I was keeping quiet about this, as it contradicts Gary Taubes, Michael R Eades & Richard D Feinman and Eugene J Fine.
Please note: This post is not criticising low-carb, high-fat diets. I'm pointing out that if someone on a low-carb, high-fat diet exercises as much gluttony as they want on roast lamb/pork/duck etc, they may not lose as much weight/body fat as they expected & they may even gain.
I don't want to start a shit-storm, but as I am in the "a calorie is a calorie" (when it comes to weight gain/loss) camp and a lot of the people whose blogs I link to aren't, I need to go public. So, here it is, copied and pasted from the comments section of Diet, Carbs, Fat and Weight Loss, corrected for spelling.
"I would like to propose a theory which explains how fat cells can acquire glucose (& thus correct a deficiency in glycerol-3-phosphate) even when serum insulin level is basal.
Consider muscle cells undergoing anaerobic activity:-
Anaerobic activity is very inefficient and uses pyruvate at a very rapid rate. A deficiency in pyruvate up-regulates all of the up-stream processes, including Glu-T4 transporters so as to maximise pyruvate production.
This explains why resistance training with weights greatly increases muscular insulin sensitivity and why resistance training with weights when depleted of muscle glycogen can cause precipitous drops in blood glucose level.
Ditto for glycerol-3-phosphate in fat cells. In this case, blood glucose level is maintained by the liver & kidneys, which convert the glycerol backbone of triacylglycerols (fats) and other substrates such as lactate, pyruvate & glucogenic amino acids into glucose."
In plain terms what this means is that, like muscle cells, fat cells can acquire as much glucose as they need, independently of carbohydrate intake.
Therefore, if an excess (beyond what the body is burning) of dietary fat is eaten, this can be stored in fat cells even if serum insulin level does not increase.
There. I've said it. I expect comments. Moderation is enabled. All comments that are free from ad-hominem, straw men & other logical fallacies will be published.
EDIT: Here's evidence that dietary fat can be stored in the absence of dietary carbohydrate. It involves doing maths on an Oral Fat Tolerance Test:- On burning, storing and recomposing.
EDIT: Here's evidence that a calorie is a calorie (where weight change is concerned):- Bray et al shows that a calorie *is* a calorie (where weight change is concerned).
As a lot of people report that they can eat dietary fat without getting fat (& actually getting lighter & slimmer), there appears to be something "magical" going on. It's generally accepted that fat is the least thermogenic of all the macronutrients & protein is the most thermogenic. I wonder if this is the case for all types of fat and all types of people.
See Butyric Acid: an Ancient Controller of Metabolism, Inflammation and Stress Resistance.
From Battle of the Weight Loss Diets: Who's Winning (at losing):-
Insulin Resistant people lose more weight on low-carb, high-fat (LCHF) diets than high-carb, low-fat (HCLF) diets.
Insulin Sensitive people lose more weight on high-carb, low-fat (HCLF) diets than low-carb, high-fat (LCHF) diets.
According to Gary Taubes's Carbohydrate Insulin Hypothesis, everyone should lose more weight on low-carb, high-fat (LCHF) diets than on high-carb, low-fat (HCLF) diets. Therefore, Gary Taubes's Carbohydrate Insulin Hypothesis is false.
It's possible that in people who do well on LCHF diets, kcals out on the right hand side of the Energy Balance Equation increase significantly. So keep on keeping on.
EDIT: With the benefit of four more years of knowledge, here's why LCHF & ketogenic diets have an advantage for people who have Insulin Resistance. How low-carbohydrate diets result in more weight loss than high-carbohydrate diets for people with Insulin Resistance or Type 2 Diabetes.
See also:-
Metabolic Advantage of Ketogenic Diets Debunked? An Intriguing Study You Will Want to Read
Is the Fable of Unfettered Fat Burning Derailing Your Low Carb Diet?
See also How stuff works & Enzymes.
56 comments:
Hi NIgel, I replied to you on my blog, but I'll repeat it here. My husband and I have different experiences with low carb. He only has to limit carbs and he stays lovely and slim, despite eating lots of cream. I, however, have to also watch my calories or I put on weight on a restricted carb diet, even at less than 20 carbs. There might be a metabolic advantage to low carb, and there are certainly plenty of other health and appetite advantages, but for some of us (very petite females who have been dieting for decades and are thus fairly screwed up) we still have to watch calories.
