Metabolism Damaging Foods
These days it’s all the rage to talk about metabolism damaging foods, and even though it’s popular to suggest that sugar kills metabolism, this is far from true. In fact it’s the opposite of the truth. Sugar is pro-metabolic, let me count the ways.
Sugar Is Fuel For Metabolism>>
Metabolism is the combination of biochemical interactions that take place in the body, as a means to ensuring proper function, utilizing food to provide energy, to enable rebuilding or regeneration, and to allow for waste removal.
Generally speaking, whether or not metabolism is able to function optimally, depends on the balance between exposure to stress (both internally and externally), and the availability of nutrition and fuel in order to meet that stress.
A stressed or slow metabolism (where provision of energy is insufficient, and the adaptive, defensive stress mechanisms are working overtime) can be mistaken for a fast metabolism, and it can run this way for long periods of time. But this is not the same as an optimally functioning thyroid energy metabolism, where stress is low, overall metabolic performance is high, and protection from degeneration and disease is robust.
Sugar is so important for the ongoing running of metabolic processes, that as soon as metabolism detects that not enough is able to be provided, stress related functions kick in to ensure that a backup is ready to go. Unfortunately this comes with a cost, involving the use of valuable tissue (including muscle, skin and organs) for energy, as well as a change in biochemical conditions which can in and of themselves, add to stress levels, and lead to further interference with optimal metabolism.
Sugar Is A Stress Antidote>>
It’s probably not too much of a shock to discover that many of the biochemical changes that begin to occur when metabolism is stressed, respond to the provision of sugar, by no longer being as necessary. When glycogen stores run low, the stress hormones cortisol and adrenaline, begin to rise, and this is often the beginning of interference with metabolism, which then leads to more stress. Sugar is known to lower the substances of stress. So in other words, the availability of sugar enables stress to go down.
Although it’s not always a black and white, immediate reversal back to optimal performance, it is fair to say that sugar is a remedy for stress. But ongoing exposure to the things that promote stress, can lead to changes in the function of metabolism, that can take time to create, and can be difficult to repair.
And to add to that, stress can have an impact that transfers from one generation to the next, and can interfere with the development of metabolism, and so metabolic function can be impeded from the beginning. This does not mean that the biological processes that keep the system going are different in every case, but it does mean that they can express themselves in a multitude of different ways depending on individual history and varying circumstances.
However you look at it though, sugar is necessary for optimal metabolic performance, and this only changes when the discussion moves to a different species, perhaps from a different planet. The problem is, that when metabolism has been damaged, the way the system deals with sugar can make it look like it is the sugar that is the problem, but there is always going to be a better explanation.
Sugar Supports Thyroid>>
Thyroid energy system function is at the heart of metabolism, to the extent that you can’t really talk about one without (at least indirectly) referring to the other. And you can’t really talk about a stress metabolism, without acknowledging that you are also saying that thyroid performance is sub-optimal.
Lack of availability of sugar prevents optimal thyroid function in many different ways, and it is not unscientific or irrational to suggest that sugar is a requirement for the proper functioning of thyroid metabolism, which is just another way of saying that sugar is pro-metabolic.
Sugar is one of the things that enables the conversion in the body of inactive thyroid hormone (T4) into active thyroid hormone (T3), and when this conversion is hampered, thyroid systems cannot run as effectively. In fact, when conversion is interfered with, this can itself become a circumstance which further inhibits thyroid metabolic function. For example, lack of T3 supply lowers thyroid performance, but interference with conversion also means that inactive thyroid hormone (T4) can accumulate in the system, which can by itself have powerful anti-metabolic effects.
On top of this, when stress is high and glycogen stores run low, many of the stress substances which begin to rise in response to this, cause additional interference with thyroid performance (including preventing optimal conversion of T4 to T3), and so a vicious circle of more stress, and greater interference with metabolism, can be set in motion.
Sugar Improves Digestion>>
When stress is high and metabolism is interfered with, digestion is one of the first things that suffers, and this fact is central to what can then go on to cause damage to the proper function of thyroid energy systems, promoting the ongoing stress state.
A slow or impeded digestive system allows for bacterial issues to build up, increasing exposure to many stress promoting, thyroid metabolism inhibiting things. Bacterial endotoxin is just one of these, although it is powerfully inflammatory and anti-metabolic.
Lack of sugar is directly involved in this process firstly because of the effect that insufficient availability of sugar has upon stress and metabolism, and hence upon digestive function. When stress rises, energy is redirected away from digestion in order to prioritize other systems that are required more for immediate survival.
Unfortunately, interference with metabolism, due to dietary problems and other stressors, can create a chronic state of stress, and chronic suppression of digestive function, even when there is no real immediate survival danger. This can then cause a situation where it becomes more difficult to assimilate nutrition, and where there is a buildup of stress promoting inflammatory things within the intestines, which then go on to interfere even more with metabolism and add to the stress levels.
To add insult to injury, endotoxin can directly interfere with the ability of cells to properly utilize sugar for metabolic function, and so it can be said that one of the things that can happen when sugar is restricted, can also lead to circumstances where there will be insufficient sugar for energy, even when there is sugar available for use as energy.
