Burn the Fat – Part 1

/Burn the Fat – Part 1
Burn the Fat – Part 1 2016-10-16T16:41:16+00:00

Burn The Fat

Part 1: Understanding fat gain and the role of fructose and uric acid

Written by: Joachim Bartoll
Classic Muscle Newsletter, June 2015 (issue #10)


This is a teaser of Burn The Fat, containing one third of part 1!
You can access the full-length article and all forthcoming parts by subscribing - starting at only 4.99 USD/month!


Burn The Fat article-series covers pretty much everything you need to know to be successful – whether it’s about lowering your weight to regain health, getting ready for a photo shoot or competing in bodybuilding. Although the series is based on my previously published 4-part series called Fettförbränning, it’s much more than a translation. It’s an updated and heavily expanded version – almost twice the size! Fettförbränning was written during 2012 and 2013 and was originally based on some of my drafts from a book started back in 2010. The first three parts were published by MM Sports, while the fourth part was published in Body Science Magazine and in its full length on my blog and here on The Classic Muscle Newsletter.

Before we begin

This series will contain the following parts:

Part 1: Looking at our evolution and understanding the mechanics of fat gain.

Part 2: Understanding how the body use fat for energy, looking at various diets and what really matters.

Part 3: Fasting and meal frequency. Understanding insulin, insulin resistance and glucagon.

Part 4: A look at the thyroid hormones, understanding your metabolism, how to repair it and a look into adiponektin and leptin.

Part 5: Understanding your body’s limitations, why fat loss slows down and/or stalls and why you should increase your calories during a diet.

Part 6: More about hormones, problem spots and competing totally shredded.

I guess we all know about the laws of thermodynamics and that you need to spend more energy (calories) than you ingest to use stored energy (fat) as a substitute for the lack of consumed energy. In other words, you need to burn more calories than you consume in order to tap into your fat stores and burn body fat.
Although this law is universal, there’s so much more going on that a lot of people simply lose focus on what’s important and what really makes a difference. At the same time, there’s so much confusion about how the body works and why it sometimes don’t seem to work as intended.

In this fat-burning series, I’ll do my best to break it all down and explain the most important bits. The first part will deal with some of the basics, but also some of the most significant underlying causes of the fat epidemic we’ve been witnessing the last 40 years.
Although the main culprit to fat gain is simply consuming more energy than you spend, there’s a lot more going on, such as inflammation, insulin resistance, leptin resistance and all the underlying hormonal imbalances caused by weight gain and poor food choices.
If you understand what happens in our bodies as we gain fat and what harm some food choices can cause, it becomes easier to correct the underlying problems and improve health and drop the weight.
Simply eating less is not always the answer. New studies from the last couple of years challenge the long-standing dogma that "a calorie is just a calorie", and suggest that the metabolic effects of food may matter as much, or even more, then its energy content.

A full list of +30 references and suggested reading is available at the bottom of the article. I’ve also included new research that strengthens my conclusions from the original articles published in 2012 and 2013.

The mechanics of fat storage

To understand why people get obese, why they develop metabolic syndrome and why some have trouble losing weight, we need to look at our history and evolution. We can also learn a lot by observing animals and how they gain weight in order to prepare for winter or migration. The mechanics are striking similar.

Animals prepare for periods of food shortage not only by storing a lot of fat, but by becoming insulin resistant, leptin resistant and even pre-diabetic. Some species even develop metabolic syndrome to help them survive (metabolic syndrome is a disorder of energy utilization and storage).

While becoming fat is highly regulated and most of the time scheduled in animals, it seems unrelated with what we can observe in humans today. Or is it?
People who get obese does not normally over consume to prepare themselves for famine, but the underlying principles might still be the same.
Many scientists believes that those of us who are becoming obese and insulin resistant have activated a “program” similar to the mammal readying itself for winter or the bird preparing for a long distance migration. There are a lot more at work than simply consuming too many calories and moving too little.

