Showing posts with label i. Show all posts
Showing posts with label i. Show all posts
Monday, March 16, 2015
2009 What I Learned Last Year
What We Eat Contributes More to Disease Risk than Genetics
I started this blog to try to understand how food, exercise, sun exposure, etc., contribute to health and disease, because I was shocked that recent, comprehensive studies demonstrated that genetic defects were only minor contributors. I am trained as a molecular biologist and I search for explanations of disease in terms of the interactions of the proteins coded by the genes in our cells. History of defective genes that code for defective proteins in sickle-cell anemia, Huntington’s disease or ALS, suggested that personal genetic defects might explain personal diseases. Fortunately, it appears that in most cases genetic defects only matter when our actions produce chronic inflammation. What we eat is far more important than our genetics in determining if we are going to suffer from allergies, autoimmune diseases, degenerative diseases, various forms of mental illness or cancer. If we eat to avoid inflammation, in most cases it doesn’t matter how genetically defective we are.
Diet-Based Inflammation Is the Major Risk
Modern diets rich in starch/sugar/fructose and polyunsaturated fats (omega-6 oils), and deficient in saturated fats and omega-3 oils produce the chronic inflammation that forms the foundation of most diseases. Vegetable oils, such as corn, soy or safflower oils are inflammatory and should be eliminated from our kitchens. We should only use olive oil, butter or lard. Saturated fats from meat, dairy and eggs are healthier than polyunsaturated vegetable oils. There was never adequate scientific data to justify the shift from saturated fats to polyunsaturated vegetable oils. That was a tragic, unscientific medical error that contributed significantly to deteriorating health in the developed/developing world.
Anti-Inflammatory Diet and Lifestyle Is the Cure
It came as a surprise to me that simply eliminating inflammatory foods could prevent most diseases. After diseases have developed, it is harder to reverse the process and return to health, but even in that case, diet is of paramount importance.
Back to Basics of a Healthy Diet (the Food Pyramid Is Wrong)
- Starch/sugar/fructose are inflammatory. Low carbohydrate is the healthiest diet.
- Grains, even whole grains, and especially cereal are a big part of the problem and should be avoided.
- Fat and not carbohydrates, should be the major source of dietary calories/energy.
- Saturated fats are healthier than vegetable oils -- use olive oil and butter.
- Meats/fish (not fed on grains) are healthy. A healthy vegetarian diet is difficult.
- Leafy vegetables are a good source of healthful antioxidants.
- Fruits and fructose are inflammatory and should be eaten sparingly.
- Healthy gut bacteria are important. Eat fermented foods with live bacteria, e.g. yogurt.
Living with Inflammation
Chronic inflammation can lead to many problems that diet and supplements can help to remedy. For example, vitamin D deficiency is an epidemic in America, because chronic dietary inflammation appears to compromise the ability to make vitamin D in the skin with sunlight. Most individuals eating a diet high in polyunsaturated fats, starch and high fructose corn syrup, are deficient in vitamin D and would benefit from a vitamin D3 supplement of at least 2,000 IU per day. Vitamin D deficiency also contributes to inflammation. Fish oil supplements can also help to reduce dietary inflammation and should always be taken with at least equal amounts of saturated fats in the same meal.
Resolve to Eat Your Way to Health
It is easy to avoid most diseases by avoiding dietary inflammation. Since chronic dietary inflammation produces depression, lethargy, obesity and a lack of energy, a healthy anti-inflammatory diet will also lead to weight loss, increased energy and reduced symptoms of aging. Most symptoms of aging and disease are actually poorly managed inflammation that exposes genetic defects. Most people increase in inflammation with age, but proper diet can avoid this risk to health and prolong youthful activity. The healthiest resolution for the new year is to stop eating blatantly inflammatory foods (starch and vegetable oils) and start eating more spicy meats, fish and leafy vegetables.
Sunday, March 15, 2015
Health in Diagrams I — Gut Flora and Diet
---All 200 posts here---
This is the first of three posts to summarize my thoughts on diet, inflammation and disease mediated by gut flora. I decided that I needed to make my points as explicit as possible by putting them down in diagrams and making references to my other posts. By the time I finish, I will reach my 200th blog post at Cooling Inflammation.