No matter what you eat, metabolic systems have developed to attempt to ensure the provision of what is needed for proper function, and sugar is one of the most important things. In this sense, how stressed metabolism becomes, also depends upon how easy it is for the system to get the things that are required. As an example, in general, it is far less costly for metabolism to get sugar from something that has lots of sugar in it, than it is to get it from something that is low in sugar and high in protein for instance, or high in all sorts of things that get in the way of the absorption of sugar.
White sugar itself is easy to digest and, in the context of a diet that provides sufficient protein and other nutrients, helps to provide energy without fueling bacterial inflammatory issues, which then helps to up-regulate the thyroid systems which provide energy and protect against bacterial issues. Sounds like a bargain.
Sugar Improves Liver Function>>
Proper liver function is crucial to metabolism, and when stress is rising and sugar is restricted many things begin to happen that interfere with the ability of the liver to do the things it does to enable optimal metabolic performance, and this then leads to suppression of thyroid metabolism, which then further inhibits the liver. Not a good idea.
Not only is the liver responsible for the provision of the majority of metabolically active thyroid hormone (T3) throughout the system, but it plays a major role in detoxification processes, including preparation for the removal of many of the stress substances which increase in circulation, when stress is high, metabolism is suppressed, and liver function is inhibited. Sugar provides the energy which is required in order for the liver to do these things optimally.
When stress goes up, and metabolism is sub-optimal, estrogen levels tend to rise, and estrogen plays a big part in the promotion of the inflammatory metabolic conditions. The liver prepares estrogen for excretion, and when sugar is restricted and liver performance is slow, estrogen levels tend to build up in circulation, and estrogen itself directly interferes with the ability of the liver to carry out detox functions.
The liver is also involved in the processes that protect against the buildup of the inflammatory, anti-metabolic stress substances, serotonin and nitric oxide, both of which also rise in response to interference with digestion and increasing exposure to bacterial endotoxin.
Slow digestion, and rising endotoxin (as well as the other inflammatory things that rise when digestion is slow) also adds to the stress load placed upon the liver, and so because lack of sugar can prevent proper digestion, this is another way that sugar can help the liver.
A good way to help reduce the toxic stress load coming from the digestive system and take the pressure off the liver so that it can start to function better and heal itself, is to do a cleanse. One of the most important things for liver and digestive system cleansing, is the provision of energy (combined with protein and other nutrients), in the easiest and least stressful way possible. Attempting to cleanse in a way that allows for metabolism to be inhibited can be counterproductive, as the cleansing organs (and metabolism in general) need to be functioning properly in order to reduce production of, and properly excrete toxins. This is why sugar is a necessary part of an effective cleanse. In fact, providing enough sugar (and some other requirements) for proper metabolic function, can be a little like doing a continuous cleanse.
Sugar Protects Against PUFAs>>
The polyunsaturated fats (PUFAs) and the substances that they break down into inside the body, suppress metabolic function in many different ways. They interfere with thyroid hormone availability and performance, they cause the stress substances to rise, they powerfully inhibit digestion and promote bacterial issues and they interfere with and damage the liver, promoting inflammation and degeneration. You could say that they are one of the most common metabolism damaging foods, although it is questionable whether they really are food for humans. Certainly not in the quantities which have only become a thing in far more recent times.
Sugar protects against the PUFAs in a number of different ways, but arguably the most important way is by suppressing stress and promoting metabolism. This is another one of those potential vicious circle type scenarios that can kick in when much of the sugar is purposefully removed from the diet.
By providing sugar for thyroid energy system function and by keeping stress at bay, the PUFAs can, at least to some degree, be prevented from being taken out of storage and brought into circulation as free fatty acids, where they cause a lot of damage to metabolic systems. At the same time, a high functioning metabolism assists with the safe removal of PUFAs via other means that do not have as much of an impact upon overall function.
The breakdown products of the PUFAs have been shown to be involved in the progression of inflammatory metabolic illness, and this includes heart disease, diabetes, cancer, autism, arthritis, MS, depression, alzheimer’s and an endless number of related conditions. This makes sugar a pretty important part of the diet, and not something to avoid intentionally.
Excess Sugar Can Be Turned Into Good Fats>>
Another way that sugar helps to protect against the PUFAs, and to assist with metabolic function, occurs if there is ever any excess which does not get used immediately for energy or as an addition to glycogen stores. Under these circumstances, sugar gets converted predominantly into saturated fats, which are protective against PUFAs, and have anti-inflammatory, pro-thyroid effects.
The only problem with this is that when sugar is available, and metabolism improves, it can be difficult to eat enough sugar in order to be able to have any excess left over for conversion into fat. And some people who have metabolic issues struggle to produce and store much excess fat too, and this can mean the stress metabolism can appear to be like a fast metabolism.
When healing metabolism in the beginning, saturated fat accumulation (from de novo lipogenesis) is probably more common, and there is reason to think that this can play a part in the processes that help reduce stress and inflammation (like a buffer) and eventually enable thyroid metabolism to start to function at a higher level.
