Study (1999) coconut oil - glycogen use reduction during/post exercise

Preexercise medium-chain triglyceride ingestion does not alter muscle glycogen use during exercise

Preexercise medium-chain triglyceride ingestion does not alter muscle glycogen use during exercise

+ Author Affiliations

1. ¹ Department of Kinesiology and Health Education, The Human Performance Laboratory, The University of Texas at Austin, Austin, Texas 78712

• Submitted 25 May 1999.
• accepted in final form 23 September 1999.

Abstract

This investigation determined whether ingestion of a tolerable amount of medium-chain triglycerides (MCT; ∼25 g) reduces the rate of muscle glycogen use during high-intensity exercise. 

On two occasions, seven well-trained men cycled for 30 min at 84% maximal O₂ uptake. Exactly 1 h before exercise, they ingested either 1) carbohydrate (CHO; 0.72 g sucrose/kg) or 2) MCT+CHO [0.36 g tricaprin (C10:0)/kg plus 0.72 g sucrose/kg]. The change in glycogen concentration was measured in biopsies taken from the vastus lateralis before and after exercise. Additionally, glycogen oxidation was calculated as the difference between total carbohydrate oxidation and the rate of glucose disappearance from plasma (R_d glucose), as measured by stable isotope dilution techniques. 

The change in muscle glycogen concentration was not different during MCT+CHO and CHO (42.0 ± 4.6 vs. 38.8 ± 4.0 μmol glucosyl units/g wet wt). 

Furthermore, calculated glycogen oxidation was also similar (331 ± 18 vs. 329 ± 15 μmol ⋅ kg^{− 1} ⋅ min^{− 1}). The coingestion of MCT+CHO did increase (P < 0.05) R_d glucose at rest compared with CHO (26.9 ± 1.5 vs. 20.7 ± 0.7 μmol ⋅kg^{− 1} ⋅ min^{− 1}), yet during exercise R_d glucose was not different during the two trials.

Therefore, the addition of a small amount of MCT to a preexercise CHO meal did not reduce muscle glycogen oxidation during high-intensity exercise, but it did increase glucose uptake at rest.

Carb restriction - fat ingestion doesn't stop adaptive response to fasting

My Carb Sane-Asylum: Carbohydrate restriction regulates the adaptive response to fasting

CarbSane said... 

 

What the lipidstudy did was to see if adding nutrition in the form of fats modified the adaptation (e.g. just the body sensing calories). It didn't. An amino acid only infusion would be another interesting study to have done.

....when I say LC puts you in "starvation mode" it is because all of the adaptive mechanisms that kick in during longer fasts are the very same ones that do with severe carb restriction. Increased NEFA (fat mobilization), insulin resistance, ketones enhanced, gluconeogenesis and glyceroneogenesis enhanced, de novo lipogenesis decreased.

February 9, 2011 12:25 PM

Glycemia, starch, & sugar in context - by Ray Peat Ph.D

Glycemia, starch, and sugar in context

A R T I C L E

Glycemia, starch, and sugar in context

============================================

Monosaccharide -- a simple sugar; examples, glucose, fructose, ribose, galactose (galactose is also called cerebrose, brain sugar).

Disaccharide -- two monosaccharides bound together; examples, sucrose, lactose, maltose.

Oligosaccharide -- a short chain of monosaccharides, including disaccharides and slightly longer chains.

Polysaccharide -- example, starch, cellulose, glycogen.

Glycation -- the attachment of a sugar to a protein.

Lipolysis - the liberation of free fatty acids from triglycerides, the neutral form in which fats are stored, bound to glycerine.
============================================

In the 1920s, “diabetes” was thought to be a disease of insulin deficiency. Eventually, measurements of insulin showed that “diabetics” often had normal amounts of insulin, or above-normal amounts. There are now “two kinds of diabetes,” with suggestions that “the disease” will soon be further subdivided.

The degenerative diseases that are associated with hyperglycemia and commonly called diabetes, are only indirectly related to insulin, and as an approach to understanding or treating diabetes, the “glycemic index” of foods is useless. Physiologically, it has no constructive use, and very little meaning.

Fat Burns In the "Flame of Lean Muscle Mass"

The Daily Lipid: When Fat Burns In the Flame of Lean Muscle Mass -- Better Put That Butter Either on Steak or Potatoes

In 1895, a biochemist by the name of Rosenfeld coined the expression "fat burns in the flame of carbohydrate." This was based on observations that cells could break down fatty acids into ketone bodies but without sufficient glucose the cells could not break them down fully into carbon dioxide and hydrogen.

The aphorism offered a simple explanation for why ketones are elevated to extreme levels in diabetes: diabetics do not use glucose efficiently, so glucose levels in the blood rise; since their cells are starved of glucose, the fat stores of these diabetics release their fatty acids and their livers break the fatty acids down into ketones, but these ketones cannot be used in the absence of glucose, so ketone levels in the blood rise and then the ketones are finally lost in the urine. Thus the diabetic is effectively in a constant state of starvation.