Health in Diagrams II -- Curing Autoimmunity and Allergies
Health in Diagrams III -- Inflammation from Cell to Tissue
Everyone Leaves Out Gut Flora
I want to first explain and diagram my current understanding of the relationship between gut flora (the complex community of hundreds of different types of bacteria and fungi in the intestines) and diet. My impression is that many people have health problems based on diet, but when they try to heal their health, they fix their diet and see only limited benefits. Medicine provides only a temporary treatment using dairy probiotics. The problem is that they failed to fix their gut flora, which was also damaged by their unhealthy diet.
Health Requires a Match between Diet and Gut Flora
It is a myth that gut flora will just adjust to diet and a healthy diet leads to a healthy gut flora.
A damaged gut flora lacks necessary species of bacteria. Antibiotics, for example, can permanently delete dozens of particular bacterial species of gut flora that can only be replaced by reintroducing the missing bacteria by eating those bacteria again. The missing bacteria may be needed to digest particular foods and the result is food intolerances, commonly mistaken for food allergies. Antibiotic use frequently leads to autoimmune diseases, that are caused by deficient regulatory T cells of the immune system that develop in the lining of the intestines in response to particular gut bacteria. The natural source of gut bacteria is eating the bacteria clinging to raw or fermented vegetables.
Antibiotics and Autoimmunity
Diagram Showing the Interaction of Food, Gut Flora and the Immune System
Food is just Protein, Fat and Soluble Fiber
The human body produces enzymes to fully digest proteins, fats and one polysaccharide, starch. All other parts of plants and animals are edible (fermented by gut flora) soluble fiber polysaccharides or insoluble, undigestible fiber consisting of cellulose or lignin, which together also make up the undigested organic matter, humus, of soil. Grains are problematical for health, because their starch is readily converted to sugar, i.e. high glycemic, and their fiber is insoluble (not fermented by gut flora) and high in phytate. Phytochemicals, plant polyphenolics, are of questionable value as antioxidants and are of unexplored importance for their antimicrobial impact on gut flora.
Phytochemicals, Natural Antibiotics and Antioxidants
Polymers (Protein, Starch) are Hydrolyzed by Enzymes to Oligomers and then Monomers (Amino Acids, Glucose)
The stomach mixes protein digesting enzymes, proteases, and starch digesting amylase, with food protein and starch. Proteases convert the long chains polypeptides, polymers of protein amino acids, into shorter fragments, oligopeptides. The specific nature of the stomach proteases leaves groups of basic amino acids (lysine, arginine), heparin-binding domains, intact. These peptides, similar to the defensins of the microvilli crypts, are anti-microbial and work with residual acidity to reduce bacterial growth in the first part of the small intestines. Pancreatic enzymes then digest the peptides further and the small peptides are ultimately digested by enzymes on the surface of intestinal epithelial cells just prior to absorption. Similarly, starch is degraded to oligosaccharide amylodextrins, which are then hydrolyzed to glucose at the intestinal surface prior to absorption. Amino acids and glucose are not normally available to bacteria in the intestines.
Antimicrobial Heparin-binding Domains
Fats are Dissolved by Bile, Digested by Lipase and Absorbed
Fats are triglycerides, i.e. three fatty acids attached to the three hydroxyl groups of glycerol. Fats are hard to digest, because they form oily droplets. The droplets are dissolved in the intestines with bile, which is an acidic form of cholesterol, that is produced in the liver and stored in the gall bladder. Fat in a meal triggers bile release from the gall bladder into the small intestines. The bile represents a huge reservoir of the cholesterol that is synthesized by the body and dwarfs the cholesterol content of any meal. Statins decrease body production of cholesterol, interfere with bile/fat digestion and lower lipid cholesterol levels. (Unfortunately, lowering lipid cholesterol levels has minimal impact on heart disease and the only impact of statins on cardiovascular disease is through weak anti-inflammatory side effects.) Pancreatic lipase removes two of the fatty acids from each triglyceride. The fatty acids (a.k.a. soap) and monoglyceride are absorbed by the intestinal cells and reformed into triglycerides that make their way to lymphatic lacteals and are dumped into the blood, where they circulate as chylomicrons surrounded in lipoprotein. Lipoprotein lipase binds to heparan sulfate on the surface of blood vessels and gradually removes fatty acids, until the diminished chylomicron is absorbed by the liver and exits as a VLDL. (Note that this is another connection between lipid metabolism and inflammation, since inflammation decreases heparan sulfate on cell surfaces. Heparan sulfate also mediates LDL binding to cells and amyloid stacking.)
