I am watching some of this video Modok posted, and it’s better than my entire physiology degree LOL.
My God that video is seriously fucking disturbing.
[quote]MODOK wrote:
[quote]CappedAndPlanIt wrote:
Oh hey, I’ve seen this. I remember there was a part where he said fruit isnt bad because it has fiber and other nutrients (“when god gives us a poison, he packages it with the antidote”).
Basically what I’ve been saying the whole thread.[/quote]
Did you happen to pay any attention to the fucking science, or are we going on with this circular argument again? Did you see the metabolic pathway of fructose? Do you understand why it can be less than ideal for physique athletes? Lustig isn’t a bodybuilder or even an athlete. I know the guy. He is pretty much a communist in his views toward government regulation of things like fructose. I posted the lecture in this thread because it contains a very concise explanation of glucose and fructose metabolism.
I have came to the conclusion that you are either:1. an imbecile. or 2. for some reason just wanting to argue on, ad infinitum, with no logical conclusion. I know that you are a smart guy, so that rules out #1. You know exactly what the discussion has been, what the points are that have been made, and why they were made. You keep taking the opposite point to further the argument. It is not constructive or enjoyable for anyone. You have certainly left an impression on me that I will not forget in future threads.
[/quote]
There’s no circular argument.
Someone who trains for MMA 4 times a week and wants to ‘lose a little for a BJJ competition coming up’ asked if he should avoid fruit.
I said no, he has no reason to avoid fruit, as long has he has a moderate intake and avoids other sources of sugar/HFCS.
Do you, MODOK, think that the OP (who trains for MMA 4 times a week and wants to ‘lose a little for a BJJ competition coming up’, and who is not a precontest bodybuilder) should avoid fruit?
[quote]MaximusB wrote:
I am watching some of this video Modok posted, and it’s better than my entire physiology degree LOL.
[/quote]
So far I’ve seen up to 45mins of that video, don’t mean to sound funny here but how far have you seen up to? And what parts were news to you? The parts about the health industry’s blunders over the past 30 years?
[quote]its_just_me wrote:
[quote]MaximusB wrote:
I am watching some of this video Modok posted, and it’s better than my entire physiology degree LOL.
[/quote]
So far I’ve seen up to 45mins of that video, don’t mean to sound funny here but how far have you seen up to? And what parts were news to you? The parts about the health industry’s blunders over the past 30 years?[/quote]
I saw all of it, what shocked me was towards the end, where with his diagrams he talks and shows how things like glucose and fructose are handled differently. How the processing of our foods has screwed us badly, which isn’t completely surprising to me because every time I go back to Italy, I destroy pasta and end up losing weight like clockwork.
Also how the FDA royally fucked ‘We the People’ really bad. They are in on the shit basically. I know they were behind the “fat is bad idea” but I didn’t realize how they also herded people in the carb industry.
Swear to God, after seeing that, makes me want to grow all my food, and I am sure that that was only the tip of the iceberg.
[quote]MaximusB wrote:
[quote]its_just_me wrote:
[quote]MaximusB wrote:
I am watching some of this video Modok posted, and it’s better than my entire physiology degree LOL.
[/quote]
So far I’ve seen up to 45mins of that video, don’t mean to sound funny here but how far have you seen up to? And what parts were news to you? The parts about the health industry’s blunders over the past 30 years?[/quote]
I saw all of it, what shocked me was towards the end, where with his diagrams he talks and shows how things like glucose and fructose are handled differently. How the processing of our foods has screwed us badly, which isn’t completely surprising to me because every time I go back to Italy, I destroy pasta and end up losing weight like clockwork.
Also how the FDA royally fucked ‘We the People’ really bad. They are in on the shit basically. I know they were behind the “fat is bad idea” but I didn’t realize how they also herded people in the carb industry.
Swear to God, after seeing that, makes me want to grow all my food, and I am sure that that was only the tip of the iceberg.
[/quote]
Too right.