We now know that fat burns in the flame of oxaloacetate, which can be derived from either glucose or amino acids.

When we break down fats or carbohydrates for energy, we turn them into acetic acid, or acetate, which is a two-carbon unit. A little shuttle called coenzyme A, which is made of pantothenic acid, carries the acetate around and together we call the complex acetyl CoA. Pantothenate is also called vitamin B5 and is found abundantly in many foods but liver and egg yolks are among the highest (along with certain mushrooms, seeds, and yeast).

In order to fully harvest energy from acetate, we need to send it through the citric acid cycle, also called the Krebs cycle or the tricarboxylic acid (TCA cycle). This cycle will break the acetate down into carbon dioxide and hydrogen. In doing so, it will also release high-energy electrons whose energy can then be harvested to synthesize ATP, a major usable energy currency of the cell. Entry into this cycle is dependent on a compound called oxaloacetate.

Image hosted by Library.Thinkquest.Org

In the presence of glucose, we convert glucose to oxaloacetate. Thus, as oxaloacetate leaves the Krebs cycle cuz it's got things to do and people to see, we can just use glucose to replenish it. In the absence of glucose, we do the opposite: we turn oxaloacetate into glucose. Thus, oxaloacetate gets depleted in the absence of glucose unless we have some other source of it. We can make oxaloacetate from a variety of amino acids, but not from fats. Thus, in the absence of dietary protein or carbohydrate, the only place to get oxaloacetate is to dig into the lean proteins found in our muscles and internal organs.

One thing I really like about The Perfect Health Diet is that although the authors advocate a low-carb diet, they devote a lot of attention to the body's need for glucose, rather than coming up with some silly aphorism like "there are essential amino acids and essential fatty acids, but there is no essential carbohydrate." The body may be able to survive without dietary glucose, but only because it can make glucose from protein. Give it only fat, and it will make that glucose — and oxaloacetate — from lean muscle tissue.

Better get a steak or potato to go with that butter!

May 4, 2011 1:48 PM

Emily Deans, M.D. said...

Chris - I doubt you need to be burning predominantly ketones for the brain to see some benefit from ketosis. Zooko sent me links to so,e interesting studies on twitter - I think I will do a post on it, actually. They are familiar papers but the graphs are very interesting.

May 4, 2011 5:26 PM

Chris Masterjohn said...

Emily, I don't doubt it, but the brain selectively gets the glucose when it is initially limiting, with muscles getting the ketones. Under more extensively glucose deprivation this shifts towards muscles using fatty acids and brains using ketones, which spares lean mass by reducing the need for gluconeogenesis. This is my understanding, at least, though I do need to look deeper at the primary literature on this and the differences between ketogenic diets and prolonged fasting. But my point in response to Dana was that even on a very low-carb diet with a moderate amount of protein, the brain, while perhaps using ketones to some degree, is probably still using primarily glucose. I'm very open to changing this view as I consider it tentative. I look forward to reading your post. Chris

May 4, 2011 5:32 PM

Emily Deans, M.D. said...

I should say that a strict anti-seizure benefit would have to be from strict ketosis to up regulate the GABA reliably and consistently. But other conditions seem to benefit from dips into ketosis, or ketosis that just turns a ketostix. Well, post coming one of these days...

May 4, 2011 5:57 PM

Chris Masterjohn said...

Hey Dr. Deans, In my experience, I can get ketostix purple just by exercising intensely and feasting on carbs. I'd be willing to bet that my brain was running almost entirely on glucose when my ketostix were as purple as they could get (granted I was eating plenty of fat including coconut fat during this time). I'm definitely not claiming dips into ketosis won't be of benefit -- I'm just saying (in my response to Dana, which I'm assuming that's what you're responding to) that in calculating the physiological glucose requirement of the brain you can't assume that a low-carb diet is going to substantially reduce it. Most low-carb diets probably keep the brain running mostly on glucose is my guess, and that's all I was saying. Chris

May 4, 2011 6:12 PM

Paul Jaminet said...

Hi Chris, Great post, and thanks for the shout-out! Here are a few thoughts I had while reading: The “fat burns in the flame of oxaloacetate” discussion is an elegant summary of why 95% fat diets are unhealthy. Re Dana’s point, the body consumes a lot of glucose whether it is consumed or no. If you want to exclude carbs from the diet, you’d better eat sufficient protein! Even if you do, it’s far from clear that manufacture from protein is the optimal way to meet glucose needs. I don’t believe it is. Re ketogenic diets, I’ve migrated to the view that the optimal ketogenic diet even for clinical use should have minimal excess ketones, few excreted ketones, and a fair amount of dietary carbs and protein. Once ketones are being excreted, few tissues are taking up marginal ketones. I think the clinical ketogenic diets often overshoot the optimal amount of ketones, and undershoot the optimal amount of carbs and protein. Re Ned’s point, I’ve eaten a moderately ketogenic low-protein diet for a long time and my albumin levels have never budged. Of course I’ve never eaten a 95% fat diet … but I would imagine you would lose a lot of lean muscle mass before serum albumin levels would start to decrease. Anyway, great thought-provoking post! Best, Paul

May 4, 2011 6:32 PM

John said...