Heparin-binding Domains
Plant Polysaccharides are Soluble Fiber and Food for Gut Flora
All that remains of food after the protein, fat and glycemic starch (glycogen) have been removed in the small intestines are plant cell wall polysaccharides, resistant starch, storage polysaccharides, e.g. inulin, plant beta-glucan, animal glycans, e.g. chondroitin sulfate and heparan sulfate, and insoluble fiber. The insoluble fiber passes on to be a minor contributor to the bulk of stools and the rest of the polysaccharide is potentially fermentable by gut flora into short chain fatty acids (formic, acetic, propionic, butyric acids). Some of the polysaccharides are simple repeating units of one or two sugars in long chains, but others are made of five to ten different sugars in complex branched structures. Simple repeating polysaccharides require just a few different enzymes for their initial synthesis and a few for their digestion. Thus, resistant starch can be digested by a couple of enzymes into glucose that can be used by most gut flora. Arabinogalactan, on the other hand, requires a dozen enzymes for plant synthesis and an equal number of hydrolytic enzymes to produce arabinose and galactose, which require further enzymes for metabolism in a select few of species of gut flora bacteria.
Resistant Starch as a Panacea
Food Intolerance/“Allergy” Indicates Missing Bacteria
Gut flora in general can produce several hundred different enzymes for digestion of diverse soluble fiber, but most soluble fiber polysaccharides can only be digested by certain bacteria and those bacteria increase, if the complementary fiber is present in the diet. If a fiber is absent from the diet, bacteria that specialize in digesting that polysaccharide will be eliminated. People living on diets limited to just a few types of soluble fiber can only digest those fibers and a shift in diet to other types of soluble fiber will lead to symptoms of dietary upset, such as bloating, gas production and food intolerance. Food intolerances reflect inadequate diversity in gut flora and a mismatch between bacteria and food. Food intolerances can be eliminated by repairing gut flora and the typical repair solution is eating homegrown fermented vegetables that provide the missing species of bacteria.
Paleo Gut Flora Repair
Immune Cells Develop in Response to Gut Bacteria
Most of the body’s immune cells are in the intestines. Cells of the immune system are constantly dividing in bones and the thymus gland, developing in the lining of the intestines and migrating to other tissues. Filamentous bacteria of the gut flora stimulate the development of aggressive immune cells that kill other cells that are infected with pathogens or viruses or are cancerous. Furrows perpendicular to the flow of food cultivate the growth of Clostridium species that ferment soluble fiber, e.g. resistant starch, and release butyric acid that stimulates the development of regulatory T cells, Tregs. It is the Tregs that control the aggressive immune cells and prevent attack on self (autoimmunity) or innocuous antigens (allergy). It appears that merely eating resistant starch, e.g. potato starch, with probiotics that contain butyric acid producing Clostridium bacteria may provide a cure for many autoimmune diseases.
Free the Animal: A Resistant Starch Primer for Newbies
Gut Biofilms Release Vitamins as Quorum Sensing Signals
The gut flora lines the intestines in numerous biofilm communities, which form from dozens of different species of bacteria that communicate by exchanging molecules called quorum sensing signals. These signals from the biofilms intimately attached to the lining of the intestines are vitamins. Thus, healthy gut flora are the major source of vitamins and other sources, such as fruits and vegetables are only needed, if the gut flora is damaged, e.g. by antibiotics.