So we men have the Metabolic Advantage? ;-p Thanks for replying.
Nige.
First, let me say that I'm not exactly sure I follow your argument. For one, I don't see necessarily that it contradicts Taubes & Feinman. I don't know that either argues that in the absence of carbs, it is impossible to store fat.
For one, I think that low carb diets typically provide enough protein so that there can be glucose (thru glycogenesis) and a related insulin response (as Patrik pointed out in the comments over on the thread on Cooling Inflamation).
That said, I do believe this question was the source of the big feud between Michael Eades and Anthony Colpo. I don't have links handy, but if you Google them, I bet you'd find their arguments on whether a metabolic advantage exists or not interesting!
But in short, I recall that Eades admits that if there is no reason to burn fat (i.e., dietary fat provides enough calories), that a low-carb diet in and of itself will not generate weight loss -- and this is the source of the low-carb diet weight plateau.
Also, if you haven't come across it, you may also want to check Eades' response on the thermodynamics question:
http://www.proteinpower.com/drmike/metabolism/thermodynamics-and-weight-loss/
He mostly couches the issue as one of entropy, but it seems to me that the other reason why a calorie isn't a calorie is the question of hormonal response to different foods. And the different responses we have to them.
Have you seen this presentation from Christopher Gardner on the Battle of the Diets?
http://www.youtube.com/watch?v=eREuZEdMAVo
The most interesting part for me was the section where he noted the different responses of the insulin sensitive and the insulin resistant to the various diets. Insulin sensitive folks did better on a high carb diet; insulin resistant did better on a low carb diet. Seems more than "a calorie is a calorie" to me!
Hi Beth.
Taubes and Feinman & Fine state "no dietary carbs = no insulin spike = no glucose entering fat cells = no glycerol-3-phosphate = no fat storage". I'm definitely contradicting this!
I read They're all MAD so I know all about the big feud between Colpo & Eades. I don't know what entropy has to do with weight loss so I can't comment on that.
I have a link to Christopher Gardner's lecture in my blog post.
When push comes to shove, I agree with most of what Taubes says. It's just the "dietary fat cannot be stored as body fat in the absence of dietary carbohydrate" that I disagree with. In practical terms, who drinks just glasses of oil or eats just knobs of butter?
Cheers, Nige.
Sorry Nige! My bad ... I did actually read the post; just spazzed on the Gardner link (so many blogs, so little time :).
I don't know that I'm that far from you, I'm just not as sure as you that Taubes and Feinman say what you say they say.
I have an entirely different issue with Taubes. As far as I can tell, he doesn't explain cultures like the Japanese or Kitavans who have diets that are high carb and yet don't have the obesity that we see.
However, I think that that means that the issue is slightly more complicated (does it involve fructose? or omega 6? or vitamin D?). But I still don't think it means that a calorie is a calorie.
Hi Nige,
I enjoy lob and dive blogging.
I must admit that I never find you controversial, but perhaps that points at me rather than you. I must admit to believing that a calorie is a calorie and marvel at where the calories go. What about brown fat proton leaking for thermogenesis?
I want to flesh out some of the molecular machinery for your controls on glucose influx.
Increase in glucose transporters can be triggered by the insulin/insulin receptor system and by pyruvate depletion. Excess intracellular glucose can result in insulin resistance by excess pyruvate leading to superoxide production by mitochondria in the presence of ample oxygen, and a shutdown of the enhancement of glucose transporters.
Are you saying that liver gluconeogenesis provides enough serum glucose so that depletion of pyruvate in adipocytes on a zero carb diet will still lead to increase in glucose transporters and enough glycerol to store serum lipids as cellular triglycerides?
Thanks for the brave blogging.
If you click on the Taubes link and fast-forward to 45 minutes, he talks about the pivotal role of glycerol-3-phosphate and its dependence on dietary carbs.
Cultures that get their carbs in rice form are eating whole grains that consist mostly of water + fibre, so although carb intake may be high in percentage terms, caloric intake is lower than cultures that get their carbs in powdered wheat & sugar form. I don't know about Kitavans so can't comment.
In the UK, we certainly eat too much manufactured junk, too much refined carbs, too much sucrose, too much omega-6, not enough omega-3 and we get nowhere near enough Vitamin D3 this far North of the Equator!
In terms of health, wellbeing etc, a calorie isn't a calorie. I'm just arguing that a calorie is a calorie when it comes to weight loss/gain.
Nige.