Another great post Chris. The way I see it is that fat can burn in the flame of anything that keeps the TCA cycle going. Even though oxaloacetate is drawn off, you can replenish it via every intermediate in the TCA cycle, because it will eventually be turned into oxaloacetate anyway. Glucose and amino acids are just two of the TCA cycle replenishing options. Another option would be odd-chain fatty acids. They can burn (somewhat) in their own flame, because the last cycle of their β-oxidation will provide propionyl-CoA, which can be turned into succinyl-CoA, a TCA cycle intermediate (not shown in the TCA cycle diagram BTW). And what about the substance that gave the cycle its name: citric acid. Perhaps that's the reasoning behind the lemon diet: burn fat in the flame of citric acid. The citric acid (and some sugar) from the lemons should be able to keep the TCA cycle going, so that would spare protein. But when you know all this, why go for the sour taste of a lemon diet? Using a sugar drink should do the trick just as well. Hmmmm, burning fat with a sugar drink? That sounds a lot like the Shangri-La diet by Seth Roberts. John

May 5, 2011 10:08 AM

Sucrose study - stress, body composition, hormones, Ray Peat etc

Proline

Tuesday, February 22, 2011

Sucrose, stress, and reactive hypoglycemia

Posted by Jannis

Several studies have demonstrated that sucrose or fructose increase the metabolic rate of humans. Individuals, eating diets high in sucrose, have a higher energy intake and a higher energy expenditure than those eating a high starch diet. The higher energy intake does not seem to cause an increase in body fat. In fact, several studies which have been conducted over a longer period of time, show that sucrose is superior in regards to fat loss and gaining lean body mass.

A Raben, I Macdonald, and A. Astrup confirmed many of the ideas Ray Peat has about sucrose. Women were divided into three groups and observed for two weeks. They received either a high fat, high starch, or high sucrose diet. On day 15, body weight, fat mass, lean body mass, blood glucose, and hormonal levels were measured and compared to the base line levels. The starch group lost a lot of lean body mass, whereas the sucrose group lost fat and gained muscle mass. Carbohydrate oxidation was also found to be much higher in the sucrose group. The whole study can be seen here

The question is: How does sucrose cause the metabolic rate to increase? One reason might be the higher costs of glycogen deposition after fructose ingestion (3.5±4.5 mol ATP/mol) than after glucose ingestion (2.5 mol ATP/mol). But the major cause seems to be something else.

According to Ray Peat, sucrose stabilizes the blood sugar, decreases stress hormones, and thus optimizes thyroid function. Therefore, I was pretty surprised to see that the sucrose group had significantly increased levels of adrenaline and noradrenaline. Additionally, lactate levels were also elevated in the sucrose group. A high lactate concentration is a sign of increased anaerobic glycolisis - the opposite of oxidative metabolism.

It seems that the increased metabolic rate on a high sucrose diet is caused mainly by the activation of the adrenal system. "[...]thermogenesis after oral or intravenous fructose, has actually been found to be suppressed by 40% by b-adrenergic blockade (propranolol)"

Peat himself has written a lot about the negative effects of adrenalin exposure. Adrenaline increases free fatty acids in the bloodstream, inhibits ATP production, and thyroid function. In general, a high level of stress hormones shifts the balance away from an oxidative metabolism towards glycolisis.

When I showed the study to Peat, he replied that he thinks that the increase in adrenaline is a temporary mechanism to compensate for low thyroid function. Whether this is correct or not, I can't say. I have been searching for a long time, but there are no studies, examining the long term effects of high sucrose diets.

Patients with reactive hypoglycemia experience episodes of hypoglycemia occurring 1–2 hours after a meal. Typical signs are cold sweety hands, headaches/ depression, anger, slugishness etc. Adrenaline, among other hormones, is part of the counterregulatory system that increases the blood sugar when it's too low. In experiments, where single doses of either glucose, sucrose, or fructose were given to patients with reactive hypoglycemia, fructose and sucrose were more efficient in stabilizing the blood sugar, as compared to pure glucose. Link

But the long term effects may be very different from that results. Hypoglycemia can be caused by endotoxin, or very high levels of PUFA or estrogen in the blood stream. But I think that it is mostly an excess of stress hormones that causes the parasympathetic nervous system to overreact, releasing too much insulin.

I was experiencing hypoglycemic episodes after meals for a long time. Two weeks ago, I reduced my intake of sucrose from more than 200g a day to 50g or less. Ever since, I haven't had a single episode of hypoglycemia. My temperature and pulse rate are stable on a higher level and my sleep improved, too. I currently eat about 300g of carbohydrates a day. 150g of starch, 100g of lactose and 50g of sugar.