Dr. Oz, Vitamins, Biofilms
Volume of Stools Reflects Gut Flora Fermenting Soluble Fiber
The bulk of bowel movements, stools, is bacteria, the compressed gut flora that accumulated in the colon while fermenting soluble fiber. We always hear that we need to eat fiber for regularity, but since insoluble fiber is only a minor contributor to stool volume and it is associated with anti-nutritive attributes, such as the binding and removal of zinc and iron by phytate, the fiber that counts for regularity is soluble fiber. Regularity results from the fermentation of soluble fiber polysaccharides producing short chain fatty acids, such as butyrate, that are the major source of energy for colon cells. And the growing bacteria in the colon provide most of the bulk of the hydrated stools. Inadequate dietary soluble fiber or damaged gut flora, dysbiosis, leave only dehydrated insoluble fiber and compact stools of constipation. Constipation can result from dehydration or excessive retention, but chronic constipation, even in the presence of adequate dietary soluble fiber, is an indication of damaged gut flora and an increased risk for diseases resulting from deficiencies of Treg production: autoimmune diseases and allergies. Constipation and associated autoimmune diseases can be cured by repairing gut flora and supplying adequate dietary soluble fiber.
Milk, Kefir and Gut Flora
Saturday, March 14, 2015
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Monday, March 9, 2015
What do I eat to build muscle
A common nutrition question for athletes is “how do I build muscle?” The most important thing to remember about building muscle is that it requires the training stimulus from the weight room along with adequate calories. Enough overall calories, not just in the form of protein, are needed for your body to have the energy to increase your lean mass. As a strength athlete, protein needs are increased slightly, but it may not be as much as you would think. A goal range of protein to be eaten throughout the day is 0.73-0.77g per pound. Eating a post-workout snack immediately after leaving the gym will help you see the effects of your training because it will be providing your body the nutrients it needs at the most effective time. Choose a snack that is a combination of carbohydrate and protein. An ideal portion of protein for a post-workout snack is around 10-20 grams. Any more than 20 grams of protein is not necessary and will not build any more muscle. Excess protein beyond will be broken down for storage rather than building extra muscle. Although protein shakes are convenient, they are not a necessity. They can be a convenient option, but whole foods give the same results and are often higher in other valuable nutrients such as vitamins and minerals.
Saturday, March 7, 2015
Sucralose Hazardous or Innocent A Review of the Review Part I Glucose Insulin GLP1 Sucralose Diabetes
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| Sweet, low and unhealthy? Is sucralose as bad as a recent review would suggest? |
First things first: What are we talking about?
As the press release informs us, an "extensive review published by Taylor & Francis"... stop, so here is our first hint. The authors of the press release are people from Taylor & Francis and have a vested interest in writing it in a way that will have people share the text and their name on the Internet (that worked pretty well, as you can see - even I am talking about it ;-)
This is part I of a multi-part series:
Sucralose, insulin, glucose, GLP-1
Appetite, Obesity & Gut Health
Cancer, Drug & Hormone Interact.
I know that Mark Sisson likes to says this, but this website is not written by a machine, but by a man who has the same "short" 24h days you have... basically, what I am trying to say is that I had to split this review of the review into a "trilogy" - and be honest, you wouldnt want an article thrice as long as this one, would you?
Based on hundreds of [...] publications?
While it is true that the review has 476 references, not all of them deal with sucralose and only few of them provide data that would by any means be relevant to the most important question of all: "Can sucralose consumption harm us". The statement "based on hundreds of [...] publications" is thus misleading, because when its used in conjunction with the word "review" people will interpret it as the number of relevant papers - or, even worse, of studies the data of which has been used in a systematic review. The paper at hand is yet everything but a systematic review - its a narrative one.
Next on the list of our "review with your critical thinking cap on the head" list are the following claims about the health / environmental effects of sucralose:
- Please note: I will address all the issues within this trilogy, but for today I will focus on the one with the asterisk (*). As you can see from the headlines in my preliminary outline above, the rest of the issues are going to follow, asap.alterations in insulin, blood glucose, and glucagon-like peptide 1 (GLP-1) levels,The best thing you can do if you want to make sure youre not going to miss a single article is to register for the SuppVersity Newsletter at the bottom of the page or - even better - like the SuppVersity Facebook Page and youll always be in the know.