Hi Art.
My previous reply was to Beth, by the way. This is the first time I've dared to "stick my head over the parapet". So far, I haven't had it shot off!
"What about brown fat proton leaking for thermogenesis?"
I think that adults don't have much if any brown fat. That said, my skinny ex-G/F always had a hot back (one location for brown fat), though her hands & feet were like blocks of ice!
"Increase in glucose transporters can be triggered by the insulin/insulin receptor system and by pyruvate depletion. Excess intracellular glucose can result in insulin resistance by excess pyruvate leading to superoxide production by mitochondria in the presence of ample oxygen, and a shutdown of the enhancement of glucose transporters."
In muscle cells, a lack of pyruvate up-regulates everything to make more pyruvate. An excess of pyruvate down-regulates everything, including Glu-T4 sensitivity to insulin, to make less pyruvate. Too much input leads to insulin resistance.
"Are you saying that liver gluconeogenesis provides enough serum glucose so that depletion of pyruvate in adipocytes on a zero carb diet will still lead to increase in glucose transporters and enough glycerol to store serum lipids as cellular triglycerides?"
In adipocytes, a shortage of glycerol-3-phosphate (rather than pyruvate) up-regulates everything to produce more glycerol-3-phosphate. Too much input can be diverted to de-novo-lipogenesis, so adipocytes don't usually become insulin resistant until they're full.
As triglycerides in the blood are hydrolysed to glycerol & fatty acids by lipoprotein lipase, the glycerol provides the liver with material to produce glucose. Dietary protein can be used to provide additional glucose as required.
That's a lot of biochemistry for just before bed-time!
Nige.
I am female,60, and have not had much success with HFLC,coconut oil etc and weight loss. I seem to have gained about 10 pounds and my husband has gained about 20. We are not diabetic. Both of us have not had the feeling of blood sugar ups and downs or hunger that we used to on the SAD. I am going to try writing down my food intake and see if that works and restrict the calories. Maybe HFLC works better on the under 60 age group. We are wheatless, sugarless, Vit D believers, try to limit Omega 6's, etc...Maybe need to spend some time lifting weights at our age.
Hi anonymous female.
LCHF definitely results in more stable appetite, blood glucose & insulin levels and you should be finding that you don't get after-meal "slumps" (if you used to).
Try using kitchen scales for a while to get a feel for portion sizes. Eyeballing portion sizes is very inaccurate.
Lifting weights is good for maintaining/increasing bone density and maintaining/increasing muscle mass. Take care, increase the weight you lift gradually & take advice from other weight lifters to achieve good lifting form.
See Dude Deadlifts 329 Pounds Then Passes Out.
Hey Nigel,
G-proteins affect the receptors for adiponectin and other hormones, and it appears the fatty acids play a mediating role. I definitely think you are on the right track that the different lengths of fatty acids have differential biochem consequences...
Fatty acid receptors are new therapeutic targets for diabetes
Oooh, more science. Keep it coming!
Nigel,
months ago I read a research paper suggesting that liver doesn't use glycerol for gluconeogenesis even under conditions of starvation. I don't remember the details but I think it was a rat study with 13C labeled glycerol backbone. Unfortunately I don't have the reference available. Maybe you or someone else can try and track this or similiar research down (I'm currently swamped with exams + no access to full text).
Adrián, I'll have a rummage through PubMed, but I can't always get access to full text. Also, rat/mouse studies may or may not be applicable to humans.
Nige.
I found Rat liver responsiveness to gluconeogenic substrates during insulin-induced hypoglycemia which states:-
"The IN group showed higher (P<0.05) hepatic glucose production from glycerol, L-alanine and L-glutamine and higher (P<0.05) production of L-lactate, pyruvate and urea from L-alanine and L-glutamine."
I also found Contribution of glycerol and alanine to basal hepatic glucose production in the genetically obese (fa/fa) rat which states:-
"The contribution of glycerol to glucose production was significantly increased in obese animals."
Nige.
Hi Nigel. I there is some kind of metabolic advantage, my guess is it is so small it can't actually be mesured. Why? Because you can't measure differences when your measurement device has an error of the same magnitude of what you pretend to measure. Please see article below and also see Attwater factors. You're an engineer, so you know what I'm talking about. Thanks for a great blog. Bookmarking!
http://www.canibaisereis.com/download/calorie-delusion-new-scientist.pdf
http://www.canibaisereis.com/2009/07/18/a-desilusao-das-calorias-new-scientist/
O Primitivo.