Having to contend with the “fats are bad” crowd is enough to drive anyone insane (I have a sister-in-law who’s always lecturing and trying to “educate” me)
I do actually grow my own veg, and eat absolutely nothing processed (unless it’s beyond my reasonable control).
[quote]MaximusB wrote:
I saw all of it, what shocked me was towards the end, where with his diagrams he talks and shows how things like glucose and fructose are handled differently.
[/quote]
Yeah. And you still have people who claim “its all just calories in/out” and ignore those differences.
Also, he makes a really good point when he’s comparing sugar and alcohol – fructose is habit forming. So its no surprise food companies pack as much HFCS into their food as possible - the more fructose, the more people get hooked on the food. Have you ever watched someone go from a high-sugar/hfcs diet to cutting it out suddenly? They appear to get sick (most have flu-like symptoms). I’m not trying to state this as an absolute fact, but that seems an awful lot like detox to me.
Back in late 2003, I was fat, I mean really fucking fat. Not too far from 300 lbs, and I am only 6’1. I was facing prison time, my dad died and I could not go to his funeral, so I ate myself into comfort. I craved carbs like crazy (which makes sense to offset a huge cortisol release.) I literally ate 3-4 meals of drive thru a day. You name it, McDonald’s, Taco Bell, Carl’s Jr, I had seen it all. I also noticed that I LOVED soda. Not diet soda, but regular Coke. No matter how much I drank, I wanted more, and I was always thirsty. My mouth would water the moment the idea of fast food popped in my head, and now I see that this was not just out of emotion. The shit food hard wires your brain to want more and more of it.
Once I started my prison time, my first month inside I lost about 35 lbs, no junk food around, soda was hard to find, and I exercised my ass off as a stress reliever. After seeing the video, it’s not only a psychological cycle, but a physiological one too. My first week in the joint, I was sick (most likely from a detox of shit food). I am not saying the food inside was great, but it was better than the pure shit I found at the drive-thru places. By the time I came home, I went from very close to 300 to around 210. Waist went from 46 to 34.
Never again, it makes me sick to even think people make money off of making other people sick. I am all for making cash money, but not at the price of fucking up someone’s life. Those fuckers (the FDA) should be in jail.
Moral of the story, go to jail lol
Whenever I helped my wife with the diet, the hardest thing by far was the coke addiction. She tried the diet version to no avail. Her diets always lasted 2 weeks maximum, then it was back to the coke again.
I used to find it hard to believe and would laugh at people (read: what I thought were “suckers”) buying coke every day, but now I’ve had first hand experience of why. My parents were sensible enough not raise us on that kind of crap so I took it for granted.
It’s truly crazy when you look around shops at lunch-time and see the rubbish kids buy day in and day out for their whole lunch (ALWAYS coke or something similar). It make me sad.
[quote]its_just_me wrote:
Moral of the story, go to jail lol
Whenever I helped my wife with the diet, the hardest thing by far was the coke addiction. She tried the diet version to no avail. Her diets always lasted 2 weeks maximum, then it was back to the coke again.
I used to find it hard to believe and would laugh at people (read: what I thought were “suckers”) buying coke every day, but now I’ve had first hand experience of why. My parents were sensible enough not raise us on that kind of crap so I took it for granted.
It’s truly crazy when you look around shops at lunch-time and see the rubbish kids buy day in and day out for their whole lunch (ALWAYS coke or something similar). It make me sad.[/quote]
Reading that with “coke” meaning the drug…is very sad :(. Ha, would also make you come across as one very cold individual.
[quote]CappedAndPlanIt wrote:
Also, he makes a really good point when he’s comparing sugar and alcohol – fructose is habit forming. So its no surprise food companies pack as much HFCS into their food as possible - the more fructose, the more people get hooked on the food.
[/quote]
Don’t be a conspiracy theorist. Just because that’s one possible outcome does not mean it was the intention. It doesn’t mean it WASN’T the intention, either, but people forget how heavily subsidized corn is and thus the preference to use HFCS as a sweetener.
So, why don’t we find something that’s naturally sweet (Stevia?) and subsidize the shit out of that? It would take 5-10 years to see the impact.