Contrary to most popular dietary health advice today, a reasonably low fat diet, with enough quality protein, as well as lots of vitamins and plenty of sugar, can provide everything required (including some synthesis of fat) in order to maintain optimal metabolic performance and keep stress at bay. Including some saturated fats from butter or coconut oil and the like, can be helpful for lowering stress and improving metabolism in the beginning, even if there is some weight gain.
Sugar Increases Cholesterol Production>>
Even though you might be thinking otherwise, you need cholesterol for the proper functioning of metabolism and for protection against stress, and the first step is to ensure that you are able to produce enough. Sugar assists with cholesterol production in numerous ways.
Equally importantly, by helping to lower stress and improve metabolic function, sugar also assists with the conversion of cholesterol into the protective anti-inflammatory hormones, pregnenolone, progesterone, DHEA and testosterone.
It probably isn’t a stretch to argue that by improving the effectiveness of metabolism and by lowering stress, provision of enough sugar can gradually, over time, lead to a reduction in the quantity of cholesterol (and of the specialized protective hormones) needed, and as such, a reduction in sugar requirements. On the other hand, increased functionality can probably also increase energy requirements, so it could go either way.
Sugar Protects Against Inflammation>>
It’s very common to hear that sugar consumption is inflammatory. Luckily this is predominantly a misinterpretation of how metabolism functions, as it would be strange if something needed to improve metabolic function and lower stress, caused an increase in inflammation, especially since dysregulated inflammatory processes are connected to basically all disease.
The confusion probably arises because of the connection between blood sugar dysregulation issues, like for instance hyperglycemia and insulin resistance, and chronic, systemic inflammation. The good news is that it is mostly PUFAs (and some other highly stressful and inflammatory things), not sugar consumption per se, that causes blood sugar dysregulation, and so there’s nothing to stress about. It all makes sense as it is intended to.
Endotoxin is another thing that leads to inflammation (even more so in combination with too much of the PUFAs), and the relationship endotoxin has with stress, lack of sugar, and thyroid suppression, is an important link in the chain which explains the real causes of chronic inflammation and metabolic illness.
Iron dysregulation has been shown to be closely involved with metabolic disease, and results in part from excessive iron intake and from too much exposure to the PUFAs and endotoxin (and stress substances like estrogen), which interact to powerfully promote oxidative stress and inflammation. Sugar, by reducing stress and improving thyroid energy metabolism, helps to protect against iron related issues, adding to the list of potential anti-inflammatory effects.
Sugar Reduces Lactate Production And Insulin Resistance>>
Regardless of the fact that a lot of people are promoting the idea, you don’t really want to use the stress of sugar restriction for too long, as a way to improve metabolic health. It’s basically a contradiction, and although it can feel good for a while, the long term consequences can be dire, particularly when metabolism is already damaged.
Increased production of lactate is associated with disease progression and mortality, and occurs as a result of interference with oxidative metabolism. It’s important to keep in mind that a high lactate producing metabolism is a stress metabolism, and this makes sense in the context of all the other things that promote stress and blood sugar dysregulation. It also makes the very popular idea that sugar causes diabetes, extremely illogical and unlikely.
However you approach it, the end result is roughly the same. PUFAs interfere with the use of sugar, and lack of sugar increases circulation of the PUFAs. Insulin resistance promotes stress, which increases lactic acid production, and excess lactate can promote insulin resistance and stress. Endotoxin causes inflammation and interferes with thyroid energy metabolism, and a suppressed thyroid, and chronic inflammatory state, increases endotoxin exposure. Sugar protects against stress, insulin resistance, lactate, inflammation, and metabolic dysfunction, but that doesn’t mean you can just eat some sugar and instantaneously make everything go back to normal. Still, when I hear talk about paradoxes, I’m inclined to believe it’s just another way to justify the continuation of a false theory.
Sugar Increases Carbon Dioxide Production>>
I’m not sure if anybody has tried to directly argue that the production of energy is bad for health, but it probably won’t be too long. In the mean time, it’s worth noting that oxidative metabolism (thyroid energy system metabolism), which involves the breakdown of sugar to carbon dioxide (CO2), is the best way to produce energy under normal circumstances.
Sure, it’s important to have a backup for extreme conditions of stress and starvation, and one of the things that happens in order to make this possible, is the suppression of metabolism as a means to reducing energy requirements. But in general, it’s supposed to be a defense mechanism, for survival, and unfortunately it comes with a long term metabolic cost.
When there is a lack of sugar availability, metabolism slows down, and more of the fat stores are used to produce energy, but this generates less CO2 than sugar, which also means that metabolism slows, and stress goes up. Increasing sugar and decreasing fat, is one way to improve CO2 production and up-regulate metabolism, and increasing CO2 levels (bag breathing for instance), is a good way to lower stress, decrease fat circulation and increase sugar metabolism. Improving CO2 levels protects against all of the substances of stress, including lactate, and increasing stress is by definition an indication that CO2 levels are reduced. Sugar is therefore, anti-stress and pro-metabolic.
