UC TV: The skinny on fat (Part 1)

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Zute
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UC TV: The skinny on fat (Part 1)

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Interesting 12 minute video that says things you don't often hear.

http://www.youtube.com/watch?v=h0zD1gj0 ... r_embedded
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Re: UC TV: The skinny on fat (Part 1)

Post by Tudamorf »

It would be interesting to see where this goes -- whether it's just a rehashing of the fructose hypothesis or something more interesting.

But, strictly for weight maintenance, a calorie is a calorie.

Americans are getting fatter because their calorie intake has been steadily rising since the 1970s (not just from sugar, but also from steadily increasing quantities of meat, added fats, and grains) and they're doing less manual work than ever.

Show me a fat person, and I guarantee you that their diet and activity level will show that they're overconsuming.

http://www.cnn.com/2010/HEALTH/11/08/tw ... index.html
Twinkie diet helps nutrition professor lose 27 pounds

Twinkies. Nutty bars. Powdered donuts.

For 10 weeks, Mark Haub, a professor of human nutrition at Kansas State University, ate one of these sugary cakelets every three hours, instead of meals. To add variety in his steady stream of Hostess and Little Debbie snacks, Haub munched on Doritos chips, sugary cereals and Oreos, too.

His premise: That in weight loss, pure calorie counting is what matters most -- not the nutritional value of the food.

The premise held up: On his "convenience store diet," he shed 27 pounds in two months.

For a class project, Haub limited himself to less than 1,800 calories a day. A man of Haub's pre-dieting size usually consumes about 2,600 calories daily. So he followed a basic principle of weight loss: He consumed significantly fewer calories than he burned.

His body mass index went from 28.8, considered overweight, to 24.9, which is normal. He now weighs 174 pounds.

But you might expect other indicators of health would have suffered. Not so.

Haub's "bad" cholesterol, or LDL, dropped 20 percent and his "good" cholesterol, or HDL, increased by 20 percent. He reduced the level of triglycerides, which are a form of fat, by 39 percent.
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Re: UC TV: The skinny on fat (Part 1)

Post by Zute »

This was good. I think a lot of people assume that skinny means healthy and it isn't the case at all.
The thin man’s diabetes

His father lost his leg to type 2 diabetes, but Jeff O’Connell – a young, slim health journalist – never thought the disease could affect him…

The first thing I saw was a prosthetic leg propped against a wall. As I passed a curtain, the man I caught sight of looked nothing like the man who had raised me, and yet it was unmistakably him. I had been out of touch with my father for 20 years. Two decades will change anyone, but he showed none of the grace or subtle shadings of ageing; this was a human body in the process of cannibalising itself. I’ve had little experience with death, but my father looked like what I’d expect a man to look like in his casket.

Then his eyes moved. From his hospital bed, my father struggled to size me up, angling his neck like a man peering hard into a foggy mirror. He had not only lost much of his body weight, but in a particularly cruel twist, he’d even lost a tall man’s defining characteristic, his stature. Where his right leg should have been was a brown corduroy pant leg, folded up and pinned together. Formerly 6ft 3in and 15st 5lb, he was now a 10st 5lb collection of bones jutting against crinkled, discoloured flesh.

He smiled, and I was taken aback that this once handsome man now had rotten teeth and horribly inflamed gums. My father extended his blood-splotched arm, his firm handshake now a feeble grasp. “It’s good to see you, Jeff,” he said. “I’m glad you came.”

“It’s great to see you too, Dad. How ya feelin’?” I cringed inside at my own question, and his face winced, perhaps the best way he could summarise all he had endured. “It’s been kind of rough. But I’m glad you came.” He continued to hold my hand, punctuating sentences like that one with a gentle squeeze.

Shifting his weight in bed seemed to require all of his remaining strength, and while he closed his eyes to summon it, I looked around. A small Phillies pennant was tacked above his bed. I saw a few photographs of children, no doubt his children, although they were strangers to me. “Your brother tells me you’re a writer, and a successful one. He showed me some of your articles and books.”

