the facts?

bopes said...

Arby, I'm with you on that. The question of whether HGs or pre-industrial Americans ate breakfast or not is interesting. But I guess I'll let personal experience answer it for me.

My experience right now is that, while not easy to maintain on a daily basis, one plus I do note from increasing a.m. protein is an increase in dream recall.

Travis Culp said...

gallier: I agree that the glycosidic bond between fructose and glucose in sucrose makes metabolism hugely different. The odds of a particular fructose bolus reaching the blood stream and glycating proteins or ending up far down in the GI tract and causing digestive issues is much higher. To be fair, the mixed fructose and glucose does occur with honey, but we 1) didn't evolve to eat it every day and 2) studies have shown that metabolism is different, for whatever reason.

There's so much talk about the Kitavans and carb tolerance in general, but I would wager that those fellows aren't sedentary, and that makes a massive difference. There are piles of studies that show a difference in glucose tolerance between the trained and untrained. It ain't the beta cells that proliferate when you lift weights....

john1 said...

A Cross-Sectional Characterization of Insulin Resistance by Phenotype and Insulin Clamp in East Asian Americans with Type 1 and Type 2 Diabetes

Peter, please delete if not interested.

Jane said...

Travis Culp,

Have you come across a link between fructose and copper deficiency?

'Dietary copper deficiency is associated with a variety of manifestations of the metabolic syndrome, including hyperlipidemia and fatty liver. Fructose feeding has been reported to exacerbate complications of copper deficiency. ...Our data suggest that high fructose-induced nonalcoholic fatty liver disease (NAFLD) may be due, in part, to inadequate dietary copper. Impaired duodenum Ctr-1 [copper transporter] expression seen in fructose feeding may lead to decreased copper absorption, and subsequent copper deficiency.'

BTW, I just read the comment you wrote yesterday on WHS. Great stuff.

Anonymous said...

This is quite a new drug, isn't it? I'm nowhere near as versed in body biology, so I probably should be keeping my mouth shut, but all the same a drug that kills off your fat cells sounds scary and potentially harmful...who knows what long-term effects it could cause? Just my emotional response..

YME said...

OT: Peter, have you had a look at this doctoral thesis:

Conclusions: High proportions of MUFA in serum cholesterol esters and a high SCD-1 index are related to increased CRP concentrations, independently of obesity, lifestyle factors and insulin resistance. In these Swedish popula
tions, these associations may partly be a reflection of a long-term high SFA intake. It may also be a reflection of a link between lipogenic activity and inflammation.
A low proportion of linoleic acid (18:2 n-6, the major dietary n-6 PUFA) in serum cholesterol esters, indicating a low vegetable fat intake, is associated with higher CRP levels.
Supplementation with a low dose of n-3 PUFA for 12 weeks did not
affect systemic inflammation and lipid peroxidation in individuals with the metabolic syndrome.
Neither the macronutrient proportions (i.e. fat versus carbohydrates) nor a diet high in MUFA from e.g. olive oil or a diet high in SFA did influence markers of inflammation or oxidative stress.
A high intake of dietary n-6 PUFA (linoleic acid) during 10 weeks does not increase systemic inflammation and lipid peroxidation. Instead it may reduce plasma levels of some inflammatory markers compared with
a diet rich in SFA.
Taken together, this thesis suggests that systemic low grade-
inflammation is to some extent associated with certain dietary fatty acids. In addition, indices of endogenous fatty acid desaturation (i.e. increased SCD-1 activity index) were also shown to be associated with higher systemic inflammation.

Peter said...