In practical terms, calories do count, as the vast majority of us aren't confined to a metabolic ward!
I'm just very picky (is that an Engineer's trait?) about things. Some people do go mad and pig-out on low/zero-carb foods thinking that "no carbs = no bodyfat gain". When the diet fails, they tell everyone how useless low-carb diets are. I believe that telling people "calories don't count" is doing low-carb/paleo diets a disservice.
I'm glad you're enjoying my ramblings.
Nige.
I think your theory is very thought-provoking!
There is another mechanism that can explain how AGP can be created during low carb dieting: glyceroneogenesis. It is a metabolic pathway that was discovered many years ago but for some reason remains obscure. It is explained a bit in this blog post: http://adipo-insights.blogspot.com/2009/09/is-fable-of-unfettered-fat-burning.html
Hi Anonymous.
Thanks for the link. Glyceroneogenesis is so obscure that it's not mentioned in my textbook on metabolic pathways! I've left a comment (awaiting moderation) inviting LynMarie over here.
Nige.
Counting calories? How dare you! ;)
In all seriousness, I like that you pointed out the insulin sensitivity component. I've pointed out a couple studies over on my site, one dealing with insulin sensitive obese women doing better on a high carbohydrate (60%c/40%f) diet and low insulin senstive women doing better on a "low carb" (40/40 even) diet. I've also posted links to individuals with hyperinsulinemia having no trouble losing fat when calories are controlled.
I like your theory, because I like exploring the details. I look forward to the acquisition of more data regarding insulin sensitivity and diet selection.
Best,
Skyler
Hi Skyler.
Thanks for the feedback. I need to read your blog now! I remember your "Low-carb Taliban" blog post and all the kerfuffle that caused. I "preached" Atkins with religious fervour from 1997 to 2003. Then I discovered PubMed.
Nige.
@Nige
Keep up the good work and don't be scared of slaying sacred cows and criticizing low-carb/high-fat. If you prove Gary Taubes & Feinman and Fine wrong, you have advanced our knowledge and done us all a huge favor.
One thought I had that stems from my reading of Taleb (also a Paleo-er BTW) is that we should embrace the concept of non-Platonicity.
See here:
http://www.fooledbyrandomness.com/glossary.pdf
Namely, sometime a calorie is a calorie and sometimes a calorie isn't a calorie. Make sense?
I think you and I agreed on this on Richard's blog.
Patrik.
Without that Glossary, I would have thought that Platonicity was where Platoni lived! I think that we have reached a consensus. In some ways, a calorie is a calorie and in some (other) ways, it isn't.
Nige.
Hi Nige,
Just thought I'd remind you that Gary Taubes himself has stated on several occasions that one of the problems with nutritional science is that the major players rarely question each other. He says that when a physicist presents a new theory/finding at a conference, he or she expects to be put through the ringer, but not scientists studying nutrition (as long as they tow the party line that is). Real science is about being vigilant to discuss all reasonable alternative hypotheses, and that's what you've done here.
Hi LynMarie.
I'm slightly bemused that I, a retired Electronic Engineer, have come up with a theory that contradicts some big names in the field of Diet & Nutrition.
I Emailed Taubes on 31st Dec 2009 but haven't received a reply yet. I Emailed Eades on 14th Jan 2010.
I'm still waiting for the loud "Bang". So far, the response has been like a damp squib!
Nige.
Update: I've just received a reply from Gary Taubes. He's got a lot on his plate at the moment so he can't give me a detailed reply just yet.
Wow Nige, that's great!
Here's a question worth discussing: Do you think a person can be truly obese on a LCHF diet? I believe people can become or remain chubby, plump, or whatever term you want to use for it, but not truly obese. Any thought?
Wow Nige, that's great!
Here's a question worth discussing: Do you think a person can be truly obese on a LCHF diet? I believe people can become or remain chubby, plump, or whatever term you want to use for it, but not truly obese. Any thought?
LynMarie Daye said...
"Wow Nige, that's great!
Here's a question worth discussing: Do you think a person can be truly obese on a LCHF diet? I believe people can become or remain chubby, plump, or whatever term you want to use for it, but not truly obese. Any thought?"
Gary told me that I need to read his book. This may take me some time. It's a shame that GCBC is not available in electronic form as I prefer to read stuff on a screen rather than on paper.