The graph above reflects very good how sucrose influenced my blood sugar. A rapid fall in blood glucose after a meal, followed by a slight increase, probably due to counterregulatory mechanisms. The study by Raben et al. didn't cause the women to get hypoglcemia, beside a slight decrease after breakfast. The study, from which I took the graph above, used high amounts of PUFA in the sucrose group, which probably is jointly responsible for the reaction. Nevertheless, I experienced the same, and I eat hardly any PUFA at all.

Even if the a level of adrenaline does not cause somebody to get hypoglycemia, other negative side effects such as insomnia, low energy levels, low sex drive, or acne are likely to occur.
Besides, adrenalin can cause T4 to be turned into RT3, which will worsen the problems, and is especially problematic, if thyroid medication is taken.

In order to quickly improve symptoms of high adrenaline, a reduction of sucrose intake seems appropriate. Milk and salty carbohydrates, like homemade french fries (made with coconut oil), are very usefull to reduce stress levels. Thyroid medication, containing T4, should be stopped, because the additional T4 might be turned into RT3. Pure T3 is a very powerfull tool to quickly restore oxidative metabolism, and to lower stress hormones and RT3.

I don't think that a high sucrose diet is necessarily bad. But under certain circumstances it seems to be counterproductive. For people with a high metabolism, sugar is probaly beneficial, but those with a low metabolism and suboptimal thyroid levels should only increase sugar consumption very carefully.

Much more research is necesarry to determine all the effects of sucrose.

116 comments

Dangers of Zero-Carb Diets - No 4 kidney stones

Dangers of Zero-Carb Diets, IV: Kidney Stones | Perfect Health Diet

Conclusion

Zero-carb dieters are at risk for

• Excess renal oxalate from failure to recycle vitamin C;
• Excess renal uric acid from disposal of nitrogen products of gluconeogenesis and ketogenesis;
• Salt and other electrolyte deficiencies from excretion of oxalate, urea and uric acid; and
• Dehydration.

These four conditions dramatically elevate the risk of kidney stones.

To remedy these deficiencies, we recommend that everyone who fasts or who follows a zero-carb diet obtain dietary and supplemental antioxidants, eat salt and other electrolytes, and drink lots of water.

Also, unless there is a therapeutic reason to restrict carbohydrates, it is best to obtain about 20% of calories from carbs in order to relieve the need to manufacture glucose and ketones from protein. This will substantially reduce uric acid excretion. If it also reduces vitamin C degradation rates, as we argued in our last post, then it will substantially reduce oxalate excretion as well.

Related Posts

Other posts in this series:

1. Dangers of Zero-Carb Diets, I: Can There Be a Carbohydrate Deficiency? Nov 10, 2010.
2. Dangers of Zero-Carb Diets, II: Mucus Deficiency and Gastrointestinal Cancers A Nov 15, 2010.
3. Danger of Zero-Carb Diets III: Scurvy Nov 20, 2010.

References

[1] Furth SL et al. Risk factors for urolithiasis in children on the ketogenic diet. Pediatr Nephrol. 2000 Nov;15(1-2):125-8. http://pmid.us/11095028.

[2] Herzberg GZ et al. Urolithiasis associated with the ketogenic diet. J Pediatr. 1990 Nov;117(5):743-5. http://pmid.us/2231206.

[3] Sampath A et al. Kidney stones and the ketogenic diet: risk factors and prevention. J Child Neurol. 2007 Apr;22(4):375-8. http://pmid.us/17621514.

[4] “Ketogenic diet,” Wikipedia, http://en.wikipedia.org/wiki/Ketogenic_diet.

[5] Groesbeck DK et al. Long-term use of the ketogenic diet. Dev Med Child Neurol. 2006 Dec;48(12):978-81. http://pmid.us/17109786.

[6] Taylor EN et al. DASH-style diet associates with reduced risk for kidney stones. J Am Soc Nephrol. 2009 Oct;20(10):2253-9. http://pmid.us/19679672.

[7] Gutman AB. Significance of uric acid as a nitrogenous waste in vertebrate evolution. Arthritis Rheum. 1965 Oct;8(5):614-26. http://pmid.us/5892984.

[8] Boyle JA et al. Serum uric acid levels in normal pregnancy with observations on the renal excretion of urate in pregnancy. J Clin Pathol. 1966 Sep;19(5):501-3. http://pmid.us/5919366.

[9] Linster CL, Van Schaftingen E. Vitamin C. Biosynthesis, recycling and degradation in mammals. FEBS J. 2007 Jan;274(1):1-22. http://pmid.us/17222174.

[10] Marengo SR, Romani AM. Oxalate in renal stone disease: the terminal metabolite that just won’t go away. Nat Clin Pract Nephrol. 2008 Jul;4(7):368-77. http://pmid.us/18523430.

[11] Taylor EN et al. Fatty acid intake and incident nephrolithiasis. Am J Kidney Dis. 2005 Feb;45(2):267-74. http://pmid.us/15685503.