Twenty years leaves a lot of ground to cover. You have to start somewhere. He wanted to know some basic information. This wasn’t the time to ask the questions I wanted answered. Maybe the right time for that would never come. “Are you married?” he said.

“Nope, not yet, although I’ve come close once or twice.” When a conversational lull arrived after several minutes, we switched over instinctively to baseball. Some things never change between a father and son. Baseball remained our default topic, just as it had been when I was seven years old. His alertness surprised me. Although it was turned off, a TV sat on the bureau across from his bed. He must have been following current events.

“So how long have you been diabetic, Dad?” I asked. I knew that anyone in his current state would be nearing the end of a long and gruelling battle with this disease. He thought. “I don’t really know,” he said. “I didn’t really watch my blood sugars. I passed out one day. I don’t remember anything after that.” His voice trailed off. “You didn’t have symptoms in your forties, fifties and sixties?” “No,” he said. It felt like the sort of lie I might have told him as a teenager. I would later learn that he had neglected his diabetes for at least a decade.

After several more minutes of conversation, all he could muster were short phrases – “I love you”, “It’s great to see you” – and he repeated them several times. So did I. I had no desire to delve any deeper under the circumstances. Nor, I suspect, did he. After what he had been through, what mattered was making him feel as comfortable as possible. The past and future didn’t seem to matter much, given that the here and now was this. I can’t possibly understand how my father must have felt, lying in that bed in such a state. But I knew how he felt at the earlier stages of the disease, despite his denial of having ever had symptoms – denial that landed him at the mercy of a surgeon’s saw.

Fifteen months earlier, and a week or so after receiving the call about my father’s amputation, I was attending a doctor’s appointment, a follow-up to a physical exam. I had sought an assessment of my health. I was wondering if there was some way to make my body function a little better, some antidote to disparate symptoms that made me feel sluggish, particularly in the mornings, and particularly after I had eaten a pizza or a burger and fries for dinner the night before.

Like many men, I had simply asked a colleague – in my case, one of the editors of Men’s Health magazine, where I worked – for a recommendation. I made this crucial decision with as much deliberation as one would give to choosing a garage for an oil change. The editor directed me to a small-town practice whose clientele included a number of the magazine’s staff members. When I entered the clinic for the first time, I met with Todd H. MD, a rotund man with thinning hair and a penchant for bad jokes told at awkward moments, like during medical exams. A clipboard and stethoscope weren’t the only baggage Dr H carried into the examination room. An extra 50lb or so settled around his waist.

As part of our initial visit, he had the nurse draw some blood for routine lab work. Like all patients, I was weighed as a matter of course and my height was measured for the umpteenth time. It hasn’t changed since I reached 6ft 6in as a 21-year-old. Height and weight allow for the calculation of a person’s body mass index (BMI), a number that’s supposed to tell you if you’re overweight. Unfortunately, BMI doesn’t account for body composition, the ratio between muscle and fat mass. An individual of 5ft 10in might work out every day but weigh the same as someone of similar stature who sits around all day. The difference: one is accumulating muscle, while the other is hoarding fat. Even though they might have a matching BMI, it is misleading to lump together such disparate populations.

Fresh on the heels of hearing about my father, I had returned to Dr H’s office for the results. After some introductory banter, he opened a folder and began scanning the results. Then he looked up. “Does diabetes run in your family?” he asked.

It doesn’t take more than a split second to fill in the blanks when a doctor poses a leading question about a disease, especially when you’re skinny and the doctor is asking about type 2 diabetes, which is normally associated with the overweight. This wasn’t idle chatter.

I had scored 116 mg/dL on my fasting plasma glucose test, indicative of prediabetes. Ten points higher, and I’d do away with the pre. I was tall and lean. Guys used to kid that I’d need to run around in the shower just to get wet. Diabetes? As life-threatening diseases go, leprosy and typhoid fever ranked higher on my things-that-might-kill-me list, even in the light of the news I had learnt about my father only a week earlier. I’ll be damned. How the hell could I have missed the signs?