Regarding your question: I honestly don't know. Many (but not all) people's appetites are suppressed by serum ketones and cholecystokinin, so I would guess that it's harder to pig-out on fatty meats/fish/eggs/nuts/seeds than on carbs, but not impossible. Bear in mind that obesity is by definition BMI > 30. My BMI > 30 even though I don't have a big belly. Life's not fair!
Nige.
P.S. What do you think of my piece on enzymes?
GCBC is available in electronic form!
Nigel,
I'd like to throw a new idea into the mix. About a year ago I began learning about gut microbes. I found out that they generate heat as they multiply; about 5 kilo calories per gram (dry weight) of dead microbes in the feces.
The digestive tract harbors about two kilograms of gut micro-biota. As digesting food moves through the digestive tract, microbes if various sorts participate in the digestive process both deriving nourishment from the food and providing important nutrients for the body as a byproduct of multiplication. In the stomach, aerobic bacteria utilize oxygen swallowed with food. In overfeeding studies subjects frequently report feelings of being overheated shortly after ingesting excessive calories. I hypothesize that heat generated by aerobic bacteria in the stomach may be responsible for the effect. To my knowledge, no one has designed an experiment to test this hypothesis. Scientists assume that the metabolism itself revs up somehow in response to overfeeding.
As far as total heat generated by but microbes is concerned, I calculate that a 160 pound man would produce lose about 250 calories to gut microbes each day if he were consuming sufficient protein, fat, and minerals to sustain efficient gut microbe multiplication activity. A diet poor in supportive nutrition would curtail gut microbe activity resulting in more efficient energy absorption into the bloodstream. That is, a higher proportion of the energy consumed would be available for metabolic needs and fat storage.
In my own experience, if I consume extra calories, I just have more bowel movements and don't gain any weight unless the extra calories are carbohydrate.
Before I new about gut microbes, I wrote to Anthony Colpo about calorie excretion. He wasn't at all receptive to my argument. Of course, I couldn't explain it fully at the time using the gut microbe model. But still, he could have been a little more open minded.
For more on gut microbes, visit Gary Tivendale's collection of documents at: http://www.scribd.com/people/documents/3737769-gary-tivendale?page=3&popular=1
Hi David.
I hadn't considered gut bacteria. There are two issues that I can think of.
1) Heat generated. As gut bacteria are inside our body, any heat generated from the consumption of proteins, carbohydrates & fats contributes to total body heat, thus requiring the body to generate less heat of its own from amino acids, glucose & fatty acids to maintain a given temperature. I would therefore expect the net effect to be zero.
2) Kcals out as combustible gas. According to What is the average amount a person fart a day?, the average person farts 12-18 times and produces about 45 ml of methane a day. As 1g of methane is likely to generate ~9kcals of energy and 22.4 litres (1 mole) of methane weighs 16g, (mean energy lost due to flatulence)/day = 0.29kcal/day. I knew that my A-level Chemistry would be useful one day! Does my answer look plausible?
Nige.
You got that right about heat generated by gut bacteria contributing to temperature regulation. But energy expended in the digestive tract is not the same as energy expended by the body itself for several reasons. First, when gut bacteria release heat energy there is no metabolic cost to the body itself in terms of using up tissue stores of nutrients. Second, if food quality is varied in ways that enhance or curtail gut microbe activity (assuming constant caloric intake) there will be corresponding variations in the proportionate amount of energy absorbed into the bloodstream. In other words, it's possible to keep caloric intake constant or even increase it, improve the nutrient profile in a way that increases bacterial multiplication, and end up losing weight because fewer calories get absorbed into the bloodstream.
One could argue that with more heat being generated in the gut, the body would downregulate heat generating metabolic processes to compensate. And I would have to ask what processes? The scientists I've discussed this with are vague. They just say the metabolism must be speeding up because they can account for all the calories expended using metabolic chamber measurements. What's really needed is to determine how much variation in fecal bacteria is possible with variations in caloric input or variations in food quality keeping caloric intake constant.
I hope I've explained this adequately. Thus far, it's been really hard for most people I've discussed this with to wrap their minds around the idea that gut microbes are capable of producing considerable heat. People on both sides of the metabolic advantage divide tend to reject the idea without it having been tested.
Hi David.
Hmmm, this is a tricky one! I know that the faeces of herbivores contain a lot of energy, as dried dung can be burned as fuel, but I don't know how much energy there is in the faeces of carnivores.