The other problem with fast food forming a habit is the CONVENIENCE. I really think that’s the cornerstone of many addictions.
I quit smoking (cigars, hooka) because I stuck to cigars and hooka, intentionally, and I knew that I would eventually get too lazy to light up a cigar for 30-45 min or breakout a hooka and then clean it up afterward.
Accessibility and portability are HUGE factors in addiction. If everyone HAD to cook their own meals, we’d have very little cases of obesity. People are naturally lazy.
Since it seems like a bunch of people are interested in the various metabolic pathways and why macronutrient breakdown tends to have a greater effect than necessarily the number of cals consumed ive copied and pasted a few sections from a paper I wrote a while ago on HFCS. Most of the info in the beginning is about hormones involved in digestion, some comorbidites of obesity and then about half way down is where fructose and its impact on those various hormones etc is discussed.
Ghrelin
One hormone that is impacted by macronutrient breakdown of the diet and should be considered in efforts to control obesity is Ghrelin. Ghrelin is an orexigenic, 28-amino-acid peptide gut hormone with growth hormone releasing activity (Kojima, 2002). It plays a pivotal role in long-term energy balance and short-term food intake. It is also recognized as a potent signal for meal initiation. Ghrelin is amongst the most powerful of the orexigenic peptides. Ghrelin works by activating Neuropeptide Y and Agouti-related protein neurons of the hypothalamic arcuate nucleus via the receptor, GHS-R1a, promoting production and secretion of their orexigenic neuropeptides to suppress Proopiomelanocortin neuronal activity while promoting food intake (Solomon, 2007).
Ghrelin levels rise sharply before feeding onset, and are strongly suppressed by food ingestion. Postprandial ghrelin response is totally macronutrient specific with isoenergetic meals of different macronutrient content suppressing ghrelin to a variable extent. Due to carbohydrates induction of insulin secretion and their rapid absorption, there is faster ghrelin response to carbohydrates. However, Protein induces prolonged ghrelin suppression and is considered to be the most satiating macronutrient, with people tending to have greater satiety ratings after a high protein meal than a high carbohydrate meal (Verhagen, 2010).
Insulin
Insulin is a hormone that is central to regulating carbohydrate and fat metabolism in the body. Any food or drink containing glucose, or the digestible carbohydrates that contain it, such as sucrose and starch causes blood glucose levels to increase. Glucose is liberated from dietary carbohydrate such as starch or sucrose by hydrolysis within the small intestine and is then absorbed into the blood (Grossman, 1986). In a normal metabolism, the elevated blood glucose level makes beta cells in the islet of langerhans, in the pancreas, release insulin into the blood in a biphasic manner. The first phase consists of a brief spike lasting approximately 10 minutes, followed by the second phase, which reaches a plateau at 2â??3 hours. Elevated concentrations of glucose in the blood stimulate the release of insulin, and insulin acts on cells throughout the body, primarily liver, muscle and adipose cells, to stimulate uptake and utilization of glucose and storage of glucose as glycogen (Steffens, 1990). This is done through the use of hexose transporters, most notably, GLUT4. When insulin concentrations are low, GLUT4 is present in cytoplasmic vesicles, where they are incapable of transporting glucose. When insulin concentrations are high, insulin binds to the insulin receptor, which is composed of two extracellular α subunits and two transmembrane β subunits linked together by disulphide bonds (Saltial, 2002). Binding of insulin to the α subunit induces a conformational change resulting in the autophosphorylation of a number of tyrosine residues present in the β subunit. These residues are recognized by phosphotyrosine-binding domains of adaptor proteins such as members of the insulin receptor substrate family. Receptor activation leads to the phosphorylation of key tyrosine residues on IRS proteins, which subsequently leads to rapid fusion of GLUT4 containing cytoplasmic vesicles with the plasma membrane and insertion of the glucose transporters, thereby giving the cell an ability to efficiently take up glucose (Berenguer , 2010). As digestion continues the beta cells reduce insulin output as the plasma glucose level falls, allowing plasma glucose to settle to a constant level. With this decrease in plasma insulin, insulin receptors are no longer occupied, and the glucose transporters are recycled back into the cytoplasm.
