One thing I notice is that I can lose weight (lots of it) and yet my body fat % stays the same… This is mostly likely for two reasons:

1) Lower water retention (water weights 8 pounds per gallon)
2) Protein (muscle tissue) atrophy(loss) because the body is using protein to feed the glycogen levels for the liver and brain, and energy when fat is not adequately supplied.

Because glycogen binds with water in our muscles, we can feel skinny, but our fat cells remain the same size. I agree that fat calories should not be too excessive. This will promote more body fat release, but also will promote muscle loss. Perhaps a way to curb muscle loss would be to workout (strength training) so that body uses more protein from the food to rebuild muscle tissue. And the energy source is more likely to come from fat.

I don’t have the science nailed down myself but this information is derived from stuff I’ve read. Feel free to research for you own.

http://www.drbriffa.com/blog/2010/02/16/higher-protein-diet-plus-resistance-exercise-aids-weight-and-fat-loss-in-type-2-diabetics/

However, you might want to read up on hemochromatosis if you haven’t already. Best wishes.

– I understood. That person is not me. I fit the perfect profile of someone who should indeed have easily reached normal weight goal.

“I wonder if the weight gain during your perimenopause years could have also permanently altered your metabolism.”

– I don’t believe so. The proof is that I lost the 65 pounds easily *after* that point. I’m convinced my metabolism was altered (but not permanently — hence the successful currently ongoing experiment at http://health.groups.yahoo.com/group/Leptin_Resistance) by becoming first leptin resistant and then thyroid hormone resistant, which occured *after* my weight loss and subsequent major surgery.

“One last idea — are your ferritin levels normal?”

– Perfectly normal.

Thank you so much for your thoughtful response. I’m sure your candid sharing of your experiences will help others.
One correction — I’m sorry — I should have said “fat extending down toward the wrists and ankles.” The point was that according to Lutz, the low carb diet can sometimes be less effective in terms of weight loss for middleaged obese women where the fat is deposited all over as opposed to mainly in the stomach area.

I wonder if the weight gain during your perimenopause years could have also permanently altered your metabolism. I agree so much that we women — especially at peri and post menopause have much more difficulties with weight control. So unfair… I definitely believe that thyroid problems (many undiagnosed and many under or incorrectly treated) are part of the puzzle.

One last idea — are your ferritin levels normal or at the high end of normal? MIne are high end of normal and I intend to donate blood.

I am still having periods but my ferritin is always at the high end of normal. I have been eating paleo — organic or grass fed red meat (with fat), daily sardines (for calcium), fish, eggs and and some chicken/turkey/duck plus veggies and some 85% dark chocolate — but the mainstay is meat and it’s high in iron. I drink black coffee and green/white/black/oolong teas so figured that would help make the iron from meat less available — I was wrong. For much of the fall winter (sadly, like every year), I was completely overdosing on nuts and nutbutters — really awful binging — so I have to cut them out completely. Dairy products would undoubtedly allow more low-iron choices — but philosophically, I don’t think adult humans should need milk products…thoughts/suggestions?

– That’s a complex question. Let me try and sort it out. I first ate a low calorie, low fat diet with lots of carbs for years during peri-menopause and went from being slightly overweight to morbidly obese with measured body fat of 53.5%.

– Then I got ‘educated’ and switched to a very high fat, very low carb, moderate (1500-1700 cals a day) WOE. I lost 65 pounds and my bf fell to 27%. At that point I was only 15 pounds from my goal of being slim. I was no longer obese at all, just slightly overweight, with still more stored body fat than was ‘normal’.

– Within a month of having lost the full 65 pounds, I had major surgery. From that day forward, no matter what I did, ate, didn’t eat, etc (went to 1200 high fat cals a day for a full month, weighing and measuring and tracking every mouthful), I could not lose a pound more, nor another inch of fat).

– However, I kept the weight off for a full 18 months, no problem. I weighed exactly the same every single day within an ounce or two. Then, suddenly, I gained 15 pounds in just a few weeks. And it was fat, not water. I had to go up a dress size, and my measured bf went up to 29%. And I can tell you that no matter what — upping fat, lowering fat, lowering calories, doing lots of exercise — that weight would NOT budge for another 18 months, during which my cholesterol starting rising and my temperatures began to drop. A lot.

So now I was 30 pounds from goal, and definitely overweight though still not obese, thank goodness.

“I recall in Wolfgang Lutz’s book, Life Without Bread, there is the admission that low carb diets do now work for everyone and the chances for efficacy are lowered.”

Yes. And Kwasneiwski mentions the same thing. I believe my hypothesis explains it: low carb diets DO work for everyone — at first. In some people however, whether due to extremely low carbs and/or calories over an extended period of time, or due to other stress, physical or psychological, leptin resistance begins. And when it does, it no longer matters what WOE you choose, what nutrients or calories: the body WILL conserve ingested energy and stored fat. In fact, the advice to ‘eat less, exercise more’ only makes things worse over time!