Sugar Helps Protect Against Obesity And Illness>>
Alzheimer’s, depression, diabetes, cancer, and the inflammatory metabolic illnesses in general do not only happen to people who are obese, and obesity is not caused by excessive sugar consumption.
The link between obesity and the metabolic illnesses, is biochemical stress and inflammation. The things that promote excessive metabolic stress and inflammation, and interfere with energy production, prevent the proper use of sugar. I’m not a doctor or nutritionist, and none of this is meant as health or dietary advice, but it makes sense to me, that dealing with stress related issues, by taking sugar consumption out of the picture, only makes matters worse over the long term.
There are lots of things in the environment and in modern diets that are harmful to metabolic function, and many of them can no longer be easily avoided. From what I have come to understand, the PUFAs are one of the main things that have become ubiquitous in recent decades, and one of the things that can be largely removed.
Inflammation, and oxidative stress, and insulin resistance, and HPA dysfunction, and endotoxemia, and iron dysregulation, and hypothyroidism, and cholesterol oxidation, and chronic hypoxia, and many things that result from ongoing metabolic stress, and are known to promote disease, are closely associated with excessive exposure to the PUFAs and their breakdown products. Some say PUFAs are practically a necessary component for inflammatory disease.
Sugar isn’t the solution to everything, and often will not help as much as it can when other things are out of balance. Liver function, nutrient deficiencies, protein requirements, nervous system issues, lack of light, stressful environments, and lots of other things get in the way of thyroid metabolism and overall function. But sugar is very important, and is something that keeps the PUFAs, metabolic dysfunction, and stress in general, at bay. If you want to quit something, for starters, quit PUFAs.
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Physiol Rep. 2017 Feb;5(4). pii: e13171. Suppressed sympathetic outflow to skeletal muscle, muscle thermogenesis, and activity energy expenditure with calorie restriction. Almundarij TI, Gavini CK, Novak CM.
J Clin Endocrinol Metab. 2015 Jun;100(6):2239-47. Excessive Sugar Consumption May Be a Difficult Habit to Break: A View From the Brain and Body. Tryon MS, Stanhope KL, Epel ES, Mason AE, Brown R, Medici V, Havel PJ, Laugero KD.
Ciba Found Symp. 1982;87:168-91. Review. Some hormonal influences on glucose and ketone body metabolism in normal human subjects. Johnston DG, Pernet A, McCulloch A, Blesa-Malpica G, Burrin JM, Alberti KG.
BMJ Journals, Volume 8, Issue 2. Does high-carbohydrate intake lead to increased risk of obesity? A systematic review and meta-analysis. Kurt Sartorius, Benn Sartorius, Thandinkosi E Madiba, Cristina Stefan.
Diabetes Care. 2012 Feb;35(2):375-82. High Fat Intake Leads to Acute Postprandial Exposure to Circulating Endotoxin in Type 2 Diabetic Subjects. Harte AL, Varma MC, Tripathi G, McGee KC, Al-Daghri NM, Al-Attas OS, Sabico S, O’Hare JP, Ceriello A, Saravanan P, Kumar S, McTernan PG.
Immunity. 2016 Apr 19;44(4):833-46. Human Monocytes Engage an Alternative Inflammasome Pathway. Gaidt MM, Ebert TS, Chauhan D, Schmidt T, Schmid-Burgk JL, Rapino F, Robertson AA, Cooper MA, Graf T, Hornung V.
Mol Nutr Food Res. 2015 Aug;59(8):1563-72. High fat challenges with different fatty acids affect distinct atherogenic gene expression pathways in immune cells from lean and obese subjects. Esser D, van Dijk SJ, Oosterink E, Lopez S, Müller M, Afman LA.
Am J Clin Nutr. 2004 Apr;79(4):682-90. Increase in intranuclear nuclear factor κB and decrease in inhibitor κB in mononuclear cells after a mixed meal: evidence for a proinflammatory effect. Aljada A, Mohanty P, Ghanim H, Abdo T, Tripathy D, Chaudhuri A, Dandona P.
Am J Physiol Regul Integr Comp Physiol. 2007 Nov;293(5):R1864-74. Social stress and recovery: implications for body weight and body composition. Tamashiro KL, Nguyen MM, Ostrander MM, Gardner SR, Ma LY, Woods SC, Sakai RR.
Br J Nutr. 2014 Jan 28;111(2):342-52. Dietary intake of carbohydrates and risk of type 2 diabetes: the European Prospective Investigation into Cancer-Norfolk study. Ahmadi-Abhari S, Luben RN, Powell N, Bhaniani A, Chowdhury R, Wareham NJ, Forouhi NG, Khaw KT.
J Clin Endocrinol Metab. 1996. Fasting as a metabolic stress paradigm selectively amplifies cortisol secretory burst mass and delays the time of maximal nyctohemeral cortisol concentrations in healthy men. Bergendahl M, et al.
J Clin Endocrinol Metab. 2005 Jul;90(7):4019-24. Small differences in thyroid function may be important for body mass index and the occurrence of obesity in the population. Knudsen N, Laurberg P, Rasmussen LB, Bülow I, Perrild H, Ovesen L, Jørgensen T.
