The effect of extreme carbo-loading

Carbo-loaders

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59 Comments

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  1. murray
    The case of Tim Noakes is instructive.

    An acquaintance was a world-class mountain biker for his age group (around 40). He rode hard every day for hours at remarkably high heart rates and had done so for years. He carb-loaded, as typical. He did not gain weight, but he had a medical procedure and, after examining him, the physicians informed him he had one of the more advanced cases of atherosclerosis they had seen. He was in disbelief, as he had always exercised hard and been lean his entire life. He now reports that he has found out this is not uncommon among high-intensity endurance athletes. He was unsure whether to attribute it to the exercise intensity, the carb-loading or the combination of both.

    Read more →
  2. Peggy Holloway
    All of the people we cycle with on multi-day rides carbo-load like crazy. They really think that because they are biking 60+ miles a day they need lots of calories and that carbs are there best bet. They snack on cookies and gatorade all day and eat pancakes, muffins, etc. for breakfast and pasta or baked potatoes for dinner. My partner and I have to work hard to find low-carb, high-fat options for the main meals. Of course, we don't eat anything at the rest stops. I overheard a woman who was rinsing out her water bottle comment that the water tasted like Gatorade. I remarked that I didn't think I'd ever tasted Gatorade. She looked at me incredulously and asked "What do you drink." My answer "water." She continued to look dazed and confused.
    It makes me dazed and confused to see how many of our fellow bikers are considerably overweight.
    Reply: #3
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All Comments

  1. Peggy Holloway
    All of the people we cycle with on multi-day rides carbo-load like crazy. They really think that because they are biking 60+ miles a day they need lots of calories and that carbs are there best bet. They snack on cookies and gatorade all day and eat pancakes, muffins, etc. for breakfast and pasta or baked potatoes for dinner. My partner and I have to work hard to find low-carb, high-fat options for the main meals. Of course, we don't eat anything at the rest stops. I overheard a woman who was rinsing out her water bottle comment that the water tasted like Gatorade. I remarked that I didn't think I'd ever tasted Gatorade. She looked at me incredulously and asked "What do you drink." My answer "water." She continued to look dazed and confused.
    It makes me dazed and confused to see how many of our fellow bikers are considerably overweight.
    Reply: #3
  2. Vincent
    That's not carb loading gone wrong, that's just excess calorie consumption.

    You could easily change the headline and transcript into this:

    Low-carb gone wrong

    "My running's is so-so, but i'm one of the nation's top five low-carbers".

    Reply: #4
  3. FrankG
    I was going to mention that I have a friend at work, who runs just about every day, trains for and runs marathons several times a year. He also seems to have a regular supply of carb-laden snacks and meals. Without meaning any unkindness, he is no more lean in build than I am. I eat freely of LCHF and walk almost every day :-)
  4. So you're saying he just gained weight because he gained weight?

    http://www.dietdoctor.com/why-calorie-counters-are-confused

    Reply: #6
  5. murray
    The case of Tim Noakes is instructive.

    An acquaintance was a world-class mountain biker for his age group (around 40). He rode hard every day for hours at remarkably high heart rates and had done so for years. He carb-loaded, as typical. He did not gain weight, but he had a medical procedure and, after examining him, the physicians informed him he had one of the more advanced cases of atherosclerosis they had seen. He was in disbelief, as he had always exercised hard and been lean his entire life. He now reports that he has found out this is not uncommon among high-intensity endurance athletes. He was unsure whether to attribute it to the exercise intensity, the carb-loading or the combination of both.

  6. Vincent
    No i'm not saying he had gained weight because he gained weight. If you start with the premise of conservation of energy then when you ingest 3000 calories, all 3000 calories has to be accounted for since energy can't be created nor destroyed. In my view, when there is more energy from food ingested then is leaving the body in a x period of time the "excess calories" are going to be stored in the body as a form of chemical energy.

    What does not make sense to me, is that some people appear to say that insuline causes the body to convert energy ingested through food into chemical energy stored in the body as adipose tissue. This would mean that if i consume 2000 calories while over a x period of time 3000 calories worth of energy are leaving my body my adipose tissue would still increase in size? And when insuline levels are low the amount of energy ingested does not matter because somehow all of that energy is leaving my body? This is a line of thought without empirical i'm not keen on accepting.

    Replies: #7, #8, #23
  7. FrankG
    Your problem is in comparing the human metabolism with the energy consumption of a steam engine.

    J. Stanton over at GNOLLS.ORG has (in my view) an excellent 4 Part series discussing your dilemma, starting with Part 1...

    There Is No Such Thing As A “Calorie” (To Your Body)
    http://www.gnolls.org/3374/there-is-no-such-thing-as-a-calorie-to-you...

    “The problem with explaining complicated systems to the layman is this: it’s easy to simplify a concept to the point that it’s no longer true.”

    If you need further empirical evidence that energy leaves your body when insulin levels are low or absent, you might discuss it with any Type 1 Diabetic :-)

    Reply: #10
  8. Christopher
    Here we go again, I give up.
    Reply: #9
  9. markus aurelius
    If you only did, Christopher, if you only did...
    Reply: #31
  10. Vincent
    Yes, I know energy is lost through urination in the form of glucose by diabetics. And I agree with your quote about the problem with oversimplification, that's also why I have a difficulty with the name of this post and for every subjects regarding human metabolism for that matter, heck for almost everything in life :) But my main point is that all the energy ingested must in some way be accounted for since energy can't be lost nor created? But if someone claims that he or she is consuming 4000 calories worth of energy and loses weight, those 4000 still has to go somewhere regardless if the subject is a steam engine or a human being. It all depends on the level of measurement and accuracy

    About the role of insuline, this is a nice article to read http://weightology.net/weightologyweekly/?page_id=319.

    Among other things he discusses the point that muscles cells don't need insuline to take up glucose from the blood. In the article you provided, the author states

    "because high blood glucose is toxic, our muscles and liver are not already full of glycogen, and insulin will quickly force it into one of them, whereupon it will be stored as glycogen and used as needed."