I left the doctor’s office in a fog. I looked at my legs as I walked back to my car. Would I, too, lose one of them eventually? After sliding behind the wheel, I sat still for a moment and closed my eyes, trying to imagine the claustrophobia of a darkness that would never lift. Would impotence lie somewhere in my future as well? Adding up everything that diabetes could take away sobered me. I realised that in the end this disease could leave a man with nothing but regret.

That grim thought must loop through my father’s mind dozens, if not hundreds of times a day, I thought. Then again, maybe he doesn’t think of it at all. During the drive back to the office, my thoughts were filled with my past, not my muddled present, or even a future that had just turned overcast. Like many skinny people whose blood sugar regulation goes haywire, I had misinterpreted being thin for being healthy. I had a hunch that my DNA wasn’t centenarian material – men in my extended family are often buried too early – but I didn’t think I was booby-trapping my own body. I had never smoked. Recreational drugs and excessive drinking held no interest for me. I wasn’t overweight.

My lifestyle seemed comparatively healthy to me, a fact that I thought would help stack the odds against premature sickness and disease. Yet over those two decades, I had somehow acquired a disease of the overweight, or at least what I thought was a disease only for the overweight. Unfortunately I had been eating a lot of unhealthy foods with impunity because they didn’t cause me to pack on pounds. But they were unhealthy nonetheless.

Up until the autumn of 2006, I ate and drank a lot of sugar, largely unaware of type 2 diabetes, because only the old and the overweight need worry about it, I thought. How wrong I was. My ignorance is inexcusable, given that I write for a magazine called Men’s Health, but it also goes a long way towards explaining why the disease has spread across America with the persistence of a glacier and the devastation of a wildfire. As it stands, one in three American adults has type 2 diabetes or its preamble, prediabetes. [In Britain, the figure is one in twenty.] Remarkably one in four diabetics is in the dark about his or her condition.

Diabetes has sneaked up on America because insulin resistance, its root cause, sneaks up on Americans. It’s the invisible cause of an invisible disease. By the time someone learns they’re prediabetic, insulin resistance is already in charge, and probably has been for many years.

After you eat a meal, the pancreas releases insulin in an amount proportional to whatever the glucose load happens to be. Insulin arrives at receptors and is recognised as such, and cells know what to do in response: absorb glucose from the bloodstream. So your blood glucose never shoots too high. As this process unfolds, a feedback loop signals the pancreas to produce less insulin, to keep the messengers home. So your blood glucose never falls too low, either. The normal blood sugar response to a meal is a slow rise followed by a reasonable drop.

Insulin resistance occurs when insulin tries but fails to bind with receptors and glucose is left stranded. Instead of taking five units of insulin to produce a certain amount of energy from glucose, it’s now taking your body, say, twenty. All the pancreas knows is that insulin isn’t doing its job, so it keeps secreting more and more of the stuff, to little avail. This creates an energy crisis for each cell, not to mention for your entire body.

No one – young or old, thin or overweight, man or woman – should assume they’re safe from this deadly disease. Diabetes sneaked up on me because I was neither old nor overweight, and because I was ignorant of my own family history. When I knew the truth, I was stunned and dazed, and a little frightened.

Because I didn’t know any better. I didn’t know, for example, that the chemicals released by sugar consumption travel the same brain pathways that heroin does, and that when we’re stressed or sad, the foods that can produce this feeling exert a magnetic pull.