J Clin Endocrinol Metab. 2000 Dec;85(12):4515-9. Acute fructose administration decreases the glycemic response to an oral glucose tolerance test in normal adults. Moore MC, Cherrington AD, Mann SL, Davis SN.
Cell Cycle. 2011 Apr 15;10(8):1271-86. Ketones and lactate increase cancer cell “stemness”, driving recurrence, metastasis and poor clinical outcome in breast cancer. Martinez-Outschoorn UE, Prisco M, Ertel A, Tsirigos A, Lin Z, Pavlides S, Wang C, Flomenberg N, Knudsen ES, Howell A, Pestell RG, Sotgia F, Lisanti MP.
Int J Gen Med. 2011 Jan 7;4:29-33. End-tidal CO2 levels lower in subclinical and overt hypothyroidism than healthy controls; no relationship to thyroid function tests. Ansarin K, Niroomand B, Najafipour F, Aghamohammadzadeh N, Niafar M, Sharifi A, Shoja MM.
Cancer Prev Res (Phila). 2017 Apr;10(4):235-243. Metabolic Obesity, Adipose Inflammation and Elevated Breast Aromatase in Women with Normal Body Mass Index. Iyengar NM, Brown KA, Zhou XK, Gucalp A, Subbaramaiah K, Giri DD, Zahid H, Bhardwaj P, Wendel NK, Falcone DJ, Wang H, Williams S, Pollak M, Morrow M, Hudis CA, Dannenberg AJ.
Diabetes. 2002 Jul;51(7):2287-93. Hyperketonemia increases tumor necrosis factor-alpha secretion in cultured U937 monocytes and Type 1 diabetic patients and is apparently mediated by oxidative stress and cAMP deficiency. Jain SK, Kannan K, Lim G, McVie R, Bocchini JA Jr.
Sci Rep. 2016 Oct 6;6:34909. Hypothalamic sensing of ketone bodies after prolonged cerebral exposure leads to metabolic control dysregulation. Carneiro L, Geller S, Hébert A, Repond C, Fioramonti X, Leloup C, Pellerin L.
Carcinogenesis, Volume 20, Issue 11, November 1999, Pages 2095–2100. Corn oil rapidly activates nuclear factor-κB in hepatic Kupffer cells by oxidant-dependent mechanisms. Ivan Rusyn, Cynthia A. Bradham, Leslie Cohn, Robert Schoonhoven, James A. Swenberg, David A. Brenner, Ronald G. Thurman.
Arch Gen Psychiatry. 1998 Feb;55(2):130-6. Plasma cortisol concentrations preceding lactate-induced panic. Psychological, biochemical, and physiological correlates. Coplan JD, Goetz R, Klein DF, Papp LA, Fyer AJ, Liebowitz MR, Davies SO, Gorman JM.
J Clin Invest. 2010 Jan;120(1):142-56. Pharmacologic inhibition of fatty acid oxidation sensitizes human leukemia cells to apoptosis induction. Samudio I, Harmancey R, Fiegl M, Kantarjian H, Konopleva M, Korchin B, Kaluarachchi K, Bornmann W, Duvvuri S, Taegtmeyer H, Andreeff M.
PLoS One. 2013;8(1):e55113. Lactate and risk of incident diabetes in a case-cohort of the atherosclerosis risk in communities (ARIC) study. Juraschek SP, Shantha GP, Chu AY, Miller ER 3rd, Guallar E, Hoogeveen RC, Ballantyne CM, Brancati FL, Schmidt MI, Pankow JS, Young JH.
J Nutr Biochem. 2015 Apr;26(4):319-26. A high-fat diet rich in corn oil reduces spontaneous locomotor activity and induces insulin resistance in mice. Wong CK, Botta A, Pither J, Dai C, Gibson WT, Ghosh S.
JAMA. 2012 Jun 27;307(24):2627-34. Effects of Dietary Composition on Energy Expenditure During Weight-Loss Maintenance. Ebbeling CB, Swain JF, Feldman HA, Wong WW, Hachey DL, Garcia-Lago E, Ludwig DS.
Antioxid Redox Signal. 2012 Jun 1;16(11):1264-84. Warburg Meets Autophagy: Cancer-Associated Fibroblasts Accelerate Tumor Growth and Metastasis via Oxidative Stress, Mitophagy, and Aerobic Glycolysis. Pavlides S, Vera I, Gandara R, Sneddon S, Pestell RG, Mercier I, Martinez-Outschoorn UE, Whitaker-Menezes D, Howell A, Sotgia F, Lisanti MP.
Neurology. 2003 Mar 25;60(6):1026-9. Elevated polyunsaturated fatty acids in blood serum obtained from children on the ketogenic diet. Fraser DD, Whiting S, Andrew RD, Macdonald EA, Musa-Veloso K, Cunnane SC.
FASEB Journal, Vol. 31, No. 1 supplement, April 2017. The Ketogenic Diet Alters Endocrine Regulation of Energy Metabolism in Ultra-Endurance Athletes. Vincent J Miller, Parker N Hyde, Ryan Dickerson, Richard A LaFountain, Carl M Maresh, William J Kraemer, and Jeff S Volek.