    So, the point being discussed in the a for mentioned article makes it seem that the above quote is a oversimplification?

    Anyway, I'm just baffled by the fact that people constantly mistake correlation for causation and make claims that are totally unjustified or worse just flat out false, or at least an oversimplification:)

  11. FrankG
    As you say Christopher "here we go again"

    Sorry Vincent but I know a great deal about insulin being a Type 2 Diabetic and injecting myself with it for many years, and formerly a Registered Nurse.

    I'm not about to read an "article" written by someone who describes themselves using a joke/made-up name like "weightologist".

    He may be right that insulin has been done a great disservice and has been badly beaten up in recent years but NOT by people who support LCHF eating. It is only those who are negative to this approach who distort what is said in order to fabricate straw-men such that insulin seems to be the devil incarnate, second only in danger to that wicked substance carbohydrate!

    No I of course realise that both of these are necessary for human health although arguably there is no essential carbohydrate that must be ingested NOT that a low carb diet equals a NO carb diet.

    You also seem to be rapidly slipping into the other favourite naysayer's straw-men which suggests that those who support LCHF eating claim you can force feed yourself on unlimited quantities of anything so long as it is not the wicked carbohydrates, and never gain an ounce of excess fat mass.

    Eating freely simply means you do not necessarily have to weigh, measure, count or any such thing your food -- eat until satisfied. Neither consciously over or under-feed. To that end I personally find that LCHF eating enables me to rely on my own body to tell me when enough is enough. I have significantly less fat mass, and healthier and happier in every regard since realising the myths of the conventional wisdom which I had been following for several past decades.

    Sorry of that upsets your view of the world but that is tough. If you find discussion of LCHF so hard to digest, may I suggest you make you own life less stressful by reading blogs where you feel more comfortable.

    ---

    And please do explain exactly how insulin not being necessarily required for glucose uptake, translates to therefore high levels of insulin doesn't rapidly move glucose into cells..?

    Reply: #12
  12. Vincent
    Hmm so you wont read an article because of the name of the website? So you will read articles on a websites called "diet doctor" but not on a website called "weightology"? And what does a name anyhow means if the research is sound?

    "Sorry of that upsets your view of the world but that is tough. If you find discussion of LCHF so hard to digest, may I suggest you make you own life less stressful by reading blogs where you feel more comfortable."

    Maybe more people should do the opposite so that the can challenge there axioms and consider there believes could be false.

    And I don't refute any health benefits of LCHF nor that it helps to maintain a desirable weight for some people. But I'm critical to the people who make more general claims, to hold them sacred and so above critique. Regarding the subject of weight, BBC made a nice documentary. "Why are thin people not fat?" http://www.youtube.com/watch?v=SeeFrcvt3KA

    Yes you are right, insuline does speed up glucose uptake by the muscle cells. But if you have an article that is highly critical about oversimplification, the mention that insuline is not needed would be a fuller explanation.

    Replies: #13, #14, #15, #16
  13. FrankG
    Sure.. I am so naive and shallow as to base how I filter where to read on the interweb purely on the name of the web site :-P

    Or do you think that I should just blindly accept the word of everyone on the web without applying any filters or skepticism?

    Let's compare how each of these sites author's describe themselves:

    http://weightology.net/weightologyweekly/?page_id=2

    "Meet your personal weightologist
    James Krieger is the founder of Weightology, LLC. He has a Master’s degree in Nutrition from the University of Florida and a second Master’s degree in Exercise Science from Washington State University. He is the former research director for a corporate weight management program that treated over 400 people per year, with an average weight loss of 40 pounds in 3 months. His former weight loss clients include the founder of Sylvan Learning Centers and The Little Gym, the vice president of Costco..."

    So not only does he describe HIMSELF as a "weightologist" which strikes me as a fundamental misunderstanding which I see as not "weight" but excess fat mass and all the associated health issues. But the site is also representing an LLC which sounds to me like he has financial interests at stake.. what is he trying to sell me?-- not necessarily a bad thing but not something I am interested in (my choice where I read surely?) AND most importantly he has no qualifications related to health which is where I am particularly interested. He strikes me as more of a personal trainer than anything else and I'm not interested in that way of thinking thanks! I could get that for free by watching such trash as "The Biggest Loser"

    --

    Now for the The Diet Doctor"...
    http://www.dietdoctor.com/about

    "About Diet Doctor

    My name is Andreas Eenfeldt and I am a Swedish medical doctor specialized in family medicine. I want to find out how to get as healthy as possible using natural methods such as diet, exercise and perhaps a supplement (vitamin D) or two.

    The idea to eat less fat and less saturated fat was certainly a mistake. Inadvertently that advice may be the biggest reason behind the epidemics of obesity and diabetes. More and more people realize this. It’s time for a health revolution.

    This blog is a place to learn about this for free. Do you want real food, better health and weight loss without hunger?"

    An MD with actual clinical experience in the area of which I am interested. NOT trying to sell me anything.. in fact offering free advice AND -- from having read his blog -- I know that he not only writes about LCHF but he and his young family also apply this way of eating it daily.

    Please forgive me for choosing where I read; while still always applying my own critical thinking to what is said or written, NO MATTER who they are or what their qualifications.. claimed or otherwise.

    Reply: #17
  14. FrankG
    For many decades I DID accept that calories are all that matters so I have ALREADY challenged these axioms! You will need to come up with something new to convince m that my change of direction was wrong.

    I am well aware of the BBC documentary and have offered it myself in comments, on many occasions.

    Do you assume that folks here have not already discussed at length these basic ideas that you feel free to trot out yet again? Please read back over previous blog posts and comments.

    Does the fact that J. Stanton did not write a 600 page textbook on the subject make his statement incorrect? You agree that insulin facilitates the access of glucose to cells and more does it to a greater degree. That insulin is not necessarily required for any access is a separate issue surely? Are you saying that every time insulin is mentioned we need to trot out EVERYTHING about it? What is being oversimplified?