Certain foods are craved precisely because they contain so much energy in so little volume. To feed the addiction, we’re mainlining sugar in progressively larger doses. That’s part of the problem. The other part of the problem – the real problem, some might say – is the degree to which food-processing technology concentrates sugar and the energy density of foods as a result. The sweet science goes back to those Indian scientists who first crystallised sugar. The most recent game-changer was the discovery by Japanese food scientists, made in the Sixties, that cornstarch could be turned into a clear, sweet goop called high-fructose corn syrup [HFCS; glucose-fructose syrup in the UK]. Producers now had something sweeter and cheaper than cane sugar and with a shelf life that could be measured in presidential administrations.

HFCS and soft drinks were a perfect match, but not the only one. HFCS found its way into nearly everything we eat and drink. Ketchup, crackers, cereal, yogurt, baked goods, salad dressing, condiments and seemingly everything else on the supermarket shelves contain it. The first ingredient in low-fat mayonnaise? HFCS. During the two decades leading up to 1990, HFCS consumption in the US increased tenfold.

Ominously, type 2 diabetes is also setting its sights on the young in record numbers. A recent study in Diabetes Care found that between 1993 and 2004, hospital stays for diabetes among those 29 years or younger increased by nearly 40 per cent. Eventually, those stays will be for heart and kidney transplants. At the current pace, one in every three people born in the US in the year 2000 will become diabetic. For minorities, the rate will be one in two.

We have plenty of company too; the American epidemic is really a global pandemic. Type 2 diabetes affects 285 million people worldwide, according to the International Diabetes Federation, and its estimate may well fall on the low side, since the disease is so hard to detect. One person around the world develops diabetes every five seconds, swelling the ranks by more than 17,000 a day. That’s more than seven million new cases of diabetes a year. The World Health Organization expects the number of people with diabetes worldwide to double by 2030. Distant lands are gaining ground on the US economically, but many of them are acquiring our morbidities at an even faster pace.

One reason is that for the first time in human history, the overweight outnumber the malnourished. “Diabetes, along with obesity, is looming as the biggest epidemic in human history,” says Paul Zimmet, director of international research at the Baker IDI Heart and Diabetes Institute in Australia.

Food technology moves much faster than human evolution; most of our foods are recent inventions and it takes us humans many, many generations to adjust to shifts in the food supply. If you had to forage for your sugar, like our distant ancestors did, you would have an awfully hard time finding and eating enough fruits, vegetables and grains to develop type 2 diabetes, especially considering all the energy that the search would take.

However, turning into the drive-through lane of a fast-food establishment demands virtually no energy expenditure, and yet a nearly limitless supply of sugar – buns, fries, soft drinks, and desserts – instantly comes within reach. Processing allows for huge quantities of sugar and other unhealthy nutrients to hit our system unencumbered by the fibre and other constituents that once made us feel full. As a result, our body’s ancient sensors for hunger and satiety are now easily tricked by food technology.

My body certainly fell for it. For too many years, I asked my metabolic system, my body’s carburettor, to handle fuel it was never designed to handle. Eventually it broke.

When I arrive in Los Angeles for my second visit with my father, he looks far worse off than he did 18 months earlier, when I last saw him. I’ve been told he hasn’t been eating, and his body is now cadaverous. During my last visit, the stump remaining from his amputation had been covered; now it’s exposed. The sight shouldn’t surprise me, but I’m taken aback. His torso is covered with a polo shirt; his lower half by a diaper. His remaining leg is propped up and parchment flaps from the bone. His eyes widen when he sees me. Slowly, he extends an emaciated arm covered with blotches to hold my hand.

We don’t speak much when I first arrive. It will take him several minutes to get his bearing and marshal his strength in the presence of a visitor, especially a son he hasn’t seen in a year and a half, and for 20 years before that. I ask him if I can pull up a chair and he nods yes while beginning the elaborate process of sitting up a bit in his bed.

His nurse, Jennifer, comes in and asks him to take a medication called Reglan. When a diabetic’s nerve damage affects the stomach, a condition called diabetic gastroparesis, food just sits there because the muscles are no longer signalled to contract. The stomach is paralysed. The resulting nausea, vomiting, heartburn and fullness would kill anyone’s appetite. Reglan is designed to increase stomach and small intestine contractions. In theory, this should aid with digestion, except my father can’t swallow it and spits it back up. I pick up a washcloth from his tray table and gently wipe his mouth.