Proc Natl Acad Sci U S A. 2009 Sep 8;106(36):15418-23. Vascular effects of a low-carbohydrate high-protein diet. Foo SY, Heller ER, Wykrzykowska J, Sullivan CJ, Manning-Tobin JJ, Moore KJ, Gerszten RE, Rosenzweig A.
Nat Commun. 2016 Mar 1;7:10634. Chronic stress in mice remodels lymph vasculature to promote tumour cell dissemination. Le CP, Nowell CJ, Kim-Fuchs C, Botteri E, Hiller JG, Ismail H, Pimentel MA, Chai MG, Karnezis T, Rotmensz N, Renne G, Gandini S, Pouton CW, Ferrari D, Möller A, Stacker SA, Sloan EK.
Am J Clin Nutr. 2017 Aug;106(2):506-518. Fructose replacement of glucose or sucrose in food or beverages lowers postprandial glucose and insulin without raising triglycerides: a systematic review and meta-analysis. Evans RA, Frese M, Romero J, Cunningham JH, Mills KE.
The Journal of Clinical Endocrinology & Metabolism, Volume 92, Issue 11, 1 November 2007, Pages 4480–4484. Dietary Macronutrient Content Alters Cortisol Metabolism Independently of Body Weight Changes in Obese Men. Roland H. Stimson, Alexandra M. Johnstone, Natalie Z. M. Homer, Deborah J. Wake, Nicholas M. Morton, Ruth Andrew, Gerald E. Lobley, Brian R. Walker.
Med Hypotheses. 2008;70(2):298-304. Chronic cellular hypoxia as the prime cause of cancer: what is the de-oxygenating role of adulterated and improper ratios of polyunsaturated fatty acids when incorporated into cell membranes? Peskin BS, Carter MJ.
Dev Cell. 2016 Mar 7;36(5):540-9. Amino acids rather than glucose account for the majority of cell mass in proliferating mammalian cells. Hosios AM, Hecht VC, Danai LV, Johnson MO, Rathmell JC, Steinhauser ML, Manalis SR, Vander Heiden MG.
Nutrients. 2017 Feb 20;9(2). pii: E167. Fructose and Sucrose Intake Increase Exogenous Carbohydrate Oxidation during Exercise. Trommelen J, Fuchs CJ, Beelen M, Lenaerts K, Jeukendrup AE, Cermak NM, van Loon LJ.
J Endocrinol. 2015 Jun;225(3):147-58. 11β-HSD1 reduces metabolic efficacy and adiponectin synthesis in hypertrophic adipocytes. Koh EH, Kim AR, Kim H, Kim JH, Park HS, Ko MS, Kim MO, Kim HJ, Kim BJ, Yoo HJ, Kim SJ, Oh JS, Woo CY, Jang JE, Leem J, Cho MH, Lee KU.
Cell Rep. 2015 Jun 16;11(10):1529-34. Dietary protein to carbohydrate ratio and caloric restriction: comparing metabolic outcomes in mice. Solon-Biet SM, Mitchell SJ, Coogan SC, Cogger VC, Gokarn R, McMahon AC, Raubenheimer D, de Cabo R, Simpson SJ, Le Couteur DG.
PLoS One. 2015 Jul 22;10(7):e0132672. Soybean Oil Is More Obesogenic and Diabetogenic than Coconut Oil and Fructose in Mouse: Potential Role for the Liver. Deol P, Evans JR, Dhahbi J, Chellappa K, Han DS, Spindler S, Sladek FM.
Metabolism. 1995 May;44(5):645-51. Differential effects of fat and sucrose on the development of obesity and diabetes in C57BL/6J and A/J mice. Surwit RS, Feinglos MN, Rodin J, Sutherland A, Petro AE, Opara EC, Kuhn CM, Rebuffé-Scrive M.
Am J Physiol Endocrinol Metab. 2016 Jul 1;311(1):E56-68. Glucocorticoid antagonism limits adiposity rebound and glucose intolerance in young male rats following the cessation of daily exercise and caloric restriction. Teich T, Dunford EC, Porras DP, Pivovarov JA, Beaudry JL, Hunt H, Belanoff JK, Riddell MC.
Diabetes. 2005 Dec;54(12):3458-65. Free Fatty Acids Produce Insulin Resistance and Activate the Proinflammatory Nuclear Factor-κB Pathway in Rat Liver. Boden G, She P, Mozzoli M, Cheung P, Gumireddy K, Reddy P, Xiang X, Luo Z, Ruderman N.
Diabetes Care. 2010 May;33(5):991-7. Differential Effects of Cream, Glucose, and Orange Juice on Inflammation, Endotoxin, and the Expression of Toll-Like Receptor-4 and Suppressor of Cytokine Signaling-3. Deopurkar R, Ghanim H, Friedman J, Abuaysheh S, Sia CL, Mohanty P, Viswanathan P, Chaudhuri A, Dandona P.
Metabolism. 2012 Mar;61(3):395-406. Arachidonic acid and docosahexaenoic acid supplemented to an essential fatty acid-deficient diet alters the response to endotoxin in rats. Ling PR, Malkan A, Le HD, Puder M, Bistrian BR.