  15. Zepp
    Well, Vincent.. I did read the articel you linked to.. its the same missconception as usaly!

    Insulin is an absolutly nesecary hormone in our bodys, for a lot of purposes.. and he got it wrong.. its not carbs> insulin>obesety!

    Thats a pretty good explanation on how its works for healty persons!

    Its Hyperinsulinemia>obesety/diabetes thats the bad thing.. its a medical condition, caused by genetic predisposition and bad diet!

    And did you know, some amino acids get even a higher insulin respons then sugar, and thats nesecery, to get those in to cells!

    Its when one eat more carbs then ones body uses/can handle thats this condition apears.. and to that, more and more peopel have desktop jobs and a sedentary lifestyle.. then one need to lower carb intake!

    Even our kids living more sedentary lifes!

    And the rising consumption of carbs, sugar, sodas and other fast digesting carbs takes its toll!

    Nearly 1 in 4 U.S. Teens Has Diabetes or Prediabetes

    In less than a decade, the proportion of kids ages 12 to 19 with diabetes or prediabetes has jumped from 9% in 1999-2000 to 23% in 2007-2008.

    Read more: http://healthland.time.com/2012/05/21/nearly-1-in-4-u-s-teens-have-di...

    And in Sweden we are soon coming in parity of USA, as a new report is telling us!

    "More than one in six children in Sweden who are obese also have pre-diabetes."

    http://ki.se/ki/jsp/polopoly.jsp;jsessionid=aBYnJAh_wu-ewtEXX-?l=en&#...

    Soo, the problem is how hyperinsulinemia is developed.. its when insulin levels is chronicaly elevated and not in comparity of blood sugar levels!

    "Hyperinsulinemic diseases of civilization:

    more than just Syndrome X"

    "Abstract

    Compensatory hyperinsulinemia stemming from peripheral insulin resistance is a well-recognized metabolic disturbance that is at the root cause of diseases and maladies of Syndrome X (hypertension, type 2 diabetes, dyslipidemia, coronary artery disease, obesity, abnormal glucose tolerance). Abnormalities of fibrinolysis and hyperuricemia also appear to be members of the cluster of illnesses comprising Syndrome X. Insulin is a well-established growth-promoting hormone, and recent evidence indicates that hyperinsulinemia causes a shift in a number of endocrine pathways that may favor unregulated tissue growth leading to additional illnesses. Specifically, hyperinsulinemia elevates serum concentrations of free insulin-like growth factor-1 (IGF-1) and androgens, while simultaneously reducing insulin-like growth factor-binding protein 3 (IGFBP-3) and sex hormone-binding globulin (SHBG). Since IGFBP-3 is a ligand for the nuclear retinoid X receptor a, insulin-mediated reductions in IGFBP-3 may also influence transcription of anti-proliferative genes normally activated by the body’s endogenous retinoids. These endocrine shifts alter cellular proliferation and growth in a variety of tissues, the clinical course of which may promote acne, early menarche, certain epithelial cell carcinomas, increased stature, myopia, cutaneous papillomas (skin tags), acanthosis nigricans, polycystic ovary syndrome (PCOS) and male vertex balding. Consequently, these illnesses and conditions may, in part, have hyperinsulinemia at their root cause and therefore should be classified among the diseases of Syndrome X."

    http://www.direct-ms...insulinemia.pdf

    Insulin Resistance and Hyperinsulinemia Is hyperinsulinemia the cart or the horse?

    "Insulin resistance, recently recognized as a strong predictor of disease in adults, has become the leading element of the metabolic syndrome and renewed as a focus of research. The condition exists when insulin levels are higher than expected relative to the level of glucose. Thus, insulin resistance is by definition tethered to hyperinsulinemia. The rising prevalence of medical conditions where insulin resistance is common has energized research into the causes. Many causes and consequences have been identified, but the direct contributions of insulin itself in causing or sustaining insulin resistance have received little sustained attention. We examine situations where insulin itself appears to be a proximate and important quantitative contributor to insulin resistance. 1) Mice transfected with extra copies of the insulin gene produce basal and stimulated insulin levels that are two to four times elevated. The mice are of normal weight but show insulin resistance, hyperglycemia, and hypertriglyceridemia. 2) Somogyi described patients with unusually high doses of insulin and hyperglycemia. Episodes of hypoglycemia with release of glucose-raising hormones, postulated as the culprits in early studies, have largely been excluded by studies including continuous glucose monitoring. 3) Rats and humans treated with escalating doses of insulin show both hyperinsulinemia and insulin resistance. 4) The pulsatile administration of insulin (rather than continuous) results in reduced requirements for insulin. 5) Many patients with insulinoma who have elevated basal levels of insulin have reduced (but not absent) responsiveness to administered insulin. In summary, hyperinsulinemia is often both a result and a driver of insulin resistance."

    http://care.diabetes...ent_2/S262.full

    Hyperinsulinemia Drives Diet-Induced Obesity Independently of Brain Insulin Production
    Hyperinsulinemia is associated with obesity and pancreatic islet hyperplasia, but whether insulin causes these phenomena or is a compensatory response has remained unsettled for decades. We examined the role of insulin hypersecretion in diet-induced obesity by varying the pancreas-specific Ins1 gene dosage in mice lacking Ins2 gene expression in the pancreas, thymus, and brain. Age-dependent increases in fasting insulin and β cell mass were absent in Ins1+/−:Ins2−/− mice fed a high-fat diet when compared to Ins1+/+:Ins2−/− littermate controls. Remarkably, Ins1+/−:Ins2−/− mice were completely protected from diet-induced obesity. Genetic prevention of chronic hyperinsulinemia in this model reprogrammed white adipose tissue to express uncoupling protein 1 and increase energy expenditure. Normalization of adipocyte size and activation of energy expenditure genes in white adipose tissue was associated with reduced inflammation, reduced fatty acid spillover, and reduced hepatic steatosis. Thus, we provide genetic evidence that pathological circulating hyperinsulinemia drives diet-induced obesity and its complications."

    http://www.cell.com/...ract/S1550-4131(12)00453-6

    Banting Lecture 2011
    Hyperinsulinemia: Cause or Consequence?