Insulin stops the use of fat as an energy source by inhibiting the release of glucagon. When insulin is absent, glucose is not taken up by body cells and the body begins to use fat as an energy source. Any food or drink containing glucose, or the digestible carbohydrates that contain it, such as sucrose and starch causes blood glucose levels to increase(Dugani, 2006).
Excessive circulating insulin due to overconsumption of carbohydrates is a strong contributor to insulin resistance via down-regulation of insulin receptors. This down-regulation occurs due to prolonged and repeated elevations of circulating insulin, which occurs by consumption of frequent carbohydrate meals, or very large meals high in carbohydrates.
Leptin
Along with Ghrelin, Leptin plays a key role in metabolism and the macronutrient affect on leptin should not be ignored when trying to reduce obesity. Leptin is an adipocyte derived peptide hormone with numerous actions, including influences on energy homeostasis and neuroendocrine and immune function. Leptin goes from adipose tissue to the arcuate nucleus in the hypothalamus where there are 2 different types of neurons, orexigenic and anorexigenic. Both neurons have leptin receptors and the binding of leptin to both orexigenic and anorexigenic neurons is necessary for energy homeostasis (Jovanovic ,2010). When leptin binds to Orexigenic neurons: neuropeptide Y (NPY) and agouti-related peptide (AgRP) are released. When little body fat is present or a meal low in dietary fat is consumed, Orexigenic neurons are stimulated by leptin signaling the body to eat more. When leptin binds to Anorexigenic neurons preproopiomelanocortin (POMC) is stimulated and releases α-melanocyte-stimulating hormone (αMSH) (Flavien, 2011). When high amounts of body fat are present, or high fat meals are consumed, the Anorexigenic neurons signal the body to reduce caloric intake and become more active.
More importantly than the maintenance of energy homeostasis is leptinâ??s role in insulin biosynthesis and pancreatic secretion which is the result of the presence of leptin receptors on the pancreas. In return, insulin stimulates leptin secretion from adipose tissue establishing a hormonal regulatory feedback loop, called the adipo-insular axis (Fehmann, 1997). Leptin also signals back to the pancreas that no more insulin is required to replenish fat stores. Thus, the adipoâ??insular axis has two branches: insulin and glucagon are signals to the adipocyte which releases leptin, which then acts as a mediator of the respective feedback to the pancreas. A defective leptin suppression of insulin secretion could contribute to insulin resistance and its associated problems (Berthou, 2011).
Physiological Impact of Obesity
Obesity influences many physiological processes and thus, increases the risk of numerous diseases such as Type 2 Diabetes, Dyslipemia, Cardiovascular disease, Non-fatty acid liver disease and various joint diseases. Diseases associated with obesity can arise from two mechanisms: from the metabolic changes associated with excess fat, as is the case in Type 2 Diabetes and cardiovascular disease, or mechanical changes, which arise from the increased fat mass itself, as seen in joint diseases (Formiguera, 2004). The metabolic changes that occur with excess fat are due to adipose tissueâ??s ability to behave as and endocrine organ. Central type obesity leads to an imbalanced production of several metabolic products, hormones and cytokines. These fat cell-derived products include leptin, resistin, adiponectin, free fatty acids, tumor necrosis factor-α and interleukin 6 (Panagiotakos, 2005).