[12] Taylor EN, Curhan GC. Oxalate intake and the risk for nephrolithiasis. J Am Soc Nephrol. 2007 Jul;18(7):2198-204. http://pmid.us/17538185.

Danger of Zero-Carb Diets - No 3 Scurvy

Danger of Zero-Carb Diets III: Scurvy | Perfect Health Diet

Conclusion

Zero-carb dieters are at high risk for vitamin C deficiency, glutathione deficiency, and selenium deficiency. Anyone on a zero-carb diet should remedy these by supplementation.

These deficiencies are exacerbated by chronically low insulin levels. Insulin helps recycle vitamin C, which supports glutathione status. Lack of insulin increases vitamin C degradation and loss.

The failure of the body to efficiently recycle vitamin C and maintain antioxidant stores on a zero-carb diet is evidence of an evolutionary maladaption to the zero-carb diet.

There was no reason why our ancestors should have become adapted to a zero-carb diet; after, all they’ve been eating starches for at least 2 million years. It seems a risky step to try to live this way.

Related Posts

Other posts in this series:

1. Dangers of Zero-Carb Diets, I: Can There Be a Carbohydrate Deficiency? Nov 10, 2010.
2. Dangers of Zero-Carb Diets, II: Mucus Deficiency and Gastrointestinal Cancers A Nov 15, 2010.
3. Dangers of Zero-Carb Diets, IV: Kidney Stones Nov 23, 2010.

References

[1] Willmott NS, Bryan RA. Case report: Scurvy in an epileptic child on a ketogenic diet with oral complications. Eur Arch Paediatr Dent. 2008 Sep;9(3):148-52. http://pmid.us/18793598.

[2] Willmott NS, personal communication.

[3] “Dehydroascorbate,” Wikipedia, http://en.wikipedia.org/wiki/Dehydroascorbate.

[4] Fain O et al. Hypovitaminosis C in hospitalized patients. Eur J Intern Med. 2003 Nov;14(7):419-425. http://pmid.us/14614974.

[5] Tyml K et al. Delayed ascorbate bolus protects against maldistribution of microvascular blood flow in septic rat skeletal muscle. Crit Care Med. 2005 Aug;33(8):1823-8. http://pmid.us/16096461.

[6] Rivas CI et al. Vitamin C transporters. J Physiol Biochem. 2008 Dec;64(4):357-75. http://pmid.us/19391462.

[7] Huang J et al. Dehydroascorbic acid, a blood-brain barrier transportable form of vitamin C, mediates potent cerebroprotection in experimental stroke. Proc Natl Acad Sci U S A. 2001 Sep 25;98(20):11720-4. http://pmid.us/11573006.

[8] Qutob S et al. Insulin stimulates vitamin C recycling and ascorbate accumulation in osteoblastic cells. Endocrinology. 1998 Jan;139(1):51-6. http://pmid.us/9421397.

[9] Will JC, Byers T. Does diabetes mellitus increase the requirement for vitamin C? Nutr Rev. 1996 Jul;54(7):193-202. http://pmid.us/8918139.

[10] Seghieri G et al. Renal excretion of ascorbic acid in insulin dependent diabetes mellitus. Int J Vitam Nutr Res. 1994;64(2):119-24. http://pmid.us/7960490.

[11] Linster CL, Van Schaftingen E. Vitamin C. Biosynthesis, recycling and degradation in mammals. FEBS J. 2007 Jan;274(1):1-22. http://pmid.us/17222174.

[12] Bank IM et al. Sudden cardiac death in association with the ketogenic diet. Pediatr Neurol. 2008 Dec;39(6):429-31. http://pmid.us/19027591. (Hat tip Dr. Deans.)

Dangers of Zero-Carb Diets - No 2 mucus & cancerstinal Cancers | Perfect Health Diet

Dangers of Zero-Carb Diets, II: Mucus Deficiency and Gastrointestinal Cancers | Perfect Health Diet

Conclusion

A healthy diet should be robust to faults. The Optimal Diet is not robust to glucose deficiency.

There’s good reason to suspect that at least some of the Optimal Dieters developed mucin deficiencies as a result of the body’s effort to conserve glucose and protein. This would have substantially elevated risk of gastrointestinal cancers. Thus, it’s not a great surprise that many Optimal Dieters have been coming down with GI cancers after 15-20 years on the diet.

We recommend a carb plus protein intake of at least 600 calories per day to avoid possible glucose deficiency. It’s plausible that a zero-carb diet that included at least 600 calories per day protein for gluconeogenesis would not elevate gastrointestinal cancer risks as much as the Optimal Diet. But why be the guinea pig who tests this idea? Your body needs some glucose, and it’s surely less stressful on the body to supply some glucose, rather than forcing the body to manufacture glucose from protein.