    "In this conceptual model, insulin resistance is caused
    by hyperinsulinemia and is an appropriate adaptation to the increased need to store fat in adipose tissue without causing hypoglycemia. Thus, insulin resistance is an adaptive response that successfully maintains normal circulating levels of fat and glucose as long as the b-cell is able to maintain sufficiently elevated insulin levels (57). Perhaps the time has come to expand our research focus to carefully investigate the environmental changes that have accompanied the epidemic of obesity and diabetes"

    http://diabetes.diab...61/1/4.full.pdf

  16. FrankG
    I am still open to all ideas and actively seek out contrary views IF they appear to be trustworthy.

    But I have learned that not all web site are trustworthy or even readable:

    Some are just spite-filled examples of vitriol and hate; so even if there are worthwhile facts available there, I have no desire to wade knee-deep through $h1t to find it.

    Another by a PhD who passes himself off as an Obesity Researcher, has repeatedly shown himself to be unreliable by making assertions based on primary source material which are not born out by those same primary sources... I can only assume he trusts his loyal readers not to follow up by reading his linked sources.

    Having tried to debate these points on his blog and either being ignored or rebuffed, why on earth would I choose to continue reading there?

    Reply: #19
  17. Vincent
    No, one should never blindly accept what's being said on the web. And i'm not trying to dictate what one should be reading or listen to. I'm my view, for discussions to be meaningful, one has to adopt an attitude towards his own convictions that although they are being perceived as true, they could in primo be proven false. This entails that one should have an open mind to arguments that are contrary to ones own believes and accept or reject those arguments after careful deliberation . If people start holding there own believes as infallible discussion becomes pointless. So I don't care if someone has a MD, PHD or GOD as a title all that matters to me are the strength of there arguments. If you haven't looked at the evidence and have held it against your own believes and weight both sides then being a "expert" in a certain area shouldn't mean diddly :)

    (I know, the problem is that i'm making a relativistic claim while holding an absolute position. What a conundrum)

    Reply: #18
  18. FrankG
    So every time someone offers a link to "weightology" (and you are far from the first) or ANY other site, my only recourse is to read it or else I cannot have an opinion on it, or even an impression of it?

    Dang.. guess I need to give up my day job and spend all my time reading the interwebs.

    Here is how it works for me: on the first encounter I generally give people the benefit of the doubt. I work from the basis that we all start out as good and decent members of society.

    If, however fallibly, I personally judge a site or writer to be untrustworthy then they lose my respect and it is up to them to regain it.

    I choose where I read on the internet. If you have NEW evidence that I am wrong about how LCHF works then please feel free to present the primary sources -- NOT someone else's interpretations. Trotting out the same old same old CICO/ELMM nonsense will get you nowhere with me.

    If you think people who advocate LCHF are making false claims then please feel free to provide a quote in context, so that we may discuss it reasonably; rather than making sweeping assertions.

    Reply: #21
  19. Vincent
    Yes you are right. The problem is, that people who try to prove something, are only looking at evidence that would prove there claim. So everything that refutes there hypothesis is being rejected, consciously or unconsciously. This means that a lot of research is manipulated in a way to suit there view. But apart from this, research has to be interpreted and there lies a major problem. And it depends a lot on the level of knowledge to even interpret seemingly objective data. For example inferential statistics is being presented as an objective conclusion. So if data shows that X en Y are congruent, this only shows a correlation, not a causation. But a lot of articles blandly say: "Research show that X causes Y". This is subject matter is just something that intrigues me a lot. :)
  20. murray
    There are several problems with the caloric input/output approach. The most significant flaw is that some calories are not just calories--they are metabolic signals or metabolic activators that differ qualitatively from other source of calories. If there is a pattern of high carbohydrate diet, then glucagon responsiveness in pancreas A cells is down-regulated (making the high-carber prone to low blood sugar and the need to snack every 3-4 hours) and the ability to produce ketones is down-regulated, among many other factors. Indeed, research published last month found that the complexes in the mitochondria adapt by reorganizing and forming supercomplexes to optimize fuel burning capacity depending on the relative proportion of fat and sugar it receives to oxidize. So a high-fat diet will make the mitochondria more efficient at burning fat, a high-carb diet makes the mitochondria less efficient for burning fat. As shedding stored fat means burning fat in mitochondria, the capacity to burn fat is important. Phinney and Volek found that with cyclists who ketoadapted, their fat-burning capacity more than doubled, to exceed 900 kcal per hour. For someone who is not keto-adapted with full capacity to burn fat, they will need carbohydrates to keep up the energy level, which means snacking on carbs, which raises insulin, which diminishes further the capacity to burn fat (while insulin has been raised).

    Other research has shown that cells low in energy send signals to the liver that result in more bile being produced to ingest fat from the gut. This implies that otherwise not all fat in the gut is taken up, as bile is required. To test this, I ate thousands of calories daily for three weeks (80+% fat and low carb) with no weight gain. Others report the same, including Dave Asprey who eats about 4500 calories per day with minimal exercise. There is no mystery--fat simply passes through the gut into the feces.

    Then one has to consider how many calories are consumed by the gut flora and how nutrients are transformed. In a healthy flora, leafy greens, for example, are to a large extent transformed into butyrate, a short-chain saturated fat. Lactobasillic bacteria convert sugars into lactate. Propionic bacteria convert lactate into propionic acid, a saturated fat triggers the lowering of blood pressure. Etc., etc. How many calories do these processes consume and how much of this goes on depending on the state of the flora (which is affected by the nature of calories consumed over a length of time) and whether the flora gets the right types of calories to increase caloric consumption by the flora.

    I could go on (especially concerning affects on subjective appetite), but the general point is that the body is not calorie neutral, blind in its response to the nature of the calorie.