Insulin resistance and type 2 diabetes mellitus
Insulin resistance is defined as the decreased effect of insulin on glucose uptake, metabolism and storage. In insulin resistance there is a diminished insulin-stimulated glucose uptake in skeletal muscle and adipose tissue, and impairment in the suppression of hepatic glucose output (Bloomgarden, 1998). These defects may occur due to impaired insulin signaling or by the down-regulation of the glucose transporter, GLUT4. In relation to the signaling defects in obesity, it is important to consider that the initial signal for insulin action is the activation of a tyrosine kinase on the insulin receptor. The activated tyrosine kinase then determines the phosphorylation of several other tyrosine residues. In muscle and adipose tissue of obese people, there is an increased expression and activity of several protein tyrosine phosphatases, which dephosphorylate and terminate signaling pathways. Additionally, a reduction in the expression of several insulin signaling molecules has been shown in skeletal muscle in the morbidly obese. In the case of GLUT4 expression, it typically functions normally in skeletal muscle of obese and diabetic subjects; however, defective glucose transport that is seen in these people most likely occurs due to the impairment of translocation, docking, or fusion of GLUT4-containing vesicles with the plasma membrane.
Insulin resistance can also come as the result of changes in the smallest blood vessels that make up the capillary bed. These changes are caused by hyperglycemia and the hyperinsulinemia that subsequently follows, resulting in vasoconstriction in the capillary bed (Carmassi, 2005). It has been demonstrated that a constricted and inflamed endothelium is a physical barrier to the transportation of insulin to the receptor sites of the muscle, adipose and liver cells. The bodyâ??s natural response to this barrier is to instruct the pancreas to produce more insulin in an attempt to force the insulin through the thickening arterial wall. Because of this thickening; in an insulin-resistant person, normal levels of insulin do not have the same effect in controlling blood glucose levels (Zepter, 2006). During the compensated phase on insulin resistance, insulin levels are higher, and blood glucose levels are still maintained. If compensatory insulin secretion fails, then either fasting or postprandial glucose concentrations increase. Eventually, type 2 diabetes occurs when glucose levels become higher throughout the day as the resistance increases and compensatory insulin secretion fails (Matsumoto, 2001).
Dyslipidemia
Dyslipidemia, or high plasma cholesterol and triglycerides, plays a crucial role in the development of atherosclerosis and cardiovascular disease in obese subjects. This occurs due to the various elements of dyslipemia that are normally associated with the disease, which have been shown to be atherogenic (Howard, 2003).
Obesity is associated with increases in plasma triglycerides, and decreases in HDL cholesterol. Along with this, a change in LDL composition occurs in obese individuals. There LDL particles are smaller and more dense, which increases the risk of cardiovascular disease as compared to those with large LDL particles for the same level of total cholesterol (Paccuad, 2000). Because of this, the levels of cholesterol are similar in older obese people; however the structure of that cholesterol differs, subsequently increasing the risk of heart disease. The increase in the risk of heart disease is due to the reduced diameter of these particles favoring movement through the endothelial fenestrations, allowing them to locate in the sub-endothelial space where they form plaque (Denke, 1994). This obesity associated pattern of high triglyceride levels is also related to insulin resistance. In the insulin resistant state typically found in obese people, there is a decreased ability of insulin to suppress hepatic glucose output and release non-esterified fatty acids from adipose tissue. This in turn results in a decreased clearance of triglyceride-rich lipoproteins in the circulation due to decreased lipoprotein lipase activity (Nieves, 2003).
Cardiovascular disease
The connection between obesity and Cardio vascular disease involves multiple pathways. The atherosclerotic process is regulated by inflammatory mechanisms and systemic inflammation has been linked to insulin resistance. In cases of Hypertension, increase of intravascular volume, and an abnormal peripheral vascular resistance unable to respond correctly to the enhanced intravascular volume lead to the induction of hypertension (Lavie, 2009). The primary defect leading to the increase in intravascular volume appears to be an increase in sodium retention along with increased sympathetic activity which are both commonly found in obese hypertensive people. However, the mechanism behind the increased intravascular volume and sodium retention isnâ??t fully understood. This Hypertension then results in an increase in the risk for Left ventricular hypertrophy (Martin, 2008). Hypertension forces the left ventricle to work harder. As the workload increases, the walls of the chamber grow thicker, lose elasticity and eventually may fail to pump with as much force as a healthy heart. The hypertrophy of the left ventricle leads to changes in the right ventricle as well. As a consequence of left ventricular dysfunction, pulmonary heart disease can occur (Ritchie, 2007).