– That’s because the body always takes the least ‘expensive’ and most elegant way to do anything, and in terms of conserving energy, that ‘way’ is to simply turn down the metabolism by stopping T3 production, and ensuring remaining T3 doesn’t enter the cells by upping RT3 production.

“They mention that middle-aged women and those with excess fat extending to the wrists and ankles (as opposed to mostly “apple-shaped” people) may not lose their excess fat and it is unclear why.”

Not a clue, and probably because I don’t believe it’s true. I have *extremely* slim wrists and ankles and always have had, even at my most obese.

“Do you think this reverse t3/leptin issue could arise in someone who is basically maintaining their weight on a VLC diet?”

It can happen to anyone, at any time. Or may not happen at all. It is true that, anecdotally anyway, women rather than men seem to be affected by this. Maybe because we have more hormones to mess with in the first place.

Do you think this reverse t3/leptin issue could arise in someone who is basically maintaining their weight on a VLC diet?

Sorry you’re not familiar with Yahoo Groups. There are now tens of thousands of them on every topic under the sun, and they are completely FREE. There’s nothing to sell (or buy) and not even a need to ‘log in’. You can choose to have all posts go directly to your email address if you prefer. You never, ever have to go to the site itself. And Yahoo Groups are open to all.

Ellen

“To demonstrate the power of the lack of this hormone, I want to show you a video of a little girl whom I’m pretty sure is leptin deficient. Nothing much else could account for this situation. Maybe a pituitary tumor, but I doubt it. I don’t know if she is leptin deficient, but I would bet a fair amount of money that she is. In any case, this is what kids with a leptin deficiency look like.”

It’s also what leptin resistance looks like. The young girl may indeed have a damaged genetic leptin component (the equivalent of mice where this is ‘knocked out’), but most of us who eat a low carb diet and who have low TG’s yet are STILL too fat, most likely have leptin resistance instead.

Mike also wrote: “There is a critical point in the cycle described above. That critical point is when the leptin crosses the BBB. If the leptin can’t get across the BBB, it can’t get to the brain. If it doesn’t get to the brain, it doesn’t shut off the hunger response irrespective of how much is circulating in the blood.”

This is true, but it’s only a small part of the picture, which is why the even older Japanese article you quote about high TG’s blocking leptin’s ability to reach the hypothalamus is outdated. Yes, in grossly LR people hunger rages for the reason you list. But that’s not the only thing LR does. My TG’s are 42. I eat a low carb diet (though not a VERY low carb diet any longer, not after my intensive research on this), and certainly do not suffer raging appetite in the least. I eat quite modestly in fact.

Yet I am still over-fat. And that’s because of the primary response of the brain to LR — to conserve what it perceives to be a lack of energy intake by manipulating the metabolism downward. And it does this primarily through the thyroid hormones, specifically through the T4 to T3 conversion signal.

As you know, T3 is the metabolically active component of the thyroid hormone system. Convert lots of T4 to T3, and you easily burn any excess ingested energy.

However, in Leptin Resistant people, the hypothalamus (which normally receives the leptin signal and which not surprisingly also controls the liver and the peripheral thyroid hormones made therein) sends a different set of instructions. It stops conversion of T4 into T3, and into Reverse T3 (a mirror image of T3 with two crucial differences: RT3 is metabolically inert, and it does not contain the important 5′ molecule that signals the liver that sufficient cholesterol is in the body).

Thus, T3 production falls, and what little is left pools in the blood instead of reaching the cell receptors, because as RT3 increases, it blocks those receptors like a moat before a castle gate. Upshot? You either stop losing weight if you were losing before on low carb, and/or perhaps gain an unexpected ten pounds. Your temperatures go down — and your TC begins to rise, rise, rise — even though all other lipid markers show very low risk for heart disease.

It was in fact my outlier insanely high TC number that made me realize something was systemically wrong, and to do the research necessary to finding out the cause and the cure.

After just two months on the proper medication to pharmacologically override the instructions of my LR hypothalamus, my TC and LDL each dropped by over 120 points, after rising steadily with each blood test for nearly two years. My T3 is now reaching my cell receptors, and my RT3 has dropped by over 500%.

In other words, given the tools at it’s disposal, a leptin-deprived brain doesn’t need to care about whether your TG’s are low due to a low carb diet, or that you’re not overeating: it simply takes whatever steps are necessary to conserve as much fat as possible from the little food you are eating.

Mike wrote: “I would love to see the paper (papers) that have “established” the fact that the main cause of leptin resistance is stress on the endoplasmic reticulum. And why a very-low carb intake would make it worse.”

Happily. You have my email address. Send me the email you’d like to use to join the Leptin Resistance group and I’ll send you an invitation. The full Cell Metabolism article (and many others) as well as other research is available to any member on our site.

Ellen