    Reply: #42
  21. Vincent
    The problem with the internet is that there is just to much being said and to little time to digest is all. If of course you still want time to pursue the things in live that matter to you :) I agree that when someone on first glance looks likes he is full of bs then of course you can filter that out. What I would like to stipulate is that most people lack the knowledge when reading raw date to interpret that in a meaningful way, and i'm not a exception. I find statistics very hard to comprehend. And that comes back to what you said earlier, for most people things have to be simplified to such a degree that things become very distorted. And so many arguments in my experience with people go like this: Q "How do you know what you say is true?" A "Because everybody says it is" Q "Yes but how do you know they are right" A"Because they just are, that's just common sense".
    Reply: #22
  22. FrankG
    You need to understand that I grew up in the UK during an era when black & white TV was just starting. When the BBC brought out an expert (in a white coat or otherwise) they really were a knowledgeable and trustworthy source.

    Having read Gary Taubes' Good Calories Bad Calories (which too many misleadingly paraphrase as just saying carbs->Insulin->obesity) one of the biggest lessons for me is that: we can no longer trust just the opinion of "experts", no matter their qualifications. Objective evidence is what convinces me these days.

    Now I agree that there is a certain amount of human nature that falls into traps and I accept that after a while of someone showing me that they are trustworthy, I am less skeptical of what they assert but if it doesn't make sense or ring true, then I will still of course question it... no matter the source.

    After diagnosis with Type 2 Diabetes I had to learn how to read nutritional labels and in the same way I see it is a survival skill and have learned (still always learning) how to read primary source research material. By which I mean more than just even the author's own conclusion but their objective findings. Did they ask all the pertinent (and impertinent) questions? Are there other possible interpretations of the data that they either ignored or failed to consider?

    I don't subscribe to the thinking that one needs to have a science degree to be a scientist, or to apply scientific reasoning. In fact it seems clear to me that some leave academia with minds already closed by what their mentor "knows" to be true.

    One of my all time favourite quotes from Jacob Bronowski and one which I repeat often to my son at University is, "It is important that students bring a certain ragamuffin, barefoot irreverence to their studies; they are not here to worship what is known, but to question it."

  23. What does not make sense to me, is that some people appear to say that insuline causes the body to convert energy ingested through food into chemical energy stored in the body as adipose tissue. This would mean that if i consume 2000 calories while over a x period of time 3000 calories worth of energy are leaving my body my adipose tissue would still increase in size?

    Of course not. That's just silly.

    If your insulin levels are abnormally high your body will tend to store fat though, meaning that it's going to be an uphill battle to get lean. Lower those insulin levels and if you're overweight you'll WANT to eat less calories than you burn.

  24. Ondrej
    Reply: #26
  25. Ray
    I think Anthony should give up his blog. It isn't becoming, and he does a much better job when writing a book. In the context of a book, he drops all macho pretext and sticks to documented facts. I really dislike his online persona. It almost makes me wish I didn't buy his books (but they are pretty good).
  26. Zepp
    Hyperinsulinemia make your body store fat, inhibiting fat oxidation and lipolysis.. then you need to eat more calories to have enough energy for your bodily functions!

    "In this conceptual model, insulin resistance is caused
    by hyperinsulinemia and is an appropriate adaptation to the increased need to store fat in adipose tissue without causing hypoglycemia. Thus, insulin resistance is an adaptive response that successfully maintains normal circulating levels of fat and glucose as long as the b-cell is able to maintain sufficiently elevated insulin levels (57). Perhaps the time has come to expand our research focus to carefully investigate the environmental changes that have accompanied the epidemic of obesity and diabetes"

    http://diabetes.diab...61/1/4.full.pdf

    And did you know this CICO things is just a tautology, its obvius, means nothing but the obvius.. and are sertanly no advice at all for those how is obese!

    Do you think they dont know that they are eating more then they burns?

  27. grinch
    Frank,

    "Objective evidence is what convinces me these days."

    Like what? Taubes would have us believe none of this has even been tested yet.

    ----

    Doc,

    "If your insulin levels are abnormally high your body will tend to store fat though, meaning that it's going to be an uphill battle to get lean. Lower those insulin levels and if you're overweight you'll WANT to eat less calories than you burn."

    How do you explain someone who is overweight even with low or normal insulin levels? How do they eat less or lose weight if calorie intake doesn't play a causal role in weight management?

    Reply: #30
  28. grinch
    So you make fun of people who carb-load, but what about the thousands of runners who perform at their best because of it? I don't think some population of unfit runners who inappropriately carb load running at low mileage or intensity would represent those who do it appropriately. Don't you think?
  29. FrankG
    None of what?

    Does saying that "If your insulin levels are abnormally high your body will tend to store fat" make abnormally high levels of insulin a prerequisite for excess fat storage?

    Here we go again.... ((yawn))

    Reply: #33
  30. Zepp
    It seams that your favorite word is calories, becuse you wright it all over the blogg, but you never wright about why this is important and why its stored.. or even why its consumed, or how different calories affect our bodys different?

    I have alredy written to you about other bad conditions that could make you fat.. but I can wright it again!

    Hypothyreosis, leptin resistance, eating disturbances, lipolytic ensym defiencys, Insulinom, Cushings disease.. and others, fill in what you missing!

    You seems to think that etaing disturbance is the major problem with obesety/diabets/hyperinsulinemia/metabolic syndrome?

    Well figure out how this could happen, a pandemia of behavioral disturbances?

  31. Christopher
    Thank you father.
    Your always loving son Commodus.

    Meditations, The Sixth Book: III.

  32. Vincent
    It is interesting to observe that neither the protagonistic nor the antagonistic stances brought up any evidence based on clinical trials involving human subjects that would substanciate the claims being put forth. Something along the line of: "Hey, read the report of this clinical trial where what I claim was tested and showed a positive result, so how would you like them apple's? :)"
    Reply: #34
  33. grinch
    "Does saying that "If your insulin levels are abnormally high your body will tend to store fat" make abnormally high levels of insulin a prerequisite for excess fat storage?"

    So what is a prerequisite?

  34. sten
    Here is one for you.
    http://abcnews.go.com/Health/Healthday/story?id=4507131&page=1
    It specifically tied high insulin to success with low carb diet.