Fasting and low-carb ketogenic diets are therapeutic for various conditions. But anyone on a fast or ketogenic diet should carefully monitor eyes and mouth for signs of decreased saliva or tear production. If there is a sign of dry eyes or dry mouth, the fast should be interrupted to eat some glucose/starch. Rice is a good source. The concern is not only cancer in 15 years; a healthy mucosal barrier is also essential to protect the gut and airways against pathogens.

Related Posts

Other posts in this series:

1. Dangers of Zero-Carb Diets, I: Can There Be a Carbohydrate Deficiency? Nov 10, 2010.
2. Danger of Zero-Carb Diets III: Scurvy Nov 20, 2010.
3. Dangers of Zero-Carb Diets, IV: Kidney Stones Nov 23, 2010.

References

[1] Sonksen P, Sonksen J. Insulin: understanding its action in health and disease. Br J Anaesth. 2000 Jul;85(1):69-79. http://pmid.us/10927996.

[2] Peek RM Jr, Crabtree JE. Helicobacter infection and gastric neoplasia. J Pathol. 2006 Jan;208(2):233-48. http://pmid.us/16362989.

[3] Bornschein J et al. H. pylori Infection Is a Key Risk Factor for Proximal Gastric Cancer. Dig Dis Sci. 2010 Jul 29. [Epub ahead of print] http://pmid.us/20668939.

[4] Guang W et al. Muc1 cell surface mucin attenuates epithelial inflammation in response to a common mucosal pathogen. J Biol Chem. 2010 Jul 2;285(27):20547-57. http://pmid.us/20430889.

[5] Velcich A et al. Colorectal cancer in mice genetically deficient in the mucin Muc2. Science. 2002 Mar 1;295(5560):1726-9. http://pmid.us/11872843.

[6] An G et al. Increased susceptibility to colitis and colorectal tumors in mice lacking core 3-derived O-glycans. J Exp Med. 2007 Jun 11;204(6):1417-29. http://pmid.us/17517967.

[7] Paz HB et al. The role of calcium in mucin packaging within goblet cells. Exp Eye Res. 2003 Jul;77(1):69-75. http://pmid.us/12823989.

[8] Schmidt DR, Mangelsdorf DJ. Nuclear receptors of the enteric tract: guarding the frontier. Nutr Rev. 2008 Oct;66(10 Suppl 2):S88-97. http://pmid.us/18844851.

[9] Go?kowski F et al. Iodine prophylaxis–the protective factor against stomach cancer in iodine deficient areas. Eur J Nutr. 2007 Aug;46(5):251-6. http://pmid.us/17497074.

Dangers of Zero-Carb Diets - No 1 introarbohydrate Deficiency? | Perfect Health Diet

Dangers of Zero-Carb Diets, I: Can There Be a Carbohydrate Deficiency? | Perfect Health Diet

Dangers of Zero-Carb Diets, I: Can There Be a Carbohydrate Deficiency?

Filed under: Carbohydrate Deficiency, Low-Carb Diets, Zero-Carb Dangers

It’s frequently said in the Paleo blogosphere that carbs are unnecessary. Here’s an example from Don Matesz, an outstanding blogger who eats a diet extremely close to ours:

Protein is essential, carbs are not…. You can only cut protein so much, but you can cut carbs dramatically.

Dr. Michael Eades has mocked the idea of a carbohydrate deficiency disease:

Are there carbohydrate deficiency diseases, Mr. Harper, that you know about that the rest of the nutritional world doesn’t?  I’ll clue you in: there aren’t.  But there are both fat and protein deficiency diseases written about in every internal medicine textbook.

Such statements made an impression on me when I first started eating Paleo five years ago. But several years and health problems later, I realized that this view was mistaken.

How Should We Look for a Carbohydrate Deficiency Disease?

To find a carbohydrate deficiency syndrome in humans, we should look at populations that eat very low-carb diets, such as:

• The Inuit on their traditional hunting diet.
• Epilepsy patients being treated with a ketogenic diet.
• Optimal Dieters in Poland, who have been following a very low-carb diet for more than 20 years.
• Very low-carb dieters in other countries, who took up low-carb dieting in the last 10 years as the Paleo movement gathered steam.

We should also have an idea what kind of symptoms we should be looking for. Major glucose-consuming parts of the body are:

• Brain and nerves.
• Immune system.
• Gut.

The body goes to great lengths to assure that the brain and nerves receive sufficient energy, so shortfalls in glucose are most likely to show up in immune and gut function.
So, we’ve mapped our project. Over the coming week, or however long it takes before we get tired, we’ll investigate the evidence for carbohydrate deficiency conditions in humans.

Related Posts

Other posts in this series:

1. Dangers of Zero-Carb Diets, II: Mucus Deficiency and Gastrointestinal Cancers A Nov 15, 2010.
2. Danger of Zero-Carb Diets III: Scurvy Nov 20, 2010.
3. Dangers of Zero-Carb Diets, IV: Kidney Stones Nov 23, 2010.