- metabolism of sucralose in the gastrointestinal tract to metabolites whose identity and safety profile are unknown,
- induction of cyctochrome P450 and P-glycoprotein in the gastrointestinal tract to levels that may limit the bioavailability of therapeutic drugs,
- reduction in the number and balance of beneficial bacteria in the gastrointestinal tract,
- histopathological findings in gastrointestinal tract including lymphocytic infiltrates into epithelium, epithelial scarring, mild depletion of goblet cells and glandular disorganization in the,
- decomposition and generation of chloropropanols (a potentially toxic class of compounds) during baking, and
- mutagenic alterations using several types of biological assays
Claim I: Sucralose messes w/ blood glucose management
I have to admit I was very curious to see the evidence on which Schiffman & Rother base this claim and was pretty disappointed, when I saw an extensive list of rodent and cell model studies, like those by Jang et al. and Margolskee et al., in which human NCI-H716 cells (Jang. 2007) and mouse enteroendocrine cells (GLUTag; Margolskee. 2007) were used to support the claim that sucralose would lead to an increase in GLP-1 - which is, by the way you usually wont hear as an argument against artificial sweeter use ... anyways, we are going to see why later, for now it should suffice to say that this intrigued me.
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| In view of the physiological role of GLP-1 its by no means clear whether the mentioned increase is actually something to be afraid of (see "Eat More, Burn More and Lose Fat Like on Crack with GLP-1!? Roux-en-y Bypass Study Sheds a Whole New Light on Satiety(Hormone)-Induced Weight Loss" | learn more) |
The thing wed have to fear is thus not the release of GLP-1 (for a large majority of the increasingly overweight population this could actually be beneficial), but a "dysregulation" GLP-1, GIP, C-peptide, insulin, glucose, and so on and so forth....
I dont say that its impossible that this is going to happen, but by no we have no convincing evidence that it will and in view of the fact that a scarcity of glucose is not exactly something to be afraid of in this day and age, an increase in GLP-1 could actually be an advantage for the majority of SAD-dieters. Unfortunately, the real-world (=non-petri dish) evidence from a 2009 study by Ma et al. tells us that this is not going to happen in humans.
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| Figure 1: GLP 1 (left) + insulin (right) response in healthy individuals to sucrose, saline (control) or 80mg and 800mg sucralose (theoretically this would be as sweet as 48g and 480g of pure sugar; Ma. 2009). |
Granted: Even the authors cite evidence against the GLP-1 hyothesis
I know, not everyone is willing to briefly type "GLP1 subjects sucralose" into a search engine, wait for the results to pop up and follow the link to the previously cited study by Ma et al. I understand that, but if that was you, you would actually just have to scroll down to the bottom of sensationalist press release, I cited on Facebook and click on the link (or enter the doi) to the (free) full-text, to find the following line on page 402:
"Oral consumption of sucralose without co-administration of glucose (Brown et al.,In other words, contrary to the author(s) of the press release, Schiffman and Rother are well aware that their evidence is far from being conclusive. What I am not so certain about, though, is whether they are also aware that their reference to a study by Brown et al. from 2009, where the coningestion of sucralose with acesulfame-K in 240 ml of caffeine-free diet soda (Diet Rite cola) produced an increase in the GLP-1, but not insulin or glucose (see figure 2), could actually be interpreted as a highly beneficial result.
2011) produced no significant effect on blood glucose levels. Sucralose delivered by intraduodenal infusion in combination with glucose also exerted no marked effect on blood glucose or plasma GLP-1 (Ma et al., 2010)."
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| Figure 2: Glucose, insulin and GLP1 response to oral glucose tolerance test conducted 10min after the ingestion of 240 ml of caffeine-free diet soda (Diet Rite cola; boxes) or carbonated water (circles; Brown. 2009) |
reduced the fasting and 8h post-meal free fatty acid levels of type II diabetics by -25% and 30%,The WM-HDP ↔ GLP-1 ↔ fatty oxidation connection | reread "Waxy Maize Reloaded" read more - improved the 8h blood glucose levels,
- decreased the HbA1c value from 9.2% to 7.9%,
- normalized the levels of cell-toxic fructosamine,
- slowed down gastric emptying
- decreased their ravenous appetite,
- improved insulin sensitivity and β-cell function, and
- induced a -3% reduction in total body fat.
