Well, for those of you that were interested, here are the preliminary results of my refeed or carb-up last Monday.

Pre-carb-up weight, Monday am: 238.4 lbs.
Monday - ate whatever I wanted, high carb foods, candy, sugared fruit ice, etc. It was about 3500 calories all together.
Tuesday am weigh-in - up three pounds. Tuesday, back on LC, carbs below 20 grams.
From Wednesday to Sunday I kept eating low-carb.
On Friday I added some exercise too (which I haven't been doing enough of), 20-30 minutes cardio and upper body weight training exercises.
On Saturday I went for a 45 minute brisk walk outdoors (very cold).
Sunday - no exercise.
Monday am weight: 236.2 lbs - loss for the week 2.2 lbs.

My interpretation of the results: I lost a decent amount, but still lower than my average loss per week over the past 23 weeks (avg loss has been 2.6 lbs per week), so I'm thinking the carb-up didn't have much effect for me. Now my weight loss hasn't been consistent, so maybe this would have been a week with no weight loss and it was better, but I don't know this for sure. And maybe the 2.2 I lost this week was more a result of the added exercise than anything else, so not only would I not have lost weight without it, but the refeed would have had no effect whatsoever? As someone pointed out to me, though my weight loss rate had slowed, I was still doing relatively well before the refeed. So, I'm thinking that maybe my leptin levels and metabolism didn't need a jolt, they were working just fine before and that's why this didn't produce great results. Maybe the result would have been different if I'd been truly stalled when I tried it.

Summary conclusion: I don't have a clue if it worked or not, but it didn't seem to have hurt me at least! Thank goodness!

Valerie

Below is an article from today's Washington Post on lepin. It seems to provide support for the idea that lepin levels are involved in the rate at which our body burns fat. I hope that someone, somewhere, is doing some research on whether or not losing a certain amount of weight adversely affects lepin levels in ways that can't just be explained by saying that we now have fewer fat cells. The more I read about lepin, the more I think that may be where the explanation of why our weight loss SUDDENLY slows down to a crawl, lies. You can't explain the suddenly slowdown just by saying that we now weigh less and therefore our bodies need fewer calories. If that were the case, it would be a gradual slowdown.

Washington Post article (February 16, 2004):


A Dream of Burning Fat Cells

In what sounds like every dieter's dream, scientists have figured out a way to turn fat-storing cells into little fat-burning machines. Unfortunately, it has only been done in laboratory rats, and the human applications remain in the future.
Nevertheless, the scientists say it could eventually lead to new ways to help Americans fight their expanding waistlines.

"This is in no way a cure for obesity," said Roger H. Unger of the University of Texas Southwestern Medical Center in Dallas, who led the work. "But it is a road map. It's a strategy for future research."

Unger and his colleagues injected rats with a virus genetically engineered to carry the gene for the hormone leptin, which is normally produced by fat cells. The virus infected the animals' livers, causing the organ to produce leptin. The resulting high levels of leptin in the animals' bloodstreams made the rats rapidly lose weight.

When Unger and his colleagues examined the animals' fat cells, they discovered that they had shriveled in size and were chock-full of an unusually large number of structures known as mitochondria, tiny energy-producing powerhouses inside cells, said a report last week in the Proceedings of the National Academy of Sciences.

"We turned them into fat-burning machines full of mitochondria," Unger said in an interview.

The findings indicate that fat cells normally develop a defense against their own leptin, which would explain why injecting the hormone into the body has failed to make people lose weight. But when the hormone comes from another part of the body, it appears to bypass that defense. If researchers could identify that mechanism and harness it, that could lead to new weight-loss treatments, Unger said.

"The fat cell builds a defense against its own leptin. This study really shows what it's defending against," Unger said. "What we need to do is find that barrier and bypass it."

-- Rob Stein

"The fat cell builds a defense against its own leptin."

I agree with Liz--now we're talking! The body is finding ways not to lose its "precious" fat.

I think I will buy and read Schwarzbein II. I understand that she talks a lot about lepin in there. I'm a little skeptical about what she has to say -- she was such a strong pusher of HRT and we all know what has happened with that -- but just because someone was wrong on one thing does not mean that they are wrong on everything else.

Very interesting article Liz. Thanks for sharing. I found the abstract online and you have to be a researcher just to be able to read it. I'm glad the Post translated it. It sounds very promising.

abstract

Rapid transformation of white adipocytes into fat-oxidizing machines

Lelio Orci *, William S. Cook , Mariella Ravazzola *, May-yun Wang , Byung-Hyun Park , Roberto Montesano *, and Roger H. Unger
*Department of Morphology, University of Geneva Medical School, Rue Michel Servet 1, CH 1211 Geneva 4, Switzerland; Gifford Laboratories of the Touchstone Center for Diabetes Research, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Y8.212, Dallas, TX 75390-8854; and Veterans Affairs Medical Center, Dallas, TX 75216

Contributed by Roger H. Unger, December 15, 2003

Adenovirus-induced hyperleptinemia rapidly depletes body fat in normal rats without increasing free fatty acids and ketogenesis, implying that fat-storing adipocytes are oxidizing the fat. To analyze the ultrastructural changes of adipocytes accompanying this functional transformation, we examined the fat tissue by electron microscopy. After 14 days of hyperleptinemia, adipocytes had become shrunken, fatless, and encased in a thick basement-membrane-like matrix. They were crowded with mitochondria that were much smaller than those of brown adipocytes. Their gene expression profile revealed striking up-regulation of peroxisome proliferator-activated receptor coactivator 1 (an up-regulator of mitochondrial biogenesis not normally expressed in white fat), increased uncoupling proteins-1 and -2, and down-regulation of lipogenic enzymes. Phosphorylation of both acetyl CoA carboxylase and AMP-activated protein kinase was increased, thus explaining the increase in fatty acid oxidation. The ability to transform adipocytes into unique fat-burning cells may suggest novel therapeutic strategies for obesity.