Neither of us is a stellar conversationalist, but after a few minutes we begin talking to the extent that he is able to in this state. “I’m sorry I haven’t seen you since the last time,” I say. “I really haven’t flown anywhere for the past year because, frankly, I’m terrified of it.” “That makes two of us,” he says with a slight grin.

Normally, this would be one of his better days, he says. There’s no dialysis scheduled. But he says that he’s feeling particularly under the weather today and is dreading the prospect of having his blood cleaned again tomorrow.

For him to have survived for as long as he has, after what he’s been through, is truly remarkable. “I’m not a quitter,” whispers my father at one point. “I’d still like to have a few more good years.” I suspect he has only a few weeks or months left, at the very most, but I tell him how great it will be when he leaves this place behind. He nods his head in agreement. A month and a half earlier, he had a seizure, which isn’t unusual when diabetes advances to this stage. He’d been depressed ever since, I was told. That’s typical, too.

My father says that he needs a nap. I promise him I’ll be here when he wakes up. When his eyes flutter back open after five minutes, he extends his arm for my hand, and we chat a little more. I tell him I’ll be in LA for a few weeks and that I want to spend as much time with him as he can manage. I ask him if I can accompany him to a dialysis session. He’s surprised, but grants my request. “Nothing happens… it’s really boring,” he says. I tell him I’ll bring reading material; he manages a laugh.

The next morning, a pair of twentysomething paramedics, Kevin and Frederico, show up to transport my father to his dialysis session at another facility. “These guys are my buddies,” my father says. Transferring his skeleton from hospital bed to trolley is a delicate dance. They end up grasping two corners each of the blanket underneath him, and then, on a synchronised count, lift him and the blanket from the bed to the trolley in one sweeping motion.

After my father’s been wheeled out of the facility, one of the guys slides in behind the wheel of the ambulance. I pile into the back with my father, who remains on the trolley, and the other tech. During the 15-minute drive, Kevin explains that we’re in a basic ambulance, lacking only drugs and a defibrillator. I ask him how many of their transports involve dialysis. He says 90 per cent, noting that his company specialises in those calls. The business of kidney cleansing isn’t cheap.

The paramedics wheel my father into the kidney dialysis centre. With stations arrayed around the large room, TVs hung from the ceiling and technicians moving from person to person, it looks like a nail salon or launderette. Then I see that the frail, sickly bodies of patients, most of them elderly and swaddled in blankets, are hooked up to artificial kidneys. When the goal of diabetes care is simply to manage complications over time, rather than going to the source and addressing insulin resistance, this is where you wind up.

“I guess you know what’s going on with your father,” a young technician named Sarah says to me. “Uh, sort of,” I reply, with more than a hint of embarrassment. I can’t imagine the severe judgment she must be passing on a son who pleads ignorance when asked about his own father’s suffering, which she witnesses several times a week. She fills me in on his weight loss and worsening mental outlook.

What I didn’t know was that my father had been cutting short his dialysis treatments. Whereas healthy kidneys work round the clock, dialysis has only 12 hours each week to attempt the same job. Short-changing it will result in a nitrogen build-up in the blood and other harmful consequences.

Given my father’s frailty, I can’t picture how he would stop a session even if he wanted to. When Sarah leaves to tend to another patient, I turn to my father: “Dad, you have to try to make it through the whole session each time, OK? It’s important. You’ll feel better if you can do that.”

After we return to the care facility and my father has been lifted back in his bed, he and I discuss our next visit. We plan it for two days hence. I hold his hand and tell him to sleep well, that I’ll see him very soon. “Oh, call first,” he says softly as I turn to leave. When I arrive on a Monday afternoon, I haven’t called ahead, but he’s expecting me. I can tell something is on his mind. I barely settle into a chair before he launches into a speech of sorts: “A long time ago, my wife and I decided to hide the fact from our kids that I had you kids from a previous marriage, to protect them. I remember it being her decision, and she says it was mine, but either way, it was a mistake.”