High Fructose Corn Syrup
High fructose corn syrup is any type of corn syrup that has undergone enzymatic processing to convert some of its glucose into fructose to produce a desired sweetness. The most widely used varieties of high-fructose corn syrup are: HFCS 55 mostly used in soft drinks, which is composed of approximately 55% fructose and 42% glucose; and HFCS 42 used in many foods and baked goods, which is made up of approximately 42% fructose and 53% glucose.
High Fructose Corn Syrup has a cheap and easy production method which has led to a significant increase in its consumption since its advent in the 1970s. Shortly after High Fructose Corn Syrupâ??s introduction in the mid 1970â??s, Americans consumed an estimated 80kcals per day of the sweetener. By 1998 that number had increased to 132kcals per day and 228kcals per day in 2008. To produce High Fructose Corn Syrup, first corn kernels are shelled and soaked in a solution of water and sulphur dioxide in order to soften them. Following this, the softened kernels are sent to a degerminating mill, where the lighter weight germ is separated from the remainder of the kernel and used to make corn oil. The rest of the kernel, however, is mixed with water and passed through a series of screens and hydroclones which further extract and purify the corn starch. After this, the pure corn starch is treated with the enzyme Glucose Isomerase, which converts glucose to fructose. Finally, the fructose syrup is purified one last time, yielding true High Fructose Corn Syrup. Thus, due to the ease with which High fructose corn syrup is produced, transported, and utilized, it has become a staple sweetener and a preservative in all manner of products. This increase in High Fructose Corn Syrup consumption potentially increases the risk of various metabolic problems associated with high fructose intake, such as the following:
Non Alcoholic Fatty Liver Disease
Chronic intake of fructose has been linked to non alcoholic fatty liver disease. Due to high fructose corn syrups high fructose content, there is a higher risk of non fatty acid liver disease when compared to other sweeteners. Fructose is readily absorbed and transported through enterocytes to the portal bloodstream by a fructose-specific hexose transporter GLUT5 (Annania, 2005). Fructose is phosphorylated by fructokinase to fructose-1-phosphate, which is metabolized to the triose phosphates glyceraldehydes and di-hydroxy-acetone phosphate (Ouyang, 2008). As fructose is metabolized through this route in the liver, its metabolism bypasses the main rate-limiting step in glycolysis, which is catalyzed by phospho-fructo-kinase. So while glucose metabolism is tightly regulated through the allosteric inhibition of phospho-kinase by citrate and ATP, fructose can continuously and uncontrollably enter the glycolytic/gluconeogenetic pathway resulting in the production of glucose, glycogen, lactate and pyruvate. Pyruvate and lactate are both precursors of the formation of acyl-glycerol molecules, which, can contribute to an increased formation of triglycerides and, subsequently, production of very-low-density lipoproteins (Gaby, 2005).
Besides bypassing the phospho-fructo-kinase-controlled step of glycolysis, chronic intake of fructose may lead to bacterial overgrowth, increased intestinal permeability and, subsequently, elevated endotoxin levels in the portal blood as well as to an activation of Kupffer cells, increased formation of reactive oxygen species (ROS) via TLR-4-dependent signalling pathways and an NFκB-dependent induction of Tumor Necrosis Factor-α, which can then cause insulin resistance in hepatocytes, which in turn may alter hepatic triglyceride secretion of very low density lipoproteins (Kanuri, 2010).
Malonyl- CoA signaling
High fructose corn syrups ability to bypass the rate limiting glycolyitic step also has an impact on Malonyl-CoA signaling, which is part of the leptin signaling pathway. Unlike glucose, which suppresses food intake, fructose increases food intake when metabolized by the Central Nervous System (Lane, 2009). Although glucose and fructose utilize the same signaling pathway to control food intake, they act in an inverse manner and have reciprocal effects on the level of hypothalamic malonyl-CoA.