References

[1] Holman RT. The slow discovery of the importance of omega 3 essential fatty acids in human health. J Nutr. 1998 Feb;128(2 Suppl):427S-433S. http://pmid.us/9478042
[2] Aiello LC, Wheeler P. The expensive tissue hypothesis: the brain and the digestive system in human and primate evolution. Current Anthropology 1995(Apr); 36(2):199-211.

Carbo loading - Athletes not using it

The Correct Nutrition and Diet for Athletes. Part 3: So what is wrong with carbo-loading, UK

There are two problems that those who recommend carbo-loading don't appear to realise:

• Firstly, the body can't store carbohydrates in large quantities and most people already get more than enough carbohydrates to fuel their bodies' daily activities. All carbohydrates, whether they are bread, pasta, sugar or jam when you put them in your mouth, enter the bloodstream as glucose. And the bloodstream can only hold so much. The body, being a well-run power plant, puts the leftovers in storage to use in the future if it's needed. Some is stored as a type of starch called glycogen, but as it can't store much of this, the body turns most of the excess into fat and keeps it on deposit in the body's fat cells. And we see it walking around the streets wherever we go, hanging off bodies in a most unattractive way. Put simply, carbo-loading cannot work simply because excess carbs are not stored in a readily usable way.
• The second problem lies in how the body uses its various options for fuel. Each of our body's cells contains lots of very small power plants called mitochondria . It is they that produce the energy we need from the food that we consume. Glucose is usually called the body's 'preferred fuel' because, if it is available, our bodies have been conditioned from birth to use it first. But it is not the best fuel. That distinction belongs to fats - or fatty acids, to give them their scientific name. Before the mitochondria can use either glucose or fatty acid as a fuel, it has to be transported into the mitochondria.

Fatty acids are transported into the mitochondria as completely intact molecules. Glucose, on the other hand, can be transported only after it has been broken down first into pyruvate by the process of glycolysis . This is then used anaerobically to produce energy with lactate as a by-product.

The by-products of the energy-production process when fatty acids are used are carbon dioxide and water, both of which are easily excreted. But when glucose is used, the lactic acid produced in the conversion process can build up in muscle cells and make them ache. It is this that is the cause of the aching muscles or pain involved in strenuous exercise - 'the wall' as athletes call it. This 'wall' severely limits an athlete's performance.

But it is not necessary ever to 'hit the wall'. If you do, your diet is wrong.

Now let's look at a real athlete

It was 1968 at the Mexico City Olympic Games. The spectators at the marathon went wild as a relatively unknown Ethiopian, Degaga (Mamo) Wolde, won the marathon. Not only was the thirty-six-year-old runner the oldest man ever to win this prestigious event, he did it in a time that has not been bettered to this day.

So what was Wolde's secret?

Wolde was a member of the Oromo or Galla, a traditionally pastoral tribe who live in West and South Ethiopia and part of Kenya. Traditionally the Oromo were nomadic herders like their neighbours, the Maasai and Samburu tribes.⁽¹⁾ His life consisted of herding and running after and hunting wild game on foot. His diet, like other similar tribes, was one high in animal meat and fat, with practically no carbohydrate. Subsequent tests showed that Wolde's body, under conditions of physical load, readily burned fat as its main energy source. Wolde had no concept of 'hitting the wall'. It had never happened to him.

low carb & paleo related studies - 78 reference links

library of low carb and paleo related study links - 78 of them:

American Journal of Clinical Nutrition:
• Carbohydrate nutrition and inflammatory disease mortality in older adults
• Carbohydrate quantity and quality and risk of type 2 diabetes in the European Prospective Investigation into Cancer and Nutrition–Netherlands (EPIC-NL) study
• Dietary intake of saturated fatty acids and mortality from cardiovascular disease in Japanese: the Japan Collaborative Cohort Study for Evaluation of Cancer Risk (JACC) Study
• Effect of a low glycemic index compared with a conventional healthy diet on polycystic ovary syndrome
• Effects of glycemic load on metabolic risk markers in subjects at increased risk of developing metabolic syndrome
• Gluconeogenesis and energy expenditure after a high-protein, carbohydrate-free diet
• High protein intake reduces intrahepatocellular lipid deposition in humans
• Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease
• Saturated fat, carbohydrate, and cardiovascular disease

Sucrose, stress hormones, hypoglycemia & Ray Peat - Proline Feb 2011

Proline: February 2011

Extract:

But I can’t help, considering my own experiences with high sugar diets (the first one I ever did totally eliminated all my gray hair for example, which didn’t start coming back in again for 6-7 years), thinking that sugar may have some advantages here. It’s certainly hard to make everyone who follows my work suffer with anxiety over omitting many of their favorite foods over it. In a perfect world that sugar would probably come from freshly-juiced sugarcane, what one person has written to me and called the ultimate food. But there are of course many ways of scrutinizing this as well. Ice cream could win votes too by some lines of thinking (higher calorie density, therefore greater calorie consumption, therefore greater energy level, mood, heat production, etc.).