If we look at animals and what happens once they have depleted their fat stores, we get clues to how they’re able to quickly regain their weight. Research has shown that cortisol and uric acid skyrockets. Cortisol is a steroid hormone released from the adrenal glands in periods of stress. It suppresses sleep, breaks down muscle protein for energy, raises blood pressure and causes retention of salt and water. All features that will help an animal to survive when food, water and salt supplies are low.
We already know that cortisol should be high in the morning to help us mobilize energy and get us going and that it should decline during the day, reaching a low at night so we can sleep. Elevated levels of cortisol above normal is bad news when you’re on a diet as it breaks down metabolic active muscle mass, interferes with other hormones and your sleep.
However, serum levels of cortisol are not elevated above normal in the average obese person. So this cannot be the underlying problem. But what about uric acid?


Uric Acid – much more than a waste product

Not long ago, since uric acid is produced during the breakdown of nucleotides (building blocks of nucleic acids like DNA and RNA), many physicians considered uric acid to be a waste product with little biologic function, only associated with gout and kidney stones.
However, as of late, scientists have found that elevated levels of uric acid is very common in individuals with obesity, insulin resistance and metabolic syndrome.
At first, the sentiment among many scientists was that this elevation in uric acid was a consequence of obesity and insulin resistance, and not the causation of these conditions. However, during the last 10 years that viewpoint has begun to change.
Many authorities now suggests that an elevated level of serum uric acid should be considered a criteria for these syndromes. Also, if you have increased serum uric acid above normal levels, you have a highly increased risk for developing obesity, high blood pressure, fatty liver and metabolic syndrome. Elevated levels of uric acid is not only common in obesity, it precedes and predicts its development.

If you know your biology, the mitochondria is the powerhouse of our cells that regulate cellular metabolism and produces the energy currency of the cell, ATP. Just like a factory, the mitochondria generates heat and produce energy that allows us to move, to eat, to lift weights, to breath and to think. Without ATP, the cell would shut down and eventually die.
What’s interesting and alarming at the same time, is that uric acid affects the mitochondria by increased oxidative stress, injuring specific enzymes involved in energy production. And at high concentrations, uric acid actually reduce the total number of mitochondria in the cell.
Oxidative stress to the mitochondria has also been identified as having a critical role in causing insulin resistance.

Furthermore, oxidative stress induced by uric acid inhibits an enzyme that leads to the accumulation of citrate lyase, which is an enzyme that stimulates fat production from carbohydrates. Uric acid also inhibits an enzyme required for the burning of fatty acids, leading to less ATP being produced. The net effect of high levels of uric acid is thereby increased fat synthesis, reduced burning of fat, and reduced energy (ATP) output. In other words, uric acid alter the mitochondria to convert the energy we get from food into fat as opposed to producing ATP. Also keep in mind that a reduction in ATP in the liver signals the brain to encourage more food intake. All of this is the total opposite of what we want, but it’s ideal for storing fat and prepare the species for harsh times.

To summarize. If you rapidly want to alter your physiology for increased fat storage, you should do anything that is necessary to increase serum levels of uric acid – and that is exactly what animals do when preparing for winter or migration! And if you want to be lean, healthy and full of energy, you should simply do the opposite. So, what is it that animals do to trigger this rise in uric acid?


Fructose and the Uric Acid connection

As fruit ripens, the sugar content increases while the levels of vitamin C decreases. Most animals prefer mature, ripened fruit with a high content of fructose. Many anthropologists have observed that both free and captive animals prefer ripened fruit in the autumn and early winter. Even carnivores including bears, raccoons, and foxes turn to fruits at this time if they are available.
Another example is the orangutans who will travel long distances to find fruit. When they do, they will go on a feeding binge, eating as many ripe fruit as rapidly as they can. This will ensure that they put on enough body fat that they will survive during subsequent months when food is less plentiful.
All these observations and studies suggest that there is something special about ripe fruit and its ability to rapidly increase fat stores...

Please subscribe to The Classic Muscle Newsletter to read the rest of the Burn The Fat Part 1 article (and gain access to the following parts as they are released during the summer of 2015).