I don't know how things balance out re: Gut bacteria consuming nutrients & generating heat from them vs Our bodies consuming nutrients & generating heat from them. If gut bacteria "steal" nutrients from our bodies, is there a net gain/loss of heat? That's the $64,000 question and I don't have the answer.
Colpo has cited 26 metabolic ward studies in They're all MAD! which support the theory that "a calorie is a calorie" w.r.t. weight gain/loss. The comments on here support it. However, everybody is different! I have no problem with people who do experience a metabolic advantage.
Nige.
Hi Nigee,
I am hopelessly right brained due to a left brain trauma, and have absolutely no training in science, so my opinion is not useful, only being able to share my own experience. I follow many of the same blogs you do and enjoy your blog.
One of the things I took away from my slog through Taubes' book is that a broken metabolism has a big effect on weight control and obesity. He tends to blame carbohydrates and in some ways his ideas remind me of Art's thinking on preserving health via the AID he esposes, although I eat a bit like Peter at Hyperlipid as I do not tolerate grains or starches. My health and health markers have greatly improved since moving to a LC, low fructose way of eating.
Sorry, I got away from the point of writing. Your theory and the comments over on Dr. A's blog reminded me of a post that Jenny put up back in June of 2009 -- "Metabolic Advantage of Ketogenic Diets Debunked? An Intriguing Study You Will Want to Read".
In the post Jenny references an article in Scientific American featuring Rudolf Leibel -- http://www.scientificamerican.com/article.cfm?id=interview-with-rudolph-l.
Leibel argues very convincingly that his studies show that we have a body weight set-point, which is one of the reasons that so many people stall on any kind of a diet. If you have not already read the article, I think you might enjoy it.
Hi Nick.
It's a bit too early in the morning for me and I have company, but I'll get back to you a.s.a.p!
Nige.
Hi again Nick.
I found Jenny's post at Good Science: Dr. Leibel Explains Metabolic Slowdown with Weight Loss and read the Scientific American Interview with Dr Liebel. Fascinating stuff! So should people now say "I'm not fat, I'm hypothalamically-challenged"? Thanks for your comment.
Nige.
Nigel: "In terms of health, wellbeing etc, a calorie isn't a calorie. I'm just arguing that a calorie is a calorie when it comes to weight loss/gain."
I'm not sure I get your meaning here. Could you expand a bit please.
Thanks,
Patrick
Valtor.
I don't understand your confusion. As it's gone 1:30am and I have a hospital appointment in the morning, I'll have to pass on a more detailed explanation at the moment.
Nige.
Ok here is what I think I understand.
You are saying that a calorie will always have the same effect on weight and then that regarding health and well being the type of calorie is important too?
But our healthfulness and well being state often affects the amount of food we intake and our predisposition toward exercise.
So then wouldn't the type of calorie have a very indirect effect, but an effect none the less, on weight ?
Patrick
Patrick.
The food that you eat affects you psychologically and physiologically, so eating the diet that suits you can increase kcals burned by thermogenesis and Spontaneous Physical Activity giving an apparent Metabolic Advantage.
As you can't increase kcals burned on the RHS of the Energy Balance equation ad-infinitum, eating too much will still cause weight gain, even on a low-carb diet. Hopefully you won't over-eat, but there are many reasons for eating apart from hunger. Read Dr. A's blog as she has a good understanding of reasons for over-eating.
Finally, the diet that suits you may not suit someone else. Insulin-sensitivity & activity have a big effect on what is someone's optimum diet.
Nige.
Nigel, am I getting this wrong or are you suggesting that dietary fat contains enough glycerol to make us fat?
But don't you see, you are not opposing the carbohydrate hypothesis when you suggest that it's the glycerol that makes us fat: Glycerol is a carbohydrate. You merely suggest an alternative source of carbs, i.e. the glycerol backbone of triglycerides instead of refined sugar for example.
If that's what you mean, then I see no reason to oppose your theory. All that needs to be done now is to figure out exactly how much fat we should eat to reach that obesogenic glycerol threshold.
On the other hand, there's the insulin factor. It regulates lipolysis and glycolysis. Insulin can't be dismissed no matter the theory. It must always be accounted for because its functions on fat and glucose metabolism can't be avoided.
Here's a rough idea of the importance of insulin in fat metabolism.