Since the action of 2-ketohexokinase on fructose rapidly consumes ATP, the entry of fructose into the hypothalamus produces a rapid depletion of ATP. This decrease in ATP is accompanied by an increase in AMP which lowers malonyl-CoA concentration provoking increased food intake (Gao, 2009). In contrast, the central administration of glucose leads to an increase in ATP concentration that initiates the leptin pathway to produce satiety. Thus, the downstream events in the signaling pathway triggered by fructose are the inverse of those provoked by glucose (Rajasekar, 2007).
Insulin resistance
Another problem with fructose is its impact on insulin resistance. Fructose consumption and obesity are linked because fructose consumption does not cause an insulin response. This is important because without an insulin response after consumption of high fructose food, there is no suppression of appetite which is normally induced by insulin secretion after a meal (Akgun, 1985). If there is no satiety or suppression of appetite occurring, then the person will continue eating resulting in weight gain, which, combined with the fact that fructose is favored by the liver to be metabolized into lipids, subsequently leads to insulin resistance (Bantle, 2007).
Another way High Fructose Corn Syrup can lead to insulin resistance is its impact on the adipocyte hormone, adiponectin, which also plays an important role in insulin action. The insulin sensitizer agonist, PPAR-Gamma, stimulates adiponectin production. Adiponectin is thought to be part of an antagonistic mechanism which lowers circulating fatty acids and increases fat oxidation. The net effect is to decrease liver triglycerides and increase insulin sensitivity. Chronic fructose consumption reduces adiponectin responses, which then contribute to insulin resistance (Carvalho, 2010).
Also, Fructose consumption has been linked to significant decreases in insulin receptor GLUT5 mRNA, and subsequent insulin receptor numbers in skeletal muscle and liver leading to reduced fructose transport (Hajduch, 2003). As a result of this, insulin stimulated autophosphorylation necessary for insulin action is reduced in the liver. Insulin receptor substrate protein levels are also reduced, and there are significant decreases in insulin induced Insulin Receptor Substrate phosphorylation in both liver and muscle cells. These changes are important, because it has been shown that the products of these metabolic pathways lead to the formation of advanced glycation end products (Duffey, 2008).
Formation of Advanced Glycation End Products
Reducing sugars, such as fructose and glucose, react with proteins and amino acids to form substituted amino sugars. This reaction, known as the Maillard reaction (also called glycosylation or glycation), usually occurs at the site of a lysine side-chain, but reducing sugars can also react with tryptophan, arginine and other amino acids as well. These initial products of the Maillard reaction undergo further reactions and rearrangements to form Advanced Glycation End Products (Edeas, 2010).
Advanced Glycation End Products modify and crosslink most proteins in the body and affect their structure and function, a process that is countered through continuous turnover of body proteins. However, some long-lived proteins accumulate Advanced Glycation End Products, such as collagen in the vascular wall, crystallins in the lens of the eye, and in blood proteins (Sayaka, 2011). Similar modifications also occur on membrane phospholipids and in DNA. Advanced Glycation End Products have been proposed as activators of pro-inflammatory pathways through the binding of cell surface receptors, such as RAGE, the receptor for Advanced Glycation End Products (Kim, 2007).
The rate at which the Maillard reaction occurs depends on both the concentration of the reducing sugar involved and its degree of reactivity. Fructose is much more reactive than glucose with respect to participation in glycosylation reactions (Kasper, 2001). Because of this, the large percentage increases in serum fructose concentrations that occur after ingestion of fructose may have clinical consequences. The use of fructose in cooking also has the potential to cause adverse effects. Advanced Glycation End Products form during the heating of common foods and, in contrast to in vivo Advanced Glycation End Product formation, they can develop during cooking much more rapidly and in far greater concentrations. Approximately 10 percent of ingested Advanced Glycation End Products are absorbed, of which two-thirds are retained in tissues in reactive forms (Yonekora, 2002). Dietary Advanced Glycation End Products have been shown to accelerate the progression of nephropathy and to shorten survival times in animal models of diabetes. In humans with diabetes, the mean concentration of C-reactive protein (a marker of inflammation and an independent risk factor for cardiovascular disease) was 135-percent higher when the diet was high in Advanced Glycation End Products than the diet was altered to reduce Advanced Glycation End Product consumption (Daroux, 2010).