"Indeed, both palmitoleic acid and SCD-1 index increase in response to SFA intake180, results also supported by animal data suggesting that dietary SFA induce SCD-1 activity and hence increase endogenous fatty acid synthesis of MUFA181. Moreover, in the Western societies, especially in elderly populations and decades ago, oleic acid is mainly provided by animal derived fat, and not from olive oil, which is the major source for MUFA in for example the Mediterranean countries. Thus, MUFA in cholesterol esters reflects dietary saturated fat intake rather than dietary MUFA intake14, suggesting that the present correlation between MUFA, SCD-1 index and CRP probably reflects high meat and dairy fat intake. SCD-1 index can also be influenced by a high carbohydrate intake (especially from sugars) via de novo lipogenesis182-184. This endogenous synthesis of fat is however believed to be small in Western populations due to the relatively high fat intake3,4,184,185. Whereas SCD-1 index shows a strong positive relation to insulin resistance in Amerindians living under Western conditions, this association is absent in Amerindians with traditional hunter/gatherer lifestyle despite a higher SCD-1 index. Thus, if the diet is very low in fat and high in non-refined carbohydrate the plasma SCD-1 index might reflect enzyme activity in adipose tissue rather than in the liver, whereas activity in the latter probably is the case in Western diets with a higher fat content186. SFA was not related to inflammation, perhaps because inflammation is promoted by a metabolic disordered state associated with elevated SCD-1 activity rather than the SFA intake per se."


The above quote, from pages 47-8, seems to sum up the PhD. It's very clear that HGs have a high SCD-1 index and this has no association with insulin resistance. In acculturated Amerindians there is an association between SCD-1 and insulin resistance. The thesis then speculates that HGs eat a diet very low in fat and very high in non refined carbohydrate (WTF, this reminds me of the joke I saw on facebook which goes along the lines of: What is the HG term for a failed hunter? A vegetarian) and that under these conditions SCD-1 is active in adipocytes rather than hepatocytes. Which is apparently Good. Or alternatively I could, with a high probability of being correct, speculate that acculturated people are using SCD-1 on fructose induced DNL-derived saturated fat and the fructose is the cause of the insulin resistance in these acculturated folks... Genuine HGs can eat saturated fat and use SCD-1 with impunity whenever needed to (like myself) because they eat no HFCS. Basing your PhD on looking at fat without thinking about fructose is going to be depressing and will certainly make you go far in obesity research! Like Bengt Vessby and Nils-Georg Asp.

More comments when I get the chance.


DLS said...

ding-ding-ding: evil fructose gets along just fine with evil SFA over here... btw, cant wait for dat next post peter ;)

Zorica Vuletic said...

@ Jane

There is no mechanism for iron excretion.

Iron overload may be the primary cause of carbohydrate intolerance.

How does this overload become manifested in the first place? Is this an interaction between iron and carbohydrates? I'm just a bit confused on what you think is the primary cause of this iron overload.

Yes, iron overload is of course toxic, and the mechanism you explained how it leads to oxidative stress, which leads to improper clearence of unfolded proteins makes sense. I just want to know where you stand on the cause (other than the manganese/copper deficiency standpoint). What causes these deficiencies. I will not tell for you on any carbohydrate/insulin hypothesis, since you might have a different hypothesis to explain this overload (and deficiency).


Jane said...

Hi Gladina,

'..I'm just a bit confused on what you think is the primary cause of this iron overload.'

Sorry, I haven't explained myself very well. The primary cause appears to be a diet high in muscle meat and refined carbs. The evidence suggests that the crucial thing is the ratio between iron and manganese, which in beef muscle is about 100.

Iron and manganese share an uptake system in the gut, so if you eat a lot of iron you will absorb less manganese.

White flour has had most of its manganese removed and replaced with iron. This is insane, of course. The grain has manganese because it's needed for processing the carbohydrate during germination, and we need it for the same reason.

You can see how the combination of beef muscle and white flour (McDonalds) will have an iron-manganese ratio somewhere in the stratosphere.

Mark said...

+1 for next post

montmorency said...

@Mnature (and detractors):

On what is an ideal weight:

My Pa-in-law lived to 90 and was very overweight (but still active) all the time I knew him, although he slowed down in his last few years).

My Ma-in-law lived to nearly 88, and was very overweight all the time I knew her, but was in fine health, although a bit frail in her last few years.

