Skip to comments.A Diet Manifesto: Drop the Apple and Walk Away
Posted on 01/02/2011 3:16:05 PM PST by neverdem
Another year ends, and still the war drags on. In the final salvo of 2010, the combatants are lobbing fruit.
Not literally, of course, though they might like to: The long war of the weight-loss diets has aroused passions just about as overheated as those of any military conflict.
How is a person best advised to lose extra weight and retreat from diabetes and heart disease? Count calories, cut fat and fill up on fruits and vegetables? Or turn instead to a high-protein, high-fat...
In the opposite corner we have Gary Taubes, the science journalist who has thrown in his lot with the high-fat, high-protein crowd, arguing in his new book that the overweight should just put down their apples and walk away: If were predisposed to put on fat, its a good bet that most fruit will make the problem worse, not better.
But those who are curious about the science behind it all could do worse than to pick up Mr. Taubess book Why We Get Fat: And What to Do About It.
And the only one of these hormones under even a smidgen of voluntary control is insulin. At this point Mr. Taubes merges onto the narrative highway traveled by all low-carb advocates: The bodys insulin levels are largely determined by ingested carbohydrates, and for some people the high-carb foods that stimulate insulin secretion and cravings for more high-carb foods are, in this worldview, just so much poison.
So that apple a filling package of fiber and vitamins to the Weight Watchers folks is just a serving of fructose to Mr. Taubes. Fructose is the problematic sugar our bodies turn to fat the most readily, and if you are programmed to be fat, an apple will make you that much fatter...
(Excerpt) Read more at nytimes.com ...
This paper argues otherwise. Do you have any more up to date references than this?
A high flux of fructose to the liver, the main organ capable of metabolizing this simple carbohydrate, perturbs glucose metabolism and glucose uptake pathways, and leads to a significantly enhanced rate of de novo lipogenesis and triglyceride (TG) synthesis, driven by the high flux of glycerol and acyl portions of TG molecules from fructose catabolism.
What I still don't understand is at what point does the body start the cannibalization of skeletal muscle. Is that what body-building "over-training" is about - simple lack of protein vs exercise? Using the amino acids in other muscle groups to repair the damage of the muscles just exhausted? Sort of a self-defeating Peter paying Paul cycle? So more protein will correct this cycle? Right? At what point with additional protein are you adding fat plus muscle? That's the tough one for us amateur weight lifters.
I also don't get why nutritionists suggested 5 or more small meals (Weight Watchers) rather than 2 or 3 meals of comparable calories and macro-nutrient ratios. Although with your burn formula, I do now better understand why Atkins works so well. Thanks for the feedback. What a complex system our bodies are and no wonder there has always been so much contradicting info out there to us laymen.
BTW, I should have used a plate of pasta as a contrast with saltine crackers for differences in glycemic index. A baked potato is about the same as a cracker, ~100.
“But wasn’t the eating constrained to mealtimes?”
When I was a young enlisted man, I ate only when the chow hall or mess decks were open. Got lots of exercise, too. Put on weight.
Heck, I put on fat in boot camp.
“How about it, dsc; would you lose weight at the Hanoi Hilton?”
Is it your assertion that a person should have to reduce intake to Hanoi Hilton levels to maintain a normal weight? Surely not.
I am not saying that a person cannot starve to death. I am saying that it is *not*normal* when a person must both reduce intake to a preposterous level *and* exercise like an elite athlete to avoid obesity.
I am saying that those conditions indicate that there are other factors at work.
“whatever you do, don’t put your money where your mouth is. You’ll lose whatever you have”
If I expected to live long enough to collect, I’d ask if *you* were open to a wager.
“If you want to stuff your face, sit on your butt and get fatter, its your own business.”
Arrrgh, the sumg...it’s choking me.
I used to be an elite athlete—if you call a silver medal at a US national championship elite—and an avid camper and backpacker.
In June of 1978 I walked out of the rockies at 160 pounds after two weeks without hearing another voice or a man-made sound.
I kept my weight at reasonable levels for as long as my health allowed me to exercise like an elite athlete. When I no long could do so, weight gain set in, despite extraordinary efforts to control my weight through diet. (Staying up until 2am preparing and freezing measured portions of low-glycemic-index foods, et cetera.)
My wife, at 5’5” and 120 lbs, ate more than I did. (I am—or was—right at 6’, with a large frame.)
You might want to read the post that immediately followed the one I am responding to. And another twenty or thirty articles on the latest research into the causes of fattitude.
Or continue to pat yourself on the back for accidents of birth and the vicissitudes of life.
Yes, it is NOT NORMAL. Earlier, you claimed that MOST of obesity is not related to intake/output. The fact is, when you need to starve yourself to lose weight, something is wrong.
A few years ago, I managed a Group level Air Force Fitness program. The base exercise physiologist gave the program managers an excellent explanation concerning calorie intake. He asked us to consider the number of fat paraplegics vs the number of fat quadriplegics. He said you rarely see a fat quadriplegic because they can only eat their prescribed diet. A paraplegic can feed them self and overeat.
We, the Program Managers, learned a lot of interesting stuff. For instance, drinking a lot of orange juice is NOT good for weight loss. You're still taking in a lot of sugar. Your body will convert the sugar into fat and store it. It's the same with soda and sugary "juice boxes."
“But at adulthood, many people develop a condition called insulin resistance. This condition causes your body to turn the starchy stuff you eat into fat instead of into energy. In a large percentage of the population, insulin resistance leads to type 2 diabetes in later life.”
I am very grateful for that information.