Diabetol Metab Syndr. 2010 Jun 23;2:43. Chronic consumption of fructose rich soft drinks alters tissue lipids of rats. Botezelli JD, Dalia RA, Reis IM, Barbieri RA, Rezende TM, Pelarigo JG, Codogno J, Gonçalves R, Mello MA.
Nature Medicine volume 21, pages166–172(2015). Inhibiting peripheral serotonin synthesis reduces obesity and metabolic dysfunction by promoting brown adipose tissue thermogenesis. Justin D Crane, Rengasamy Palanivel, Emilio P Mottillo, Adam L Bujak, Huaqing Wang, Rebecca J Ford, Andrew Collins, Regje M Blümer, Morgan D Fullerton, Julian M Yabut, Janice J Kim, Jean-Eric Ghia, Shereen M Hamza, Katherine M Morrison, Jonathan D Schertzer, Jason R B Dyck, Waliul I Khan & Gregory R Steinberg.
Med Sci Sports Exerc. 2011 Oct;43(10):1964-71. Fructose and galactose enhance postexercise human liver glycogen synthesis. Décombaz J, Jentjens R, Ith M, Scheurer E, Buehler T, Jeukendrup A, Boesch C.
J Cereb Blood Flow Metab. 2013 Oct;33(10):1493-9. Why does brain metabolism not favor burning of fatty acids to provide energy? – Reflections on disadvantages of the use of free fatty acids as fuel for brain. Schönfeld P, Reiser G.
J Biol Chem. 2005 Oct 21;280(42):35361-71. JNK and tumor necrosis factor-alpha mediate free fatty acid-induced insulin resistance in 3T3-L1 adipocytes. Nguyen MT, Satoh H, Favelyukis S, Babendure JL, Imamura T, Sbodio JI, Zalevsky J, Dahiyat BI, Chi NW, Olefsky JM.
J Am Geriatr Soc. 2003. Low total cholesterol and increased risk of dying: are low levels clinical warning signs in the elderly? Results from the Italian Longitudinal Study on Aging. Brescianini S, et al.
Crit Care. 2010;14(1):R13. Brain metabolism is significantly impaired at blood glucose below 6 mM and brain glucose below 1 mM in patients with severe traumatic brain injury. Meierhans R, Béchir M, Ludwig S, Sommerfeld J, Brandi G, Haberthür C, Stocker R, Stover JF.
Endocrine Reviews, Volume 31, Issue 6, 1 December 2010, Pages 817–844, Gut Microbiota, Lipopolysaccharides, and Innate Immunity in the Pathogenesis of Obesity and Cardiovascular Risk. Melania Manco, Lorenza Putignani, Gian Franco Bottazzo.
Int J Epidemiol. 2010 Dec;39(6):1647-55. Association of blood lactate with type 2 diabetes: the Atherosclerosis Risk in Communities Carotid MRI Study. Crawford SO, Hoogeveen RC, Brancati FL, Astor BC, Ballantyne CM, Schmidt MI, Young JH.
Am J Clin Nutr. 2010 Apr;91(4):940-9. Orange juice neutralizes the proinflammatory effect of a high-fat, high-carbohydrate meal and prevents endotoxin increase and Toll-like receptor expression. Ghanim H, Sia CL, Upadhyay M, Korzeniewski K, Viswanathan P, Abuaysheh S, Mohanty P, Dandona P.
Nutr Rev. 2003 May;61(5 Pt 2):S27-33. Review. Effects of a high-sucrose diet on body weight, plasma triglycerides, and stress tolerance. Kanazawa M, Xue CY, Kageyama H, Suzuki E, Ito R, Namba Y, Osaka T, Kimura S, Inoue S.
Am J Physiol Endocrinol Metab. 2002 Aug;283(2):E233-40. Lactate induces insulin resistance in skeletal muscle by suppressing glycolysis and impairing insulin signaling. Choi CS, Kim YB, Lee FN, Zabolotny JM, Kahn BB, Youn JH.
Diabetes. 2010 Jun;59(6):1349-57. Mechanisms of Insulin Resistance After Insulin-Induced Hypoglycemia in Humans: The Role of Lipolysis. Lucidi P, Rossetti P, Porcellati F, Pampanelli S, Candeloro P, Andreoli AM, Perriello G, Bolli GB, Fanelli CG.
J Diabetes Res. 2015;2015:102054. Plasma Lactate Levels Increase during Hyperinsulinemic Euglycemic Clamp and Oral Glucose Tolerance Test. Berhane F, Fite A, Daboul N, Al-Janabi W, Msallaty Z, Caruso M, Lewis MK, Yi Z, Diamond MP, Abou-Samra AB, Seyoum B.
Ann Intern Med. 2012 Feb 21;156(4):291-304. Effect of fructose on body weight in controlled feeding trials: a systematic review and meta-analysis. Sievenpiper JL, de Souza RJ, Mirrahimi A, Yu ME, Carleton AJ, Beyene J, Chiavaroli L, Di Buono M, Jenkins AL, Leiter LA, Wolever TM, Kendall CW, Jenkins DJ.