    The key reason for a low insulin profile is however that high insulin is very strongly tied to maximum risk of heart disease, the one thing most want to avoid by avoiding obesity.
    Here link to a British very large study that found elevated fasting insulin being prime indicator of heart disease risk compared to all other standard markers like HLD, LDL, blood pressure, blood sugar, HbA1c etc. Over 3,000 women were tested and followed for some 10 years, so far.
    http://www.plosmedicine.org/article/info%3Adoi%2F10.1371%2Fjournal.pm...
    Here another study summary relating high fasting insulin also to obesity.
    http://www.ncbi.nlm.nih.gov/pubmed/12243850

    These subjects have been gone over and over so many times by now so please excuse those who write "here we go again". They forget that a majority of people are influenced by the mainstream old fat bashing ideas. Please take some time to study the links before a weighted reply!

    Reply: #35
  35. grinch
    Everyone knows high insulin levels are associated with obesity. But there is little to no evidence that high insulin levels precede obesity and cause it. High insulin is a compensatory effect of insulin resistance, which seems to occur as a result from inflammation due to energy excess and obesity, lack of physical activity, genetics, and a whole host of other factors.
    Replies: #36, #37
  36. Zepp
    Noe, more and more sciens point on that that high insulin levels do promote insulin resistance!

    You never seems to react on those links I provide you, that point on that!

    And to that insulin resistance is a normal state to coop with a diet that promote a high glycemic load!

    But if you want I can give you some of the links again, not that I think you understand them, becuse you never ever comented any of them!

    "Hyperinsulinemic diseases of civilization:

    more than just Syndrome X"

    "Abstract

    Compensatory hyperinsulinemia stemming from peripheral insulin resistance is a well-recognized metabolic disturbance that is at the root cause of diseases and maladies of Syndrome X (hypertension, type 2 diabetes, dyslipidemia, coronary artery disease, obesity, abnormal glucose tolerance). Abnormalities of fibrinolysis and hyperuricemia also appear to be members of the cluster of illnesses comprising Syndrome X. Insulin is a well-established growth-promoting hormone, and recent evidence indicates that hyperinsulinemia causes a shift in a number of endocrine pathways that may favor unregulated tissue growth leading to additional illnesses. Specifically, hyperinsulinemia elevates serum concentrations of free insulin-like growth factor-1 (IGF-1) and androgens, while simultaneously reducing insulin-like growth factor-binding protein 3 (IGFBP-3) and sex hormone-binding globulin (SHBG). Since IGFBP-3 is a ligand for the nuclear retinoid X receptor a, insulin-mediated reductions in IGFBP-3 may also influence transcription of anti-proliferative genes normally activated by the body’s endogenous retinoids. These endocrine shifts alter cellular proliferation and growth in a variety of tissues, the clinical course of which may promote acne, early menarche, certain epithelial cell carcinomas, increased stature, myopia, cutaneous papillomas (skin tags), acanthosis nigricans, polycystic ovary syndrome (PCOS) and male vertex balding. Consequently, these illnesses and conditions may, in part, have hyperinsulinemia at their root cause and therefore should be classified among the diseases of Syndrome X."

    http://www.direct-ms...insulinemia.pdf

    Insulin Resistance and Hyperinsulinemia Is hyperinsulinemia the cart or the horse?

    "Insulin resistance, recently recognized as a strong predictor of disease in adults, has become the leading element of the metabolic syndrome and renewed as a focus of research. The condition exists when insulin levels are higher than expected relative to the level of glucose. Thus, insulin resistance is by definition tethered to hyperinsulinemia. The rising prevalence of medical conditions where insulin resistance is common has energized research into the causes. Many causes and consequences have been identified, but the direct contributions of insulin itself in causing or sustaining insulin resistance have received little sustained attention. We examine situations where insulin itself appears to be a proximate and important quantitative contributor to insulin resistance. 1) Mice transfected with extra copies of the insulin gene produce basal and stimulated insulin levels that are two to four times elevated. The mice are of normal weight but show insulin resistance, hyperglycemia, and hypertriglyceridemia. 2) Somogyi described patients with unusually high doses of insulin and hyperglycemia. Episodes of hypoglycemia with release of glucose-raising hormones, postulated as the culprits in early studies, have largely been excluded by studies including continuous glucose monitoring. 3) Rats and humans treated with escalating doses of insulin show both hyperinsulinemia and insulin resistance. 4) The pulsatile administration of insulin (rather than continuous) results in reduced requirements for insulin. 5) Many patients with insulinoma who have elevated basal levels of insulin have reduced (but not absent) responsiveness to administered insulin. In summary, hyperinsulinemia is often both a result and a driver of insulin resistance."

    http://care.diabetes...ent_2/S262.full

    Hyperinsulinemia Drives Diet-Induced Obesity Independently of Brain Insulin Production
    Hyperinsulinemia is associated with obesity and pancreatic islet hyperplasia, but whether insulin causes these phenomena or is a compensatory response has remained unsettled for decades. We examined the role of insulin hypersecretion in diet-induced obesity by varying the pancreas-specific Ins1 gene dosage in mice lacking Ins2 gene expression in the pancreas, thymus, and brain. Age-dependent increases in fasting insulin and β cell mass were absent in Ins1+/−:Ins2−/− mice fed a high-fat diet when compared to Ins1+/+:Ins2−/− littermate controls. Remarkably, Ins1+/−:Ins2−/− mice were completely protected from diet-induced obesity. Genetic prevention of chronic hyperinsulinemia in this model reprogrammed white adipose tissue to express uncoupling protein 1 and increase energy expenditure. Normalization of adipocyte size and activation of energy expenditure genes in white adipose tissue was associated with reduced inflammation, reduced fatty acid spillover, and reduced hepatic steatosis. Thus, we provide genetic evidence that pathological circulating hyperinsulinemia drives diet-induced obesity and its complications."

    http://www.cell.com/...ract/S1550-4131(12)00453-6

    Banting Lecture 2011
    Hyperinsulinemia: Cause or Consequence?