After my father finishes his speech about past mistakes, he falls silent. I go over and hug him, kiss him on the forehead and cheek a few times and say goodbye. I scribble my number on a notepad and place it on his tray table. “If anything changes, please give me a call,” I say, turning to leave. “You know how I feel.”

Diabetes reaches a point where the victim’s body can no longer be salvaged and the same can be said of the ties that bind human beings. A shared disease can’t heal decades of neglect. Especially when the disease is itself borne of neglect. Perhaps subconsciously, I might have thought it could, and I was wrong. But my father and I were both wrong in thinking we didn’t know each other. We knew each other better than either man would have ever cared to admit. When I walked out of his room that day, I would have bet my life that he would never pick up the phone and call the number I had left him. And he never did.


Five months after his father died, Jeff O’Connell was given a clean bill of health. He credits his recovery to daily exercise and an overhaul of his diet: eight small meals a day that are high in protein and fat and enough self-discipline to say no to chips, doughnuts and hamburger buns.

Jeff O'Connell is the author of Sugar Nation: The Hidden Truth Behind America’s Deadliest Habit and the Simple Way to Beat It, published by Hyperion on July 19.
Link to full article
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Zute
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Re: UC TV: The skinny on fat (Part 1)

Post by Zute »

Second installment. Pretty good, IMHO.

http://www.uctv.tv/skinny-on-obesity-sickeningly-sweet/
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Re: UC TV: The skinny on fat (Part 1)

Post by AbyssalMage »

Tudamorf wrote:It would be interesting to see where this goes -- whether it's just a rehashing of the fructose hypothesis or something more interesting.

But, strictly for weight maintenance, a calorie is a calorie.

Americans are getting fatter because their calorie intake has been steadily rising since the 1970s (not just from sugar, but also from steadily increasing quantities of meat, added fats, and grains) and they're doing less manual work than ever.

Show me a fat person, and I guarantee you that their diet and activity level will show that they're overconsuming.

http://www.cnn.com/2010/HEALTH/11/08/tw ... index.html
Twinkie diet helps nutrition professor lose 27 pounds

Twinkies. Nutty bars. Powdered donuts.

For 10 weeks, Mark Haub, a professor of human nutrition at Kansas State University, ate one of these sugary cakelets every three hours, instead of meals. To add variety in his steady stream of Hostess and Little Debbie snacks, Haub munched on Doritos chips, sugary cereals and Oreos, too.

His premise: That in weight loss, pure calorie counting is what matters most -- not the nutritional value of the food.

The premise held up: On his "convenience store diet," he shed 27 pounds in two months.

For a class project, Haub limited himself to less than 1,800 calories a day. A man of Haub's pre-dieting size usually consumes about 2,600 calories daily. So he followed a basic principle of weight loss: He consumed significantly fewer calories than he burned.

His body mass index went from 28.8, considered overweight, to 24.9, which is normal. He now weighs 174 pounds.

But you might expect other indicators of health would have suffered. Not so.

Haub's "bad" cholesterol, or LDL, dropped 20 percent and his "good" cholesterol, or HDL, increased by 20 percent. He reduced the level of triglycerides, which are a form of fat, by 39 percent.
So he changed 2 variables. Not sure how he proved what you where trying to point out. High Fructose Corn Syrup has been linked to wait gain but the reasons haven't been found (From everything I have read so far). But I know they are doing more experiments (One in California and one in Illinois) so their results should be out in the next couple of years ('13 or '14).
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Re: UC TV: The skinny on fat (Part 1)

Post by Tudamorf »

AbyssalMage wrote:So he changed 2 variables. Not sure how he proved what you where trying to point out.
If you consume fewer calories than you expend, you will lose weight. For weight maintenance, a calorie is a calorie, whether those calories come from sugar, broccoli, hot dogs, or some combination, and whether they're expended jogging or playing your game console.