Can you wrap that shit up in like 20 words or less ^^^ ?
[quote]PonceDeLeon wrote:
MODOK,
I don’t want to take away from what Lustig has to present, but is he the guy that Aragorn/McDonald got into a debate with regarding fructose as the main culprit driving obesity rates?
I can’t recall. I think I’ve seen this lecture but I’ll watch it again; it was informative.[/quote]
Yes he is. It was Alan Aragon he debated with. From what I gather Lustig was claiming that fructose was reason for obesity rates and Aragon said it was other factors. Aragon ruined him.
http://www.weightology.net/weightologyweekly/?page_id=19
Fructose isn’t the problem.
And from another site regarding claims by Lustig:
"The only practical difference between sucrose and HFCS is in the bonding. The glucose & fructose in HFCS is mainly free and unbonded, while it is bonded in sucrose. However, this makes no meaningful difference in regards to metabolism in the body. The bonds in sucrose are quickly broken when sucrose hits the acid environment of the stomach. This means that once sucrose hits the stomach, itâ??s no different from HFCS. Once you get to the small intestine, metabolism is exactly the same. This little bit of difference does not lead to the problems Dr. Lustig talks about. The fact is, HFCS and sucrose are identical as far as your body is concerned. The difference in bonding wouldnâ??t make a shred of difference in regards to your health.â??
[quote]PonceDeLeon wrote:
http://www.weightology.net/weightologyweekly/?page_id=19
Fructose isn’t the problem.
And from another site regarding claims by Lustig:
"The only practical difference between sucrose and HFCS is in the bonding. The glucose & fructose in HFCS is mainly free and unbonded, while it is bonded in sucrose. However, this makes no meaningful difference in regards to metabolism in the body. The bonds in sucrose are quickly broken when sucrose hits the acid environment of the stomach. This means that once sucrose hits the stomach, itâ??s no different from HFCS. Once you get to the small intestine, metabolism is exactly the same. This little bit of difference does not lead to the problems Dr. Lustig talks about. The fact is, HFCS and sucrose are identical as far as your body is concerned. The difference in bonding wouldnâ??t make a shred of difference in regards to your health.â??[/quote]
I think fructose definitely is a big part of the problem, but HFCS isn’t necessarily much worse than sucrose. they both contain a similar amount of fructose (HFCS typically has about 5% more) so to say HFCS is more of a problem isn’t really accurate, but fructose consumption in general is
[quote]MaximusB wrote:
Can you wrap that shit up in like 20 words or less ^^^ ?[/quote]
High fructose corn syrups ability to bypass the rate limiting glycolyitic step (as first mentioned by modok) also has an impact on Malonyl-CoA signaling, which is part of the leptin signaling pathway. Unlike glucose, which suppresses food intake, fructose increases food intake when metabolized by the Central Nervous System. Because of this it messes up the adipo-insular axis indirectly leading to insulin resistance. It also leads to the formation of advanced glycation end products which can accumulate in proteins in the body, however there is some debate on just how bad advanced glycation end products are as some have been shown to have antiviral, antitumor properties etc
its a little more than 20 words but i think its a pretty decent summary
go to 1:05:45
that is interesting that black people did not have the same results as white people…
pretty much shows how genetic variation can drastically impact physiological processes in the body
[quote]PonceDeLeon wrote:
MODOK,
I don’t want to take away from what Lustig has to present, but is he the guy that Aragorn/McDonald got into a debate with regarding fructose as the main culprit driving obesity rates?
I can’t recall. I think I’ve seen this lecture but I’ll watch it again; it was informative.[/quote]
It was. Aragon made him look pretty bad. Not that Lustig’s not a brilliant guy, I think it was more of the fact that obesity was being blamed solely on fructose and more so HFCS. He basically got owned by Alan and then bailed out of the discussion when it was clear he was being bested…