In order to increase fat accumulation, there must be the materials and the workers. The materials is the fatty acids and glycerol, and the workers is the enzymes and the hormones, and the cells themselves. If the material is missing, fat can't accumulate. If the workers are missing or dysfunctional, fat can't accumulate either. Insulin is one such worker and a critical one to boot. It's even more than just a simple worker, it's like the maestro conducting the orchestra.
Anyway, your theory is fine.
Martin Levac
Martin Levac said...
"Nigel, am I getting this wrong..." Yes, I'm afraid you are.
"are you suggesting that dietary fat contains enough glycerol to make us fat?" No. I'm saying that dietary fat contains enough fatty acids to make us fat, as adipocytes can make as much G-3-P as they need whatever serum insulin level is, as long as it's not zero.
"On the other hand, there's the insulin factor. It regulates lipolysis and glycolysis." Yes and no. High serum insulin inhibits HSL so it does inhibit lipolysis. low-to-normal serum insulin allows adrenaline & noradrenaline to control HSL (if the body needs more FFAs to fuel exercise, the body gets more FFAs). Zero insulin messes-up everything (including LPL). Luckily, this only applies to <0.1% of the population (undiagnosed/untreated T1DM).
"Insulin is one such worker and a critical one to boot. It's even more than just a simple worker, it's like the maestro conducting the orchestra." If it's missing, everything goes completely haywire. If it's present at low-to-normal levels, everything works normally. If it's too high, fat-burning stops. However, there's much, much more than just insulin controlling things. I'm going to add a link to LynMarie Daye's site at the end of "I have a theory", as Glyceroneogenesis is another mechanism that allows dietary fat storage as body fat due to the up-regulation of PEPCK on low-carb diets.
Cheers, Nige.
Nigel, every time somebody says we can grow fat by overeating fat in the absence of carbs, I invariably ask: Where's the evidence?
We're not talking about normal fat storage for in-between meals, that's never been contested. We're talking about growing fat, gaining weight, excess fat accumulation, obesity, that kind of thing. So where's the evidence?
Martin Levac said...
"Nigel, every time somebody says we can grow fat by overeating fat in the absence of carbs, I invariably ask: Where's the evidence?" There's the problem. Apart from the anecdotal evidence of people who are/were on virtually zero carb diets and managed to gain weight/stop losing weight, I don't think that any large, randomized, double-blinded, placebo-controlled, trial (with/without crossover) has/will ever be done.
When push comes to shove, we're both on the same side. We're both singing the praises of low-carbohydrate diets for the treatment of obesity. Where we differ is my nerdy insistence that calories still count and that the ad-lib consumption of fatty roast meats can result in failure to reach goal weight/body composition. As bodyweight reduces, (kcals out) on the RHS of the Energy Balance Equation reduce, so (kcals in) on the LHS must reduce in proportion to maintain weight/bodyfat loss.
Cheers, Nige.
Hi Nige,
I like the new look.
I hope you and your mom are OK.
I have read recently something that is similar to your idea on glycerol on Weightology. It's a more complex issue than no carbs=no insulin=no fat deposition. Even Peter says it's not about fat deposition it's about lipolysis and that insulin has an inhibitory effect. I'm really interested in the debate but it doesn't seem to be very loud/big/visible.
I haven't lost any weight all year despite low calorie low carb (except during a short period at home in the summer 2 kgs in 3 weeks, which I promptly put back on when I came back) so I stopped trying. I'm eating potatoes now.
Hi lightcan.
I thought that it was about time for a re-vamp as I got fed up with a narrow strip of text down the middle of the screen. I think that everybody now has computer displays at least 1024 pixels wide.
Mum's getting worse and I'm kinda miserable about it but there's nothing I can do to help mum any more.
Regarding insulin: Its inhibitory effects are important, but having low serum insulin when sedentary doesn't cause unfettered lipolysis as that would flood your blood with unused Fatty Acids (FAs a.k.a. NEFAs or FFAs) which would be harmful. Lipolysis is also controlled by adrenaline & noradrenaline so when you exercise, more FAs are generated to provide fuel for your muscles.
Eating fat instead of carbohydrate just shifts the fuel usage of your body away from glucose towards FAs (and vice-versa) but it doesn't make you burn more energy. When you eat, you store more stuff than you burn and in-between meals, you burn more stuff than you store. It's the overall balance between storing & burning that determines whether you gain or lose weight on average as per the green/blue graph in Insulin…an Undeserved Bad Reputation.
