is this how you spell luxuskonsumption?

In grade school health class I was taught that there were three kinds of people; ectomorphs, endomorphs, and mesomorphs. Ectomorphs tended to be lean and have smaller muscles, endomorphs had more muscle but also more fat, and mesomorphs had lots of muscle and more fat than the ectomorph but less than the endomorph.





Seen from a Taubesian cellular starvation angle, something suggests itself. There's could be a very simple difference between these three types of people;





Ectomorphs don't store much energy in their fat cells. Therefore, when in the fasting state, they are forced to metabolize lean tissue for energy. Go to Bodybuilding.com and dig around in the forum and you'll find no shortage of very lean teenage boys claiming to have a very hard time building lean mass, even when eating at very high calorie levels.





Endomorphs tend to store too much energy in fat cells, or perhaps have trouble getting out of the fed glucose-burning state and back into the fasting state. So instead of those fatty acids locked up in their fat cells, they turn to lean tissue for fuel.





Mesomorphs have excellent metabolisms. If they eat lots of food, they have no trouble at all storing away both protein and fat. They also have little trouble accessing that fat, probably switching readily between the fed and fasted state. So their muscles get lots of energy when they eat, and lots of energy when they're asleep. Sparing lean tissue.





Taubes writes about adolescent hogs, who, when fed a low-protein diet, simply eat more of it to support growth, and burn the extra calories off. He also mentions research in the late nineteenth century by Carl von Voit and Max Rubner of something like this happening in humans, with overfeeding failing to cause weight gain. This effect is termed luxusconsumption.





Do a search for more recent studies on luxusconsumption, and you get stuff like this 9


with abstracts starting with lines like this;





"In this paper, we redefine the term luxus consumption to mean food waste and overconsumption leading to storage of body fat, health problems, and excess resource utilization."





So what's changed between the late 19th century and today? The usual line is that the measurements have gotten better. We got fancy metabolic chambers, we can measure oxygen utilization and calculate RQ, (respiratory quotient. By measuring oxygen consumption, researchers can calculate how much of a person's energy use is coming from carbs, fat, protein, etc.) Blah blah blah.





It's nice that we have a fancier yardstick. But late nineteenth century researchers were perfectly capable of calculating and tabulating how much food was being consumed, and the composition of that food, and whether or not the subject consuming that food was gaining fat mass. So I don't think we just measure stuff better now really cuts it.





So the charge against Carl von Voit and Max Rubner becomes one of incompetence or of dishonesty. Always possible; but these are serious charges. Especially for a scientist.





But what if it's not the yardstick that changed? What if it was the nature of the thing being measured?





The thing being measured was the effect of overconsumption of food on human fat stores.





Is there anything that can change the effect of food on an organism?





Maybe fructose?





Peter at Hyperlipid posted this article someone sent him in an email; I'm yoinking it here for my own foul purposes;





Florida Researchers Find Consuming Fructose Can Suppress Leptin Hormone, Lead l





Fat cells put out leptin to signal that they're full to overflowing; it's sort of a signal that they have energy to spare and wish to share it. The signal is "heard" at various places in the body, but of particular importance is the hypothalamus. Triglycerides interfere with leptin's ability to send a signal prompting the hypothalamus to respond by sending it's own messengers to sort of redirect that energy. Fructose supplementation is an excellent way to up triglyceride production. Almost any carbohydrate source will do the same, but fructose really does the job.





In the study fructose interfered with the action of leptin not just while the mice ate fructose, but later on when they switched to what they called a high-fat diet, but was probably a high corn starch and high (or even just medium) fat diet.



How else have we changed?



Much is made of inactivity as a cause of childhood weight gain. Tv, computers, video games. One obvious alternative to any association of these activities to weight gain in children is that these are all indoor activities, which might affect vitamin d levels. And it's been shown that vitamin d affects all kinds of things in the body, one of them being thyroid stimulating hormone, which can affect the thyroid which has a rather obvious connection to the availability of stored fat.



I spent my pre-teen years in the 70s, and was lean. Anyone remember The Kroft Supershow? HR Puff 'n Stuff? Gilligans Island, The Addams Family, Scooby Doo, The Flintstones, The Jetsons, Captain Caveman, Bewitched, The Munsters, Happy Days, Laverne and Shirley, All in the Family, Star Trek, Rocket Robin Hood, Looney Tunes, Trouble with Tracy, Definition (some are Canadian, so you might not.) Uncle Bobby The Friendly Giant Sesame Street, Get Smart, Hogan's Heroes, Maude, I Dream of Jeanie, The Brady Bunch, Batman, I think I got in some old Superman reruns, Ponderosa, Little House on the Prairie, The Electric Company, Romper Room, the list just doesn't end. Which doesn't really back up the idea that TV is keeping kids from getting enough sun, compared to my own youth. But I do remember having a pretty dark tan by the end of every summer.



I mentioned vitamin d's connection to the thyroid. (One of them, at least.) How about other nutrients that affect the thyroid? The most obvious one is iodine. I have no idea what the iodine or the thyroid status of the people in the original luxuskonsumption studies might have been, but it's just one more thing modern researchers might need to know before dismissing the results of those studies out of hand. Table salt is iodized, by law. The salt used in industry when producing corn and potato chips or frozen dinners doesn't necessarily have any iodine supplemented. Much of the US and Canada has iodine-deficient soil. Avoiding egg yolks and whole milk (removing the whey from milk removes much of the iodine) wouldn't help any.



Thyroid disorders do seem to be more common than they probably should be. Treatment of choice seems to very rarely involve iodine supplementation, at least from what I can tell from bopping around on the web. The discussions mostly seem to revolve around supplementation of t3 and t4. It's hard to believe that iodine's never the answer. One problem with supplementing iodine in an actual case of iodine deficiency is that it can sometimes cause goiter.



http://www.ajcn.org/cgi/content/full/86/4/1040 This study, "Vitamin A supplementation in iodine-deficient African children decreases thyrotropin stimulation of the thyroid and reduces the goiter rate."



seems to show that vitamin a protects against goiter in iodine deficient areas, even in the absence of iodine supplementation. In the study, vitamin A supplementation decreased thyroid stimulating hormone levels without reducing t4 levels, and the authors suggest that this might show an effect of vitamin a of improving thyroid hormone sensitivity. (Vitamin D, on the other hand, has the reverse effect, increasing output of tsh from the pituitary gland. Which doesn't mean vitamin d bad--it just means you'd better not be vitamin a deficient, is all. It could just be that Vitamin D helps the metabolism notice a need for thyroid hormone, while vitamin A makes your body use the stuff better, in which case the two vitamins wouldn't be antagonist here at all, but rather complementary.)



I don't know if vitamin a would have this anti-goiter effect in those cases where too much iodine precedes the goiter, but it wouldn't be surprising if something involving the balance of vitamin a and d were involved there.

Okay, I wandered all over the place with this. My point was that there are any number of differences in different groups of subjects separated by nutrient status, time, country, what have you. A failure to measure something in one group of people doesn't prove that it doesn't exist in another.