    "In this conceptual model, insulin resistance is caused
    by hyperinsulinemia and is an appropriate adaptation to the increased need to store fat in adipose tissue without causing hypoglycemia. Thus, insulin resistance is an adaptive response that successfully maintains normal circulating levels of fat and glucose as long as the b-cell is able to maintain sufficiently elevated insulin levels (57). Perhaps the time has come to expand our research focus to carefully investigate the environmental changes that have accompanied the epidemic of obesity and diabetes"

    http://diabetes.diab...61/1/4.full.pdf

    "Hyperinsulinemia is associated with obesity and pancreatic islet hyperplasia, but whether insulin causes these phenomena or is a compensatory response has remained unsettled for decades. We examined the role of insulin hypersecretion in diet-induced obesity by varying the pancreas-specific Ins1 gene dosage in mice lacking Ins2 gene expression in the pancreas, thymus, and brain. Age-dependent increases in fasting insulin and β cell mass were absent in Ins1+/−:Ins2−/− mice fed a high-fat diet when compared to Ins1+/+:Ins2−/− littermate controls. Remarkably, Ins1+/−:Ins2−/− mice were completely protected from diet-induced obesity. Genetic prevention of chronic hyperinsulinemia in this model reprogrammed white adipose tissue to express uncoupling protein 1 and increase energy expenditure. Normalization of adipocyte size and activation of energy expenditure genes in white adipose tissue was associated with reduced inflammation, reduced fatty acid spillover, and reduced hepatic steatosis. Thus, we provide genetic evidence that pathological circulating hyperinsulinemia drives diet-induced obesity and its complications."

    http://www.cell.com/cell-metabolism/retrieve/pii/S1550413112004536

  37. sten
    Assuming obesity is a cause of insulin resistance makes no sense to me. That is the other option to the strong association obesity - high fasting insulin. But please, try to find references proving that point and let us know what you came up with! Then read Gary Taubes books as I have no more time to comment just now!
    Zepp's 2nd link is clear, at least for mice. A completely reversed relation for humans would be hard to think of with many other variables being similar in cause and effect.

    The key I think is that insulin is such a powerful agent in disease and obesity that if mainstream medicine accepted it as a cause of just obesity and started measuring it and then corrected it, the metabolic diseases as heart disease and obesity would reduce catastrophically, for the medical profession that is.

    Please check the 3000+ study on UK women based on fasting insulin again. Maybe there is also a clue to weight gain in the results, knowing that women over 60 sometimes tend to increase a lot in weight. The insulin levels came first in the study. N.B..

  38. Jennie
    That's not carb loading gone wrong, that's just excess calorie consumption.
    You could easily change the headline and transcript into this:

    Low-carb gone wrong

    "My running's is so-so, but i'm one of the nation's top five low-carbers".

    ^Agree with this. stop excess calorie consumption

    Reply: #39
  39. Paul
    Any comments Jennie on the interview with Prof. Tim Noakes ?
    Reply: #40
  40. FrankG
    I think "Jennie" is just here to sell something.

    http://www.youtube.com/watch?v=g8huXkSaL7o

    Reply: #41
  41. sten
    Frank, you are spot on.
    Carb-loading is as far from low carbing one can get.
    We know that low carb is both weight reduction and improved and sustained health.
    Nothing beats LCHF!
  42. Dave
    There are several problems with the caloric
    input/output approach. The most significant
    flaw is that some calories are not just
    calories--they are metabolic signals or metabolic
    activators that differ qualitatively from other
    source of calories. If there is a pattern of high
    carbohydrate diet, then glucagon responsiveness
    in pancreas A cells is down-regulated
    (making the high-carber prone to low blood
    sugar and the need to snack every 3-4 hours)
    and the ability to produce ketones is
    down-regulated, among many other factors.

    I agree with the basic idea that all calories are not equal, but there are seemingly related issues I am not clear about.

    I often eat what I think are considered high carbohydrate foods (sweet potatoes, lentils, oats, bananas) and do not "need to snack every 3-4 hours". How is that to be explained? If I eat walnuts, almonds, pistachios, or peanuts (especially after exercising) and get what I think might not be a sufficient amount of calories from those low carbohydrate foods, I will feel like eating more, or snacking. Are you sure you are not conflating all (unprocessed) high carbohydrate foods with wheat, rye, and barley which supposedly stimulate appetite?

    For someone who is not keto-adapted with full
    capacity to burn fat, they will need carbohydrates
    to keep up the energy level, which means
    snacking on carbs, which raises insulin, which
    diminishes further the capacity to burn fat (while
    insulin has been raised).

    I have not had problems burning fat or maintaining energy levels or with snacking incessantly while on a high carb diet -- with many of the carbs from wheat! I no longer eat wheat, but in general carbs (I do not eat processed foods) do not seem to have the negative effects on me that some people would have me believe they do. I suspect much, but not all, of the anti-carb hype comes from people who are fat and lazy (no offense to those who are; I have my own flaws) and/or subscribe to the "Paleo" ideology.

    To be in fat-burning mode, isn't it important to avoid eating or drinking *anything* that has a sweet taste or carbs? Not difficult to do.

    Reply: #44
  43. Zepp
    The problem is that it diferent peopel reacts different becuse of diferent activity levels/genetic predispositiatons/food choises/social and phsycoligical kontexts, and soo on!

    But when one get to middel ages and ones belly starts to grow.. one often have reached ones geneticaly limittations!

    Soo.. one often dont know how its gonna be befor that!

  44. Paul
    spam spam spam spam spam spam spam spam
    spam spam spam spam spam spam spam spam
    Reply: #45
  45. Dave
    No, not spam. You do not have any relevant answers, do you? People here are telling lies and trying to make seem like science. I am challenging them. Why aren't you?
    Reply: #46
  46. Paul
    Hi "Dave"
    check term 'science' in your dictionary

    spam spam spam spam spam spam spam spam
    spam spam spam spam spam spam spam spam

    Reply: #47
  47. Dave
    I am not spamming. Why don't you check the meaning of that word.

    You still do not have answers, do you? Any relevant questions to contribute? You evidently are not trying to engage in a serious dialogue.