My mother is 88, looks after herself, walks to town, shops, cooks for herself (and others quite often), rarely ill. She lived through the depression (her family knew unemployment and poverty, but living in the country, kept chickens and grew vegetables and ate real food, albeit not much of it), worked 12-hour-shifts in an aircraft factory in the war, worked hard all her life (retiring at 70). She has been dieting since I was a kid, and is still significantly overweight.

My Dad went through similar experiences, worked hard all his life (retired well into his 70s). He gradually put on weight from middle age onwards, and certainly would have had visceral fat, but was hardly ever ill. Died at 84.

So that's 4 out of 4 people with visceral fat, who all lived active lives till at least 80, and longer.

Can't give you an exact quote, but in Barry Groves' "Natural Health and Weight Loss", he also casts doubt on the obsession with body weight, and shows studies where higher weight than average was associated with longevity, not lower weight than average.

And of course it's a similar story with cholesterol. As perhaps most of us here know, longevity has been shown to peak on average around 270-280 mg/dl.
(If it goes much higher, then maybe something is definitely wrong, e.g. thyroid, but artificially lowering it with statins or other drugs is definitely not the answer. The answer is to find why it's going up and it is almost certainly the body's (healthy) response to some kind of stress or inflammation).


montmorency said...


I respect a lot of what you write, but no low-carbers or low-carb spokespeople that I know of say stuff your face regardless of hunger.

Most people in my experience say only eat when you are hungry. Eat until you stop feeling hungry. When you stop feeling hungry, stop eating.

The point is that on low-carb people tend to be easily sated on their low-carb fare, and know when to stop eating, and then don't feel hungry again for quite some time afterwards, usually around their next normal meal time. (This very simple point is one that the "Food Reward" crowd seem to have great difficulty getting their heads around; that or they simply don't want to understand it).

montmorency said...


British Navy "dinner":

Interesting, but as a Brit, there is an interesting class/region thing about meal names.

Working class people and people generally in the north of England (where most of the heavy industry used to be), called the mid-day meal "dinner" and the evening meal (usually quite early evening) "tea" (even if it was still a hot meal).

Middle class people and southerners tended to call the mid-day meal "lunch" and the evening meal (usually a bit later) "dinner".

I think the point is that the main meal was referred to as "dinner", and working class people had this in the middle of their working day to fuel themselves up. "Tea" would be smaller, and probably starchy, e.g. beans on toast. "Supper" was a little snack at bedtime, e.g. cocoa and a chocolate biscuit. (Middle-class people sometimes referred to "supper" when they meant their main evening meal, to confuse the issue).

Interestingly, at school (even in middle class areas) the mid-day meal was always "dinner", and I think is still referred to that way. You had to take your "dinner money" in every week.

Working patterns have now changed, heavy industry has largely disappeared, and class distinctions are more blurred, but the regional meal-name differences are still there, I am fairly sure.

montmorency said...


Despite what everyone says (even Taubes and Lustig who are sworn enemies of HFCS), it seems that HFCS is not equivalent to sucrose after all, and we are not just talking about the small 5% difference in fructose content:


Also, I've heard Ray Peat say that HFCS contains residues left over from the original corn starch, so consuming HFCS is a bit like consuming a bunch of sweetened flour.


Another thing with meat is the high phosphorous to calcium ratio.

Milk on the other hand has a more ideal phosphorous to calcium ratio so consuming both milk (and/or cheese) and meat could help balance things out. I don't know about the respective copper-zinc ratios though.


Admin said...

This is a pretty advanced discussion about adipotide and fat loss. Does anybody know if the kidney damage from adipotide was the result of higher than normal dosing or just normal dosing. I realize that the kidneys in the study returned to normal after being taken off the drug, but kidney damage is one hell of a side effect!

Humble To Learn said...

Hi, I'm very naive, so I apologize ahead of time.

1) I could be wrong here, but I thought visceral fat didn't really secrete, or at least contribute that much to circulating leptin. At least not compared to subcutaneous adipose.

2) If studies show different gene expression in different locations of adipocytes(subcutaneously) then can one infer it will do the same with visceral fat? That is to say that not all visceral fat is the equal?

This could help explain certain psychological function