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| "Science Round-Up Seconds: The Pro-Insulinogenic Effect of Artificial Sweeteners + Mechanisms & Consequences" | more |
As far as centrally mediated effects are concerned, the upcoming installments of what began as a comment and became a series of articles on sucralose may provide at least some insights into potential long(er) term effects on blood glucose management. Derangements that occur in response to changes in the gut microbiome, endocrine system or toxic effects of sucralose or its byproducts would after all only become visible after weeks or months of chronic (high dose?) ingestion of this globally approved artificial sweetener.
- Brown, R. J., Walter, M., & Rother, K. I. (2009). Ingestion of diet soda before a glucose load augments glucagon-like peptide-1 secretion. Diabetes Care, 32(12), 2184-2186.
- Ceriello, A., Novials, A., Ortega, E., Canivell, S., La Sala, L., Pujadas, G., ... & Genovese, S. (2013). Vitamin C Further Improves the Protective Effect of Glucagon-Like Peptide-1 on Acute Hypoglycemia-Induced Oxidative Stress, Inflammation, and Endothelial Dysfunction in Type 1 Diabetes. Diabetes care, 36(12), 4104-4108.
- Fujita, Y., Wideman, R. D., Speck, M., Asadi, A., King, D. S., Webber, T. D., ... & Kieffer, T. J. (2009). Incretin release from gut is acutely enhanced by sugar but not by sweeteners in vivo. American Journal of Physiology-Endocrinology and Metabolism, 296(3), E473-E479.
- Jang, H. J., Kokrashvili, Z., Theodorakis, M. J., Carlson, O. D., Kim, B. J., Zhou, J., ... & Egan, J. M. (2007). Gut-expressed gustducin and taste receptors regulate secretion of glucagon-like peptide-1. Proceedings of the National Academy of Sciences, 104(38), 15069-15074.
- Ma, J., Bellon, M., Wishart, J. M., Young, R., Blackshaw, L. A., Jones, K. L., ... & Rayner, C. K. (2009). Effect of the artificial sweetener, sucralose, on gastric emptying and incretin hormone release in healthy subjects. American Journal of Physiology-Gastrointestinal and Liver Physiology, 296(4), G735-G739.
- Margolskee, R. F., Dyer, J., Kokrashvili, Z., Salmon, K. S., Ilegems, E., Daly, K., ... & Shirazi-Beechey, S. P. (2007). T1R3 and gustducin in gut sense sugars to regulate expression of Na+-glucose cotransporter 1. Proceedings of the National Academy of Sciences, 104(38), 15075-15080.
- Panjwani, N., Mulvihill, E. E., Longuet, C., Yusta, B., Campbell, J. E., Brown, T. J., ... & Drucker, D. J. (2013). GLP-1 receptor activation indirectly reduces hepatic lipid accumulation but does not attenuate development of atherosclerosis in diabetic male ApoE−/− mice. Endocrinology, 154(1), 127-139.
- Pettus, J., Hirsch, I., & Edelman, S. (2013). GLP-1 Agonists in Type 1 Diabetes. Clinical Immunology.
- Ren, X., Zhou, L., Terwilliger, R., Newton, S. S., & De Araujo, I. E. (2009). Sweet taste signaling functions as a hypothalamic glucose sensor. Frontiers in integrative neuroscience, 3.
- Schiffman, S. S., & Rother, K. I. (2013). Sucralose, A Synthetic Organochlorine Sweetener: Overview Of Biological Issues. Journal of Toxicology and Environmental Health, Part B, 16(7), 399-451.
- Schwartz, S., & DeFronzo, R. A. (2013). Is Incretin-Based Therapy Ready for the Care of Hospitalized Patients With Type 2 Diabetes? The time has come for GLP-1 receptor agonists!. Diabetes care, 36(7), 2107-2111.
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