    I checked Wikipedia, and included the definition of science for you.
    http://en.wikipedia.org/wiki/Science
    "Science (from Latin scientia, meaning "knowledge"[1]) is a systematic enterprise that builds and organizes knowledge in the form of testable explanations and predictions about the universe"

    Murray's claims regarding the "the need to snack every 3-4 hours" on a high carbohydrate diet are false. There are other problems, too.

    But first try to figure out what spam is and is not. I doubt you are capable of it, "Paul". But if your are, then how about answering questions and/or asking relevant questions?

    Replies: #49, #50
  48. Paul
    "I doubt you are capable of it, "Paul"

    Paul is my real name - and why are you insulting me?(which I don't mind). Are you a vegan with an extremely high IQ ?

    Reply: #51
  49. Paul
    I checked and this is what it says:
    Spam
    noun
    meaning 2: - irrelevant message sent on the Internet to a large number of recipients.

    Oooo, you are spamming, o dear o dear.

    Reply: #52
  50. Paul
    One last comment. 2 comments.

    "For someone who is not keto-adapted with full
    capacity to burn fat, they will need carbohydrates
    to keep up the energy level, which means
    snacking on carbs, which raises insulin, which
    diminishes further the capacity to burn fat (while
    insulin has been raised)."

    1) One does not need to be keto-adapted to utilize fatty acids for energy

    2) you want me to "engage in a serious dialog" with someone who reasons this way ?. You kiddin' me?. Let me quote Richard Dawkins here: to have a dialog with you would be as if a reproductive biologist would have a dialog with staunch believer of Stork Truth of Babies Deliveries.

    Reply: #53
  51. Dave
    You think it is an insult if someone uses your name?! Strange.

    I am not a vegan. I have a relatively high IQ.

  52. Dave
    Check the meaning of "irrelevant". As far as I can tell, this is a notice board for a type of diet. With the exception of my posts to you, my posts have been on-topic in an effort to learn more about this way of eating and its effects on humans or to address on-topic questions others have raised. Relevant. Very relevant. Please stop wasting my time with your obnoxious and, well, irrelevant posts.

    I do not know how many people read this. I doubt few stick around very long considering all the unaddressed health concerns and what seems to be hollow bragging about how great this diet is.

  53. Dave
    So you also disagree with Murray's "science"? I know Murray's science is false because even though I sometimes eat plenty of high-carbohydrate foods I do not need to snack every 3-4 hours.

    "2) you want me to 'engage in a serious dialog' with someone who reasons this way ?."
    Please elucidate.

  54. Paul
    "You think it is an insult if someone uses your name?! Strange."

    insult referred to this comment: "I doubt you are capable of it,"
    not to using my name. Now, how someone with: "a relatively high IQ.", can not figure this out?

    (I know you are not a vegan, you indicated this several times on this blog before "Dave")

    Reply: #55
  55. Dave
    What are you going on about? I started posting here a few days ago. Dave is the only name I have used.

    Of course I doubted you were capable of it. My only experience with you, unless you have posted under different names, is that you make obnoxious, off-topic posts while hypocritically complaining about spam. How is that you evidently thought otherwise?

    Reply: #56
  56. Paul
    1) "I started posting here a few days ago" - thus your first post is No.42 on this page, yet you state in the comment No. 52: "...my posts have been on-topic..." using plural "my posts" - are you honest in all other aspects of life?, with exception of this blog?.

    2) "I do not know how many people read this. I doubt few stick around very long considering all the unaddressed health concerns and what seems to be hollow bragging about how great this diet is." - so, why are you wasting your time here - do you want to "help us" to ruin our health by eating sugar again? - be one of those who does not stick around. Enjoy your rice and potatoes.

    Reply: #57
  57. Dave
    Yes, plural. You seem to have severe cognitive disabilities. I am honest, as a functional adult would be able to tell from the following information:

    Dave Reply to comment #20 by murray 42
    Dave Reply to comment #44 by Paul 45
    Dave Reply to comment #46 by Paul 47
    Dave Reply to comment #48 by Paul 51

    My post numbered 45, 47, and 51 were to address your posts. If you think it is off topic to make relevant replies to your posts, then you imply that you are being a nuisance by making irrelevant posts.

    Other posts I made, which are further evidence of your dishonesty and stupidity:
    http://www.dietdoctor.com/lchf/comment-page-46#comments
    Dave 2294
    Dave 2299

    http://www.dietdoctor.com/lchf
    Dave 2302
    Dave 2303
    Dave 2304
    Dave 2305
    Dave 2313
    Dave 2314
    ---
    If I do not start getting some good answers soon, I might not stick around. I would like to warn people about this site, though.

    I do not eat sugar, rice, or white potatoes, and do not know why I would recommend those things, with the exception of rice, but it would have to be organic whole grain rice.

    Your assumptions are stupid and wrong. You are a waste of time; I am finished with you.

    Reply: #58
  58. Paul
    We do not have good answers here Davej. We only feel good and look good.

    Friend of mine pointed out to me a page on a vegan blog where they discuss in endless deliberations that fructose is a ketone - just a reminder, they confused ketone with ketose. With commentaries how bad ketones are, obviously.

    I suggest you go to their site - I am sure they will have all the answers for you

  59. Robin Willcourt
    Vincent's dilemma is equating energy "in" with energy "out," while true on the surface, the statement must be modified to say "energy IN that is in a usable form AND is actually able to be absorbed by the intestines must equal energy OUT for the body to remain at a constant weight."

    The caloric content of food is calculated by using a bomb calorimeter that does not take into account which part of the food is actually usable: eg, gristle and many fibers are not. Thus, right from the get go we have an inbuilt error.

    After that, not every calorie is equally available for storage. Glucose is efficiently snapped up and used/stored while fat and protein are not. Energy is also used in differing amounts based on whether it is a fat, sugar or amino acid to store and burn our basic nutrients. Thus, a calorie is NOT a calorie. Therefore, you will get fatter eating 500g of starch than you will 500g of broccoli or steak.

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