References, sources and further reading:

Sugar, Uric Acid, and the Etiology of Diabetes and Obesity.
Richard J. Johnson, Takahiko Nakagawa, L. Gabriela Sanchez-Lozada, Mohamed Shafiu, Shikha Sundaram, Myphuong Le, Takuji Ishimoto, Yuri Y. Sautin, and Miguel A. Lanaspa.
Diabetes. 2013 Oct; 62(10): 3307–3315.
Consumption of fructose-sweetened beverages for 10 weeks reduces net fat oxidation and energy expenditure in overweight/obese men and women.
Cox CL, Stanhope KL, Schwarz JM, et al.
Eur J Clin Nutr2012;66:201–208
Excessive fructose intake induces the features of metabolic syndrome in healthy adult men: role of uric acid in the hypertensive response.
Perez-Pozo SE, Schold J, Nakagawa T, Sánchez-Lozada LG, Johnson RJ, Lillo JL
Int J Obes (Lond) 2010;34:454–461
Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans.
Stanhope KL, Schwarz JM, Keim NL, et al.
J Clin Invest 2009;119:1322–1334
Sucrose-sweetened beverages increase fat storage in the liver, muscle, and visceral fat depot: a 6-mo randomized intervention study.
Maersk M, Belza A, Stødkilde-Jørgensen H, et al.
Am J Clin Nutr2012;95:283–289
Obesity-a disease with many aetiologies disguised in the same oversized phenotype: has the overeating theory failed?
Stenvinkel P.
Nephrol Dial Transplant. 2014 Oct 31. pii: gfu338
The effects of fructose intake on serum uric acid vary among controlled dietary trials.
Wang DD, Sievenpiper JL, de Souza RJ, et al.
J Nutr 2012;142:916–923
Uric acid stimulates vascular smooth muscle cell proliferation and oxidative stress via the vascular renin-angiotensin system.
Corry DB, Eslami P, Yamamoto K, Nyby MD, Makino H, Tuck ML.
J Hypertens 2008;26:269–275
Uric acid-induced endothelial dysfunction is associated with mitochondrial alterations and decreased intracellular ATP concentrations.
Sanchez-Lozada LG, Lanaspa-Garcia MA, Cristobal M., et al.
Nephron Exp Nephrol 2012;121:e71–e78
Relationship between resistance to insulin-mediated glucose uptake, urinary uric acid clearance, and plasma uric acid concentration. 
Facchini F, Chen YD, Hollenbeck CB, Reaven GM.
Inactivation of nitric oxide by uric acid.
Gersch C, Palii SP, Kim KM, Angerhofer A, Johnson RJ, Henderson GN.
Nucleosides Nucleotides Nucleic Acids 2008;27:967–978
Uric acid stimulates fructokinase and accelerates fructose metabolism in the development of fatty liver.
Lanaspa MA, Sanchez-Lozada LG, Cicerchi C, et al.
PLoS ONE 2012;7:e47948.
Relation between uric acid and metabolic syndrome in subjects with cardiometabolic risk.
Silva HA, Carraro JC, Bressan J, Hermsdorff HH.
Einstein (Sao Paulo). 2015 May 19:0.
Prospective study of serum uric acid levels and incident metabolic syndrome in a Korean rural cohort.
Yadav D, Lee ES, Kim HM, Choi E, Lee EY, Lim JS, Ahn SV, Koh SB, Chung CH.
Atherosclerosis. 2015 Apr 25. pii: S0021-9150(15)01015-1. doi: 10.1016/j.atherosclerosis.2015.04.797
Relationship between serum uric acid, metabolic syndrome and resting heart rate in Chinese elderly.
Liu P, Jiang Y, Meng J.
Obes Res Clin Pract. 2015 May 6. pii: S1871-403X(15)00061-7. doi: 10.1016/j.orcp.2015.04.007.
Fructose and uric acid: is there a role in endothelial function?
Jia G, Aroor AR, Whaley-Connell AT, Sowers JR.
Curr Hypertens Rep. 2014 Jun;16(6):434. doi: 10.1007/s11906-014-0434-z.
Uric Acid - key ingredient in the recipe for cardiorenal metabolic syndrome.
Chaudhary K, Malhotra K, Sowers J, Aroor A.
Cardiorenal Med. 2013 Oct;3(3):208-20. doi: 10.1159/000355405.