Anyone who tries to tell you otherwise a) doesn't know what he/she is talking about, and b) is (ironically) usually overweight too.

Health and disease consequences of diet are another matter entirely, but strictly in terms of weight maintenance, this is an iron-clad law.
AbyssalMage wrote: High Fructose Corn Syrup has been linked to wait gain but the reasons haven't been found
Of course they've been found. It has calories, and if you eat in excess of your maintenance requirements, you will gain weight.
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Re: UC TV: The skinny on fat (Part 1)

Post by AbyssalMage »

Maybe you haven't read the two studies but both showed a calorie =/= calorie. One was done by a chemist and the other by Doctoral student's but its been about 2 months sense I wrote the paper. They are not sure why this is but they have multiple theories why. But those results wont be published for awhile because they have to conduct all the long term experiments (1 year+) and that is only if they get positive(negative?) results which isn't guaranteed.

I can tell you one of the theories, and the one I think is the most reasonable, is that High Fructose Corn Syrup is a few steps away from alcohol and your body can't break it down as easily as real sugar so it gets stored as fat. Not saying this is actually what happens, its just one theory of many they are testing. I know there was a Youtube Video about it posted here on the forums and there is a research paper by a different person (I couldn't use Youtube as a source even though it was published by a University) stating the same conclusion that chemically speaking, that HFCS calorie > normal calorie when the body tries to break it down and they have found similar things in other chemically altered ingredients. But until there is more research its just an unproven theory :( of why they are not equal.
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Re: UC TV: The skinny on fat (Part 1)

Post by Tudamorf »

AbyssalMage wrote:Maybe you haven't read the two studies but both showed a calorie =/= calorie.
So a chemist and a doctoral student disproved the laws of thermodynamics? Seriously?
AbyssalMage wrote:High Fructose Corn Syrup is a few steps away from alcohol and your body can't break it down as easily as real sugar so it gets stored as fat.
Nonsense. HFCS is corn syrup (pure glucose) that is treated with enzymes to convert some of the glucose to fructose. HFCS 55, the type used in soft drinks, is nearly identical to sucrose, except it has 55% fructose instead of 50% fructose. More fructose may stress the liver, increase visceral fat, increase triglycerides, and so on, but strictly in terms of weight management, they are the same.

Domestic HFCS consumption has been quickly declining since peaking around 2000 (see USDA's Table 30, U.S. high fructose corn syrup (HFCS) supply and use, by calendar year, if you doubt it), but Americans have been getting fatter than ever. Total sugar consumption has been declining too.

The cause of American obesity is not sugar per se, but calories. Americans are eating more than ever (especially added fats and grains, but also more meat -- see USDA's Loss-Adjusted Food Availability spreadsheet), sitting their fat butts on chairs all day and staring at computer screens instead of doing real work, and getting fatter than ever.

Judging from the size of his spare tire on the video, Dr. Lustig easily has 30 pounds to lose himself. And if you caught that brief shot of Kelly Brownell at 7:32, he is truly obese. Don't you find it ironic that fat people are preaching about the path to being lean? If they had all the magic answers, you'd figure they'd use them themselves first.

Again, Lustig may have some good points about the diseases, but blaming obesity solely on sugar is silly.
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Re: UC TV: The skinny on fat (Part 1)

Post by AbyssalMage »

Tudamorf wrote:
AbyssalMage wrote:Maybe you haven't read the two studies but both showed a calorie =/= calorie.
So a chemist and a doctoral student disproved the laws of thermodynamics? Seriously?
A)They proved that once a "calorie" enters the body that the amino acids(?) that are responsible for breaking down your food don't have the same process and causes more food storage(fat, usually in the liver). That was the chemist who supported(proved) this did. And there has been growing support for this research, not just HFCS, that chemically modified food does this.