I am furious, but not at you, because this is the first time I have encountered that information. I have to wonder why the legions of people who should have told me about that never did.
“Read Gary Taubes Good Calories, Bad Calories for a more thorough explanation.”
What a coincidence! I was clicking around yesterday from one article on nutrition to another, and ran across references to that in several places. It seems he has another book out, Why We Get Fat: And What to Do About It.
Some people said it was a shorter, more accessible version of “Good Calories, Bad Calories,” but I don’t know, not having read either book.
I am definitely going to read “Good Calories, Bad Calories,” and soon.
Thank you for contributing to a discussion rather than exacerbating a quarrel.
The only gratuitous insult I see is you labelling my response as a gratuitous insult. I can only assume you to be an illiterate jerk. If you were literate I’d suggest that you, too, read the article.
I cut out meat for three days. On the third night I dreamed I was a big cat eating out the gut of a fresh killed water buffalo. Went out for steak ASAP.
Don’t listen to strangers who get paid by the word.
That's quite a claim when the original post (The root cause of most obesity is an overabundance of food and lack of physical activity) reflects established scientific fact.
Some people work hard to complicate the issue to support a political agenda. Some are motivated by a desire to say Oh, it isn't my fault I'm fat -- my obesity is caused by genetics.. The former is understandable. There are people who stand to gain politically from such a misunderstanding. The latter is caused by illiteracy, plain and simple.
If you were literate Id suggest that you, too, read the article.
I've read the article and you can choose to believe Taubes if you'd like. But Taubes is a fraud who learned how to sell books a long time ago. Taubes is a proponent of the Atkins diet a dubious dietary strategy not based on scientific evidence, which seems to have been designed to sell diet books by telling people that they can eat as much as they like of some foods and still go on a weight-loss diet.
Demonizing one macronutrient or another is a common trait of diet fads. We've learned from recent history that you can sell diet advice more easily if you claim that fats or carbs are the problem while the (obvious) idea that calories are the problem seems to be something that few people are willing to pay for.
Equating long time FReepers with the Obamas, because they adhere to established science, is not a formula for winning friends on the forum. But, if Kamikaze is your style, then, by all means, carry on.
Your alternate reality is very entertaining.
Since I have personal memories of JFK’s funeral I am certainly qualified to stand by statements.
Shakey’s was a treat, as was Henry’s and McDonald’s.
People then didn’t spend the time in front of the tube like they do today, nor did they gorge on fast foods like today.
Supersized hadn’t been invented yet.
So I can compare you to Hillary or Michelle and you’ll enjoy the compliment?
And that laughter you hear...we’re not laughing *with* you.
“Since I have personal memories of JFKs funeral I am certainly qualified to stand by statements.”
Oh, I don’t know. That was 1963. If you were, say, three at that time, you wouldn’t have become aware enough to develop useful opinions until about 1970. Since we’re talking about the ‘50s and ‘60s, that would pretty much time you out.
Doesn’t matter. Until something dissipates that cloud of smug, there’s no point in even trying to talk with you.
It appears that you're refering to:
Most of the metabolic effects of fructose are due to its rapid utilization by the liver and it by-passing the phosphofructokinase regulatory step in glycolysis, leading to far reaching consequences to carbohydrate and lipid metabolism. These consequences include immediate hepatic increases in pyruvate and lactate production, activation of pyruvate dehydrogenase, and a shift in balance from oxidation to esterification of nonesterified fatty acids, resulting in increased secretion of very-low-density-lipoprotein (VLDL). These effects are augmented by long-term absorption of fructose, which causes enzyme adaptations that increase lipogenesis and VLDL secretion, leading to triglyceridemia, decreased glucose tolerance, and hyperinsulinemia. Acute loading of the liver with fructose causes sequestration of inorganic phosphate in fructose-1-phosphate and diminished ATP synthesis. Consequently, the inhibition by ATP of the enzymes of adenine nucleotide degradation is removed and uric acid formation accelerates with consequent hyperuricemia. These effects are of particular significance to potentially hypertriglyceridemic or hyperuricemic individuals.
Do you have anything more recent that refutes it? I'd be happy to read it. Here a more recent citation:
Increasing consumption of sugars is one of the contributing factors to the obesity epidemic. Both cane sugar and high-fructose corn syrup(HFCS) contain glucose and fructose. Fructose, in contrast to glucose, is known to potently stimulate lipogenesis, but the mechanisms responsible are not yet fully known. This paper reviews several possible pathways that might be involved, such as activation of pyruvate dehydrogenase, and transcriptional activation of sterol regulatory element binding protein 1c by key regulators such as peroxisome proliferator activated receptor-γ co-activator 1β and the splice variant of X-box binding protein 1. Together, these pathways might establish a feed forward cycle that can rapidly increase hepatic lipogenesis. As a result, dietary fructose might promote the development of nonalcoholic fatty liver disease, which in and of itself, can result in hepatic insulin resistance, a key feature of type 2 diabetes mellitus.
I never heard of nonalcoholic fatty liver disease when I was in medical school two decades ago, but I can find stories about it in Family Practice News now. I used to think that a six carbon monosaccharide wouldn't have any different effects from another six carbon monosaccharide, but fructose makes me question that assumption. The HFCS used in soft drinks is 55 % fructose and 42 % glucose. Couldn't the excess fructose shift the equilibrium from oxidation to esterification of nonesterified fatty acids?
Using fructose and (nafld or nonalcoholic fatty liver disease or non-alcoholic fatty liver disease) at PubMed gets 40 citations.