A causal role for uric acid in fructose-induced metabolic syndrome.
Nakagawa T, Hu H, Zharikov S, et al.
Am J Physiol Renal Physiol 2006;290:F625–F631
Uric acid and metabolic syndrome: what is the relationship?
Lanaspa M, Sautin Y, Ejaz A, et al.
Curr Rheum Rev 2011;7:162–169
The role of uric acid in the pathogenesis of human cardiovascular disease.
Kanbay M, Segal M, Afsar B, Kang DH, Rodriguez-Iturbe B, Johnson RJ. 
Heart 2013;99:759–766
Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease.
Johnson RJ, Segal MS, Sautin Y, Nakagawa T, Feig DI, Kang DH, Gersch MS, Benner S, Sánchez-Lozada LG.
Am J Clin Nutr. 2007 Oct;86(4):899-906.
Consumption of fructose- but not glucose-sweetened beverages for 10 weeks increases circulating concentrations of uric acid, retinol binding protein-4, and gamma-glutamyl transferase activity in overweight/obese humans.
Cox CL, Stanhope KL, Schwarz JM, et al.
Nutr Metab (Lond) 2012;9:68.
Fructose overconsumption causes dyslipidemia and ectopic lipid deposition in healthy subjects with and without a family history of type 2 diabetes.
Lê KA, Ith M, Kreis R, et al.
Am J Clin Nutr2009;89:1760–1765
Fructose ingestion acutely elevates blood pressure in healthy young humans.
Brown CM, Dulloo AG, Yepuri G, Montani JP.
Am J Physiol Regul Integr Comp Physiol 2008;294:R730–R737
Effects of high-fructose corn syrup and sucrose on the pharmacokinetics of fructose and acute metabolic and hemodynamic responses in healthy subjects.
Le MT, Frye RF, Rivard CJ, et al.
Metabolism 2012;61:641–651
The effect of two energy-restricted diets, a low-fructose diet versus a moderate natural fructose diet, on weight loss and metabolic syndrome parameters: a randomized controlled trial.
Madero M, Arriaga JC, Jalal D, et al.
Comparison of free fructose and glucose to sucrose in the ability to cause fatty liver.
Sánchez-Lozada LG, Mu W, Roncal C, et al.
Eur J Nutr 2010;49:1–9
Sucrose induces fatty liver and pancreatic inflammation in male breeder rats independent of excess energy intake.
Roncal-Jimenez CA, Lanaspa MA, Rivard CJ, et al.
Metabolism 2011;60:1259–1270
High-fructose corn syrup causes characteristics of obesity in rats: increased body weight, body fat and triglyceride levels.
Bocarsly ME, Powell ES, Avena NM, Hoebel BG.
Pharmacol Biochem Behav2010;97:101–106
Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women.
Teff KL, Elliott SS, Tschöp M, et al.
J Clin Endocrinol Metab2004;89:2963–2972
Association of Visceral Fat Area with Chronic Kidney Disease and Metabolic Syndrome Risk in the General Population: Analysis Using Multi-Frequency Bioimpedance.
Kang SH, Cho KH, Park JW, Yoon KW, Do JY.
Kidney Blood Press Res. 2015 Apr 30;40(3):223-230.
Effect of glucose and fructose on food intake via malonyl-CoA signaling in the brain.
Lane MD, Cha SH.
Biochem Biophys Res Commun 2009;382:1–5
High rates of fructose malabsorption are associated with reduced liver fat in obese African Americans.
Walker RW, Lê KA, Davis J, Alderete TL, Cherry R, Lebel S, Goran MI
J Am Coll Nutr. 2012 Oct; 31(5):369-74.
Glucose-induced obesity, fatty liver and insulin resistance is mediated by endogenous fructose.
Lanaspa MA, Ishimoto T, Li N, et al.
Nature Commun. In press
Role of dopamine D1 and D2 receptors in the nucleus accumbens shell on the acquisition and expression of fructose-conditioned flavor-flavor preferences in rats.
Bernal SY, Dostova I, Kest A, et al.
Behav Brain Res 2008;190:59–66