Did you get treatment for your very low serum FT3? IIRC, it was having adverse effects on your weight loss efforts (due to reducing your metabolic rate making your body burn less) and your serum cholesterol levels (due to reduced cholesterol clearance from your blood). From what you've just written, I fear not.
Best wishes, Nige.
It's not hard to guess that I didn't get the help I wanted from the endocrinologist. She doesn't want to prescribe T3 (I knew it a year ago) she called me on the phone after she got some of the blood results back to say that I should take Lipitor, but at that time my free T3 and other results were still pending. She hasn't called since, and although I called and left a message twice, nothing happened for the last two months. Totally ignoring the results, not very intelligent and open, following CW, what they call evidence-based medicine, conveniently focusing on an obvious symptom for which I can get drugs from any GP instead of looking at my hormones, that is doing her job. She was also intimidating and autocratic and referred to a previous endocrinologist's opinion instead of thinking on her own.
I suffer from chronic gum disease, how can I hope to control my condition with low T3?
Regarding my own approach, do you think that increasing calories overall to 1800, let's say, is going to make a difference? Is the body going to readjust? There are studies on calorie restriction and t3 but it's not clear how low does it go, because they use averages in that group. (so what is the magnitude of the response to diet, how low it is still acceptable)
I'm taking a bunch of supps recommended for thyroid, I don't feel it's worth it. I'm a bit confused and lost at this stage.
I have to work on my Ph.D. and this makes my anxious, worried and stressed so it's not the time to diet, but I should be careful because I might binge.
Thanks for your help.
Yes, that's what I was referring to, those posts. However, there in that chart he doesn't discuss the glycogen stores. Lipolysis during fasting. I'm nowhere near understanding all the details but is the glycogen from the liver not the first source of energy? Or they both happen at the same time depending on relative concentration?
He underlines that it is context dependent.
I had a feeling that would be your reply. Is there any chance of getting referred to a different endo'?
If you eat more, you will gain some weight. Whether or not that will raise your FT3, I really don't know.
Taking supps to help your thyroid is probably futile as you have a T4 to T3 conversion problem rather than low T4.
Being stressed-out is worse for your health than having high cholesterol. I know a lady who has a total chol of 10.4mmol/L due to Familial Hypercholesterolaemia and she's 68 years old with no sign of heart trouble. Her doc wants her on statins but they give her bad muscle pains.
Have you tried Vit C & Co-Q 10 for your gums?
Liver glycogen is used to produce blood glucose which fuels red blood cells, the brain & any other tissues that need glucose.
Muscle glycogen is used only by muscles and the amount used depends on exercise intensity & fitness. At low exercise intensity, muscles use almost 100% fatty acids for energy. As exercise intensity increases, the % of energy derived from glycogen increases until the lactate threshold is reached when 100% of energy is obtained from glycogen aerobically. Above that level of intensity, 100% of energy is obtained from glycogen, some anaerobically. Increasing fitness shifts fuel usage towards fatty acids.
I wasn't talking about muscle glycogen because that its use is localised and dependent on anaerobic exercise. In between meals, when your glucose levels go down, you start to use your liver glycogen stores. Is this not one of the reasons for not snacking between meals? If your liver stores are full and you keep eating you are bound to deposit the excess as triglycerides. (Sorry if I sound silly, but I only dare to ask you questions like this)
I am taking Coq10 100 mg and vit C for a long time, no change. Also vit K2, D, Mg. I've been to the hygienist in September and he called me back after 3 months, the same deep pockets as last year, even an infection with bleeding about 2 weeks ago. He doesn't know. They don't think holistically either, but he seemed well read and up to date. After reading Paul Jaminet's blog I started adding more starches, I also take NAC for glutathione and doubled my C intake.
If you eat too much carbohydrate (particularly fructose-based stuff which is mostly absorbed by the liver) when your liver glycogen stores are full, the liver turns the excess into TGs causing high serum TGs and in the long-term NAFLD.
I can't think of anything else to help your gums that you're not already taking.
Taubes is just too stubborn on this, although I think for his 'Carbohydrate Hypothesis' which explains obesity in the population with too much carbohydrate consumption of some people, it does not matter. What matters is: Even when the body can store fat from food in the absence of carbs, how relevant is this quantitatively? Can you overeat on fat as much as on carbs? I think when you overfeed with fat, nausea and diarrhea set in earlier than when overfeeding with carbs. But I might be wrong, still this is crucial and needs to be tested.
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