Am J Physiol Regul Integr Comp Physiol. 2003 Jun;284(6):R1631-5. An oxidized metabolite of linoleic acid stimulates corticosterone production by rat adrenal cells. Bruder ED, Ball DL, Goodfriend TL, Raff H.
Diabetes Care. 2012 Jul;35(7):1611-20. Effect of fructose on glycemic control in diabetes: a systematic review and meta-analysis of controlled feeding trials. Cozma AI, Sievenpiper JL, de Souza RJ, Chiavaroli L, Ha V, Wang DD, Mirrahimi A, Yu ME, Carleton AJ, Di Buono M, Jenkins AL, Leiter LA, Wolever TM, Beyene J, Kendall CW, Jenkins DJ.
Bosn J Basic Med Sci. 2010 Feb;10(1):83-8. Lactate dehydrogenase and oxidative stress activity in primary open-angle glaucoma aqueous humour. Jovanovic P, Zoric L, Stefanovic I, Dzunic B, Djordjevic-Jocic J, Radenkovic M, Jovanovic M.
Obes Facts. 2012;5(3):384-92. Rise in plasma lactate concentrations with psychosocial stress: a possible sign of cerebral energy demand. Kubera B, Hubold C, Otte S, Lindenberg AS, Zeiss I, Krause R, Steinkamp M, Klement J, Entringer S, Pellerin L, Peters A.
J Neuropathol Exp Neurol. 2017 Jun 1;76(6):467-478. Oxidative Injury and Iron Redistribution Are Pathological Hallmarks of Marmoset Experimental Autoimmune Encephalomyelitis. Dunham J, Bauer J, Campbell GR, Mahad DJ, van Driel N, van der Pol SMA, ‘t Hart BA, Lassmann H, Laman JD, van Horssen J, Kap YS.
J Diabetes Res. 2015;2015:102054. Plasma Lactate Levels Increase during Hyperinsulinemic Euglycemic Clamp and Oral Glucose Tolerance Test. Berhane F, Fite A, Daboul N, Al-Janabi W, Msallaty Z, Caruso M, Lewis MK, Yi Z, Diamond MP, Abou-Samra AB, Seyoum B.
Free Radic Biol Med. 2005 Apr 1;38(7):882-9. Effects of oxidative stress on adiponectin secretion and lactate production in 3T3-L1 adipocytes. Soares AF, Guichardant M, Cozzone D, Bernoud-Hubac N, Bouzaïdi-Tiali N, Lagarde M, Géloën A.
The Journal of Clinical Endocrinology & Metabolism, Volume 90, Issue 1, 1 January 2005, Pages 409–413. Resting Metabolic Rate and Respiratory Quotient in Human Longevity. M. R. Rizzo, D. Mari, M. Barbieri, E. Ragno, R. Grella, R. Provenzano, I. Villa, K. Esposito, D. Giugliano, G. Paolisso
Biol Psychiatry. 2015 Apr 1;77(7):653-60. Daily Stressors, Past Depression, and Metabolic Responses to High-Fat Meals: A Novel Path to Obesity. Kiecolt-Glaser JK, Habash DL, Fagundes CP, Andridge R, Peng J, Malarkey WB, Belury MA.
Ann Neurol. 1990 Jul;28(1):57-64. Selective hypometabolism in the inferior frontal lobe in depressed patients with Parkinson’s disease. Mayberg HS, Starkstein SE, Sadzot B, Preziosi T, Andrezejewski PL, Dannals RF, Wagner HN Jr, Robinson RG.
The American Journal of Clinical Nutrition, Volume 100, Issue 4, October 2014, Pages 1133–1138. Higher fructose intake is inversely associated with risk of nonalcoholic fatty liver disease in older Finnish adults. Noora Kanerva, Samuel Sandboge, Niina E Kaartinen, Satu Männistö, Johan G Eriksson.
Free Radic Res. 2012 Jun;46(6):758-65. Fatty liver induced by free radicals and lipid peroxidation. Morita M, Ishida N, Uchiyama K, Yamaguchi K, Itoh Y, Shichiri M, Yoshida Y, Hagihara Y, Naito Y, Yoshikawa T, Niki E.
Front Neuroenergetics. 2012 Mar 2;4:3. Brain glycogen—new perspectives on its metabolic function and regulation at the subcellular level. Obel LF, Müller MS, Walls AB, Sickmann HM, Bak LK, Waagepetersen HS, Schousboe A.
Diabetes Metab. 2005 Apr;31(2):178-88. Consumption of carbohydrate solutions enhances energy intake without increased body weight and impaired insulin action in rat skeletal muscles. Ruzzin J, Lai YC, Jensen J.
Amyotroph Lateral Scler Other Motor Neuron Disord. 2002 Jun;3(2):57-62. Impaired oxidative metabolism and lipid peroxidation in exercising muscle from ALS patients. Siciliano G, D’Avino C, Del Corona A, Barsacchi R, Kusmic C, Rocchi A, Pastorini E, Murri L.