B)The Doctoral students proved that 1 calorie from HFCS and 1 calorie from Sugar were not the same. Although the rats had the the same caloric intake (i.e. the same approx. # of calories) the rats who drank HFCS gained more wait. Enough weight in fact that they are doing follow up research because they had held your hypothesis. It wasn't even what they were studying, like most science, it was an accidental observation.

So call it what you will but the evidence is there.
AbyssalMage wrote:High Fructose Corn Syrup is a few steps away from alcohol and your body can't break it down as easily as real sugar so it gets stored as fat.
Nonsense. HFCS is corn syrup (pure glucose) that is treated with enzymes to convert some of the glucose to fructose. HFCS 55, the type used in soft drinks, is nearly identical to sucrose, except it has 55% fructose instead of 50% fructose. More fructose may stress the liver, increase visceral fat, increase triglycerides, and so on, but strictly in terms of weight management, they are the same.

Domestic HFCS consumption has been quickly declining since peaking around 2000 (see USDA's Table 30, U.S. high fructose corn syrup (HFCS) supply and use, by calendar year, if you doubt it), but Americans have been getting fatter than ever. Total sugar consumption has been declining too.
HFCS consumption has risen in the US, not fallen. Nearly everything you purchase now, that isn't organic or locally produced has HFCS. It's called technology and relabeling. Americans have been doing it for years.
The cause of American obesity is not sugar per se, but calories. Americans are eating more than ever (especially added fats and grains, but also more meat -- see USDA's Loss-Adjusted Food Availability spreadsheet), sitting their fat butts on chairs all day and staring at computer screens instead of doing real work, and getting fatter than ever.
Actually, if you eat sugar you will lose weight. But I understand your point, weight gain is more than just HFCS fault. But HFCS is part of the problem, not the solution when it comes to wait gain. Sugar on the other hand is neutral when it comes to wait gain/loss.
Judging from the size of his spare tire on the video, Dr. Lustig easily has 30 pounds to lose himself. And if you caught that brief shot of Kelly Brownell at 7:32, he is truly obese. Don't you find it ironic that fat people are preaching about the path to being lean? If they had all the magic answers, you'd figure they'd use them themselves first.
Losing weight isn't easy, period. Look on Youtube of all the Athletic Trainers gaining weight for 90 days and then trying to lose it so they can better help their clients. These are people who have had a healthy life style and only gained weight to better empathize with the difficulties of their clients. It really sheds some light on the difficulties of gaining too much weight.

There used to be an interview with Sylvester Stalone on Youtube, may still be there if they didn't claim copy write protection, on when he gained weight for one of his jobs/movies. This is a guy who was at peak shape and gained 30 pounds for his role in a film and he discusses what it was like not only gaining the weight, but keeping it on, then losing it after filming was done.
Again, Lustig may have some good points about the diseases, but blaming obesity solely on sugar is silly.
I agree. HFCS isn't the sole reason.

And yes, there is a difference between HFCS and Sugar. They are not interchangeable.
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Tudamorf
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Re: UC TV: The skinny on fat (Part 1)

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AbyssalMage wrote:But HFCS is part of the problem, not the solution when it comes to wait gain. Sugar on the other hand is neutral when it comes to wait gain/loss.
No. They are the same when it comes to weight maintenance. The same. HFCS is just the current scapegoat for American gluttony, sloth, and ignorance. Once HFCS is replaced with sugar or the next magic diet fix, the problem will remain and the media will find a new scapegoat.
AbyssalMage wrote:Losing weight isn't easy, period.
Actually, it is very easy to lose weight, or maintain a healthy weight. Trivial really, compared to real athletic conditioning. I can lose or gain weight very easily by altering food quantity. Billions of humans have done it successfully for millennia, until 30 years ago in America when they were told nothing is their own fault, and there's always a magical pill around the corner that will cure their faults, and oh, would you like to supersize that?
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