Low-carb diets are a great stress - 180 Degree Health

180 Degree Health: Mark Sisson by Matt Stone

Extract:

Low-carb diets are a great stress to most people, increasing the catecholamines, advancing the rate of aging, slowing down thyroid function, increasing inflammation, and reducing many important anti-aging hormones like testosterone, progesterone, and DHEA.

While many low-carb zealots will deny reality and go about searching busily to find evidence that supports low-carb eating – that’s what they do, defend a pre-conceived conclusion – this is the simple biological truth as I understand it…

Carbs - Carbohydrate Metabolism, gluconeogenis

lecture format - covers the mechanism of gluconeogenis, ie making glucose from fat and protein when muscle and liver glycogen levels get low.  this accounts for how people can, to some extent, internally generate their own fuel for brain and muscles while on low carb and ketogenic diets:

Low carb - Gary Taubes on the evils of carbohydrates

nb: Scientists now saying carbs, not fat, are to blame for America's ills - latimes.com

below a short abc (US) feature introducing low carb proponent Gary Taubes (http://en.wikipedia.org/wiki/Gary_Taubes):



in 2002 Taubes first challenged traditional wisdom on the basis for obesity (ie: http://www.nytimes.com/2010/12/28/health/28zuger.html ) and provoked a lot of debate on accepted dogmas in the process.he advocates a high saturated fat dietary intake.

most recently he has written about the sugar-cancer connection (http://www.nytimes.com/2011/04/17/magazine/mag-17Sugar-t.html ), with parallels to the the Robert Lustig's disease/sugar thesis

some "Top Comments" from You Tube ( see all ):

• Gary Taubes is what Galileo was to Copernicus. He has basically taken the discovery of scientists prior to him, who stated that insulin causes fat accumulation, and has made that ignored information known to the masses, and for his generosity, he is experiencing a backlash from those who uphold the prevailing orthodoxy of calories in vs. calories out. I guarantee you, that a generation from now, Taubes will be revered as a science revolutionary along with Atkins, Yudkin, and Lustig.
  alphacause 1 year ago 13

• Taubes’s mention of General Mill’s donations to Harvard opened my eyes to the huge influence corporations can have on top research institutions. This is an unavoidable consequence of the fact that scientific endeavors require huge amounts of time and money. I am also surprised about the scientific validity of the Atkins diet and the examples Taubes used to counter popular conceptions of obesity e.g. the Fat Louisa paradox and early twentieth century research on adiposity.
  pattynads 7 months ago 4

links below to 3 lectures by Taubes that reveal his approach in more detail:

Gary Taubes' "Why We Get Fat" IMS Lecture On August 12, 2010 (8 parts + 5 extras)

http://youtu.be/_WWCCUPmZcQ
http://youtu.be/dSAZ1voWjGU
http://youtu.be/xGsbszZeGIo
http://youtu.be/ph5v9iSHFYI
http://youtu.be/IDa7FxG79M4
http://youtu.be/okYWkh9YXcA
http://youtu.be/MZuEn9y5MIc
http://youtu.be/sKIhYQZuLZ8
bonus 1 - http://youtu.be/Kzs3YUSUnCA
bonus 2 - http://youtu.be/v693v3D-UeA
bonus 3 - http://youtu.be/iaZ0NWzqYDI
bonus 4 - http://youtu.be/NYSbFZSukJE
bonus 5 - http://youtu.be/tGTgpGeSH_E


Gary Taubes at Dartmouth 6/5/2009 (6 parts)

http://youtu.be/jIGV9VOOtew
http://youtu.be/cQlADI7omUQ
http://youtu.be/yEP-0TNVCEw
http://youtu.be/4SNC6Q8FcBY
http://youtu.be/HiEtsVPUXmo
http://youtu.be/XMzgo932JIw
http://youtu.be/BXaPr5v1a6k


UC Berkeley: Gary Taubes 11/7/2007 (10 parts)

http://youtu.be/AVvZP2av5Mk

http://youtu.be/_Y7cVmjFRC4
http://youtu.be/hGHgOata-IA
http://youtu.be/imX5fdR5dHk
http://youtu.be/e7W1Zpy0DtU
http://youtu.be/uhyCQ0wGFWI
http://youtu.be/qcTinoYDjtk
http://youtu.be/DZwOE1OEpsY
http://youtu.be/P2NboETKEyM
http://youtu.be/SheJ6SJSaos

Taubes has some energetic detractors ( http://www.youtube.com/watch?v=i-jbDwkHzlI&feature=fvwrel )

"Sugar: The Bitter Truth" - Dr Robert Lustig

nb: Scientists now saying carbs, not fat, are to blame for America's ills - latimes.com

first an abbreviated version of the celebrated 90 minute lecture given by Dr Robert Lustig (see here: http://youtu.be/dBnniua6-oM ) on the health impact of dietary sugar:



the broader news media have now caught on to Lustig - see example here: