Re: Another Success Story - long but hopefully worth it.

[Guest guest]

That's a great question- would love to know. I thought suggests you can

go off once you are " cured " ?

Bonnie

>

> > I guess the old saying: " It's the exception that proves the rule " is right,

> > and I'm the exception. ;-)

> >

> > When I told back in October that I intended to stay on Iodoral

> > while doing my T3 therapy, she said she'd be very interested to know if it

> > worked because she hasn't seen many people for whom that is true. Well, it

> > worked, so she can now add me to the shortlist. I've continued to take a

> > single 12.5 mg tab every morning. No HC or Isocort or Iron supplements

> > either. Nothing but T3, and not all that much required for success. I never

> > took over 75mcg and that was only for a few days. And my ferritin is only

> > 47.

> >

> > Here are the stats from my latest labs:

> >

> > Began 's protocol on November 5, 2009

> >

> > After ten days, reached 75mcg per day on November 15 -- became hyper, with

> > 99+ temps and sweats, pulse in the 90's -- cycled down to zero in a week and

> > then began again on November 23 using a modified protocol. Modified in this

> > case means I began with 6.25 mcg and added more T3 very slowly, as Val

> > recommends, and also that unlike 's recommendation did not take

> > compounded time-release T3 but Cynomel.

> >

> > BLOOD TEST on Dec 4th:

> > TC and LDL dropped 100 points!

> > Triglycerides dropped from 67 to 42

> > HDL rose from 88 to 97

> > A1c dropped a bit to 5.0

> > APO B/APO a-1 = .56 -- HALF the *lowest* risk for CHD!

> >

> > FT3 = 404 (up from 291)

> > RT3 = 10 (down from 25).

> > Ratio = 40.4!!! (up from 11.64)

> > T4 Total = 3.7 (4.5-12.5)

> > FT4 = 1.0 (1.4-3.8)

> > Sodium = 143 (128-145)

> > Potassium = 4.9 (3.6-5.1)

> > Ferritn = 47 (20-288)

> > Iron = 67 (40-160)

> >

> > I reached a dose of 50mcg on 12/16. My temps reached 98.6 steady two days

> > after that. By 12/25 my temps were 99.9 so I reduced my dose to 37.5 and

> > have been there every since. My temps have been rock solid at 98.6 all day,

> > every day for the last 3 weeks. No hypo symptoms at all, and it's clear from

> > my blood tests, lack of symptoms and high energy that my T3 is reaching my

> > cells. I've lost 2 inches from my waist and abs in this time -- mostly due

> > to the excess cholesterol dump I think, since it binds to fatty acids and is

> > excreted.

> >

> > Even more importantly, I've been doing deep, deep medical research these

> > last two months and believe I have found the cause of my RT3 problem to

> > begin with: Leptin Resistance. My blood test for that revealed that I am

> > severely leptin resistant even though I'm no longer insulin resistant to any

> > degree! I've decided to write about it here in the hopes that it will ring

> > some bells for other members and perhaps help them as well.

> >

> > Leptin is the King of all the hormones. It manages and gives orders to them

> > all, including, tellingly, insulin -- yet it takes orders from no hormones.

> > It reigns supreme. It is created from your adipose fat cells, so the more

> > stored fat you have, the more leptin you will produce.

> >

> > When you begin to eat, your leptin travels up through the bloodstream to

> > the blood-brain barrier, where with the help of a protein gets folded into a

> > three-dimensional shape that lets it slip through a precisely shaped keyhole

> > to reach the hypothalamus. The leptin gives your brain a lot of information

> > that will be used to determine how to *handle* your ingested energy: burn or

> > store. And the brain has many tools at its disposal to make your metabolism

> > do exactly what it wants, from making cells insulin resistant (thus storing

> > more fat) to signaling T4 to stop converting into T3 and start converting to

> > RT3. Or, to conversely, to have it make more T3 and 'turn up the heat' to

> > burn more energy. YOU don't control this. Leptin and your brain does.

> >

> > But leptin does more. It signals the brain about how much energy *this*

> > meal contains versus how much stored fat (the brain only sees 'energy' or

> > 'not energy') you have. If the brain thinks it has sufficient energy it

> > raises another hormone to send the signal for you to stop eating. That's

> > when you get that " Can't eat another bite " feeling and you put down the

> > fork, no matter how delicious the food. Doggy bags were created to deal with

> > this hormone. And how it works is important, because that signal makes

> > glucagon (which controls insulin rise) decrease via a hormone called amylin.

> >

> > And leptin does still more. It acts like an A1c test for fat, telling the

> > brain not only about the meal you're eating now, but about how much energy

> > you've eaten over the last several days. [Which explains why we see weight

> > gains on the scale not the day after a binge, but 72 hours later]. This is

> > the crucial information, because the brain doesn't like to make sudden

> > changes. It gathers the leptin info over the course of a few days and only

> > then decides what hormones to use to either burn off excess energy or RETAIN

> > energy by changing your metabolism via your hormones and liver.

> >

> > Amazingly, leptin was only discovered in 1994! And it set off a true Gold

> > Rush among Big Pharma because of how it was discovered: mice bred to be fat

> > (no matter how little they ate) were discovered to have low levels of this

> > hormone, yet when it was synthesized and injected into the mice, they

> > overcame their fat genes and became skinny. Oh! Big Pharma thought -- the

> > Holy Grail! We'll synthesize leptin, patent it, and have the Mother of all

> > Blockbuster Drugs to sell, one that will reverse obesity with a single pill.

> >

> > They poured millions and millions into R & D, but when the first human trials

> > were done, disaster loomed. Yes, the obese people injected with it did lose

> > weight. For the first two weeks. Then they stopped losing, gained it all

> > back, and put on a bit more for good measure. And this was true for all

> > study subjects.

> >

> > Turns out, when they actually examined fat people, they had four to five

> > times MORE leptin than thin people. WTF???

> >

> > At this point, all R & D stopped, and some companies sold their leptin

> > divisions. One company -- Amylin -- bought out the biggest, and more about

> > them later.

> >

> > So, by 2000, what researchers knew is that obese people are not only often

> > insulin resistant (which begins in the liver), and not only often thyroid

> > resistant (which begins in the liver), but are almost all leptin resistant

> > -- and in all three cases, the result is the same: the correct hormone is

> > produced, but is blocked from reaching the cells, which in turn means that

> > the correct signaling cannot get through. The actual process for this is

> > that the leptin cannot be folded into the proper shape and thus cannot cross

> > the blood-brain barrier.

> >

> > With little or no leptin reaching it, the brain believes the body is in

> > danger of starvation regardless of actual calories consumed, and takes

> > immediate steps to slow down the metabolism. So you get fat, which creates

> > more pooled leptin and you become ever more leptin resistant. It's a vicious

> > circle because for hormones, the ability to reach the cells with the right

> > signal is everything.

> >

> > This was why, for instance, my cholesterol kept rising until it was

> > sky-high: T3 carries the signal the liver needs to know there is sufficient

> > cholesterol in the blood, but RT3 lacks that signal. As soon as cytomel

> > allowed T3 to once again reach my cells, the correct signal reached the

> > liver, which immediately dumped excess cholesterol out of my body.

> >

> > When leptin doesn't reach the brain, it's much, much worse. What it means,

> > in essence, is that while I see a still-overweight woman when *I* look in

> > the mirror, what my *brain* sees is a very thin woman on the edge of

> > starvation. And it will do everything in its considerable power to conserve

> > as much ingested and stored energy as possible.

> >

> > What this usually means is:

> >

> > 1: During a meal, the leptin that normally would go to the brain saying

> > 'lots of energy here, boss' doesn't get through. So the brain never sends

> > the hormonal system of 'you're full you idiot, so stop eating!' Thus, leptin

> > resistant people are usually always hungry and always eating.

> >

> > 2: In order to conserve as much energy as possible in the easiest to store

> > form (fat), the brain sends out a specific hormone that not only tells us to

> > eat, but to eat lots and lots of carbs, particularly sweets. That's because

> > the brain knows this will ultimately create insulin resistance, which means

> > more triglycerides made in the liver, which means more stored fat. This is

> > why most leptin resistant people say they 'crave' sweets. They do, but only

> > because they are being ordered by the brain to crave them.

> >

> > But what happens when the brain is stored in a body that eats high fat, low

> > carb, and is thus not only satisfied with less food, but with almost no

> > sweets? I'll tell you what happens: the thwarted brain simply pulls another

> > tool from the box for conserving energy: the thyroid hormones. By creating a

> > RT3 imbalance, energy and fat are stored not burned, and the metabolism is

> > slowed to such a state that no amount of exercise, no eating this or not

> > eating that, no calorie reduction will overcome it. In fact, the more you do

> > to lose weight, the more the leptin-deprived brain conserves energy. This

> > finally explains the mystery of how morbidly obese patients can be locked

> > into a hospital metabolic ward, fed 500 calories a day -- and gain weight.

> > Mysterious no more.

> >

> > But what to do about it, that's the question. And for that, someone needed

> > to show exactly how people become leptin resistant (and diabetic, too!). And

> > finally, someone has. In a major study done at Boston Children's Hospital

> > Research Center in 2008 and published in the January 2009 issue of " Cell

> > Metabolism " as: " Endoplasmic Reticulum Stress Plays a Central Role in

> > Development of Leptin Resistance " this mechanism was revealed. From the

> > article:

> >

> > " The endoplasmic reticulum (ER) is a sophisticated luminal network in which

> > protein synthesis, maturation, folding, and transport take place.

> > Perturbation of these processes in several different pathological states

> > creates a condition defined as ER stress and leads to activation of a

> > complex signaling network termed the unfolded protein response

> > (UPR). Previous studies have demonstrated that ER stress and activation of

> > UPR signaling pathways play a dominant role in the development of

> > obesity-induced insulin resistance and type 2 diabetes. Furthermore,

> > reversal of ER stress with chemical chaperones—agents that have the ability

> > to increase ER folding machinery—increases insulin sensitivity and reverses

> > type 2 diabetes in obese mice.

> >

> > SUMMARY

> > Leptin has not evolved as a therapeutic modality for the treatment of

> > obesity due to the prevalence of leptin resistance in a majority of the

> > obese population. Nevertheless, the molecular mechanisms of leptin

> > resistance remain poorly understood. Here, we show that increased

> > endoplasmic reticulum (ER) stress and activation of the unfolded protein

> > response (UPR) in the hypothalamus of obese mice inhibits leptin receptor

> > signaling. The genetic imposition of reduced ER capacity in mice results in

> > severe leptin resistance and leads to a significant augmentation of obesity.

> > Moreover, we show that chemical chaperones, 4-phenyl butyric acid (PBA), and

> > tauroursodeoxycholic acid (TUDCA), which have the ability to decrease ER

> > stress, act as leptin-sensitizing agents. Taken together, our results may

> > provide the basis for a novel treatment of obesity. "

> >

> > To summarize the summary: the study proved that when something/s (still

> > unknown but I believe was right about outside stress, like major

> > surgery in my case, which is when my weight loss stopped after losing 65

> > pounds but 20 pounds from goal) stresses the ER in the brain, leptin

> > resistance begins. The ER then activates the UPR (unfolded protein

> > response), which means the leptin can no longer get through. And then all

> > metabolic hell ensues.

> >

> > What is stunning about the study though, is that the researchers went

> > further. Once they'd proved the faulty mechanism, they decided to test

> > whether or not sending along a 'chaperone molecule' with the leptin would

> > undo the UPR and let the leptin through. And they not only did it, they did

> > it with two non-toxic drugs already approved by the FDA for treating other

> > diseases!

> >

> > When they gave obese mice a ten-day 'pre-treatment' of 4-PBA the mice

> > didn't lose weight or fat, but once leptin was added to the injections,

> > those mice grew thin and *lean* with lots of lost body fat. And the mice

> > stayed lean. When their hypothalamus' were harvested, it showed that indeed

> > leptin signaling (leptin sensitivity) had been restored.

> >

> > The real eye-opener was with TUDCA though. Just treatment with it alone

> > caused major weight and fat loss. And when leptin was added, just a fraction

> > of the amount used with the 4-PBA was needed for even more drastic weight

> > loss. Which was also stable.

> >

> > TUDCA is biologically identical to UDCA (sold as Actigall in this country),

> > which is used to treat liver diseases. TUDCA was used by the researchers

> > because it's an inject-able liquid, whereas the UDCA is taken orally. Isn't

> > it amazing how everything metabolic somehow leads back to the brain's

> > connection with the liver? And the 'U' in UDCA stands for 'urso' -- Bear in

> > Latin -- because it comes from bear bile. The liver. And it's been used by

> > Native Americans for centuries to treat illness. It is such an incredible

> > substance that there are now clinical trials all over the world using TUDCA

> > to treat Huntington's Disease, Cystic Fibrosis, and Altzheimer's.

> > Researchers believe they are on the verge of major breakthrough's for all

> > three, thanks to this simple substance.

> >

> > So, armed with this knowledge (and the fact that I had diagnosed my own RT3

> > and Cholesterol problem, and treated them both of them myself successfully),

> > I met with my Endo. I was there for two hours. She did most of the

> > question-asking, and I provided most of the answers.

> >

> > When we were done, she agreed that it was indeed likely that my RT3 problem

> > was originally caused by my leptin resistance, and also with my hypothesis

> > that if I did not treat and cure the original problem (LP), my brain would

> > continue to be leptin-deprived, continue to think I'm skinny, and would only

> > pull another metabolic trick out of its hat to retain my weight and fat. I

> > believe this alone can explain why some people on T3 can lower RT3 and get

> > T3 back into the cells but not lose weight. And why for many, RT3 and/or

> > hypo symptoms return when they return to dessicated thyroid.

> >

> > She agreed to support my being an experiment of one, with help from the

> > Doctor who is leading the UDCA Cystic Fibrosis study at the University of

> > Michigan, whom I contacted and spoke to at length.

> >

> > Starting this week I will begin a 'pre-treatment' of Symlin (pramlintide

> > acetate) injections with the two sample 'pens' my Endo gave me. Symlin is a

> > synthetic form of Amylin, a sister hormone of leptin that plays a huge role

> > in proper insulin use in the body as mentioned above, by signaling the liver

> > to decrease production of glucagon. Type 1 Diabetics no longer make Amylin,

> > and it is either low or missing or not working properly in Type 2's -- which

> > is not surprising given that I believe this is their form of leptin

> > resistance.

> >

> > How it works:

> >

> > " Symlin, by acting as an amylinomimetic agent, has the following effects:

> > 1) modulation of gastric emptying; 2) prevention of the postprandial rise in

> > plasma glucagon; and 3) satiety leading to decreased caloric intake and

> > potential weight loss. "

> >

> > For me, the most important point is reduction of glucagon, which does not

> > work properly in leptin resistant people.

> >

> > Symlin is made by the company Amylin, which was the company I mentioned

> > earlier, that purchased the R & D and rights to patent leptin back in 2000. In

> > fact, Symlin has been shown to cause rapid weight and fat loss in type 1 and

> > type 2 diabetics who take it with their insulin (because I believe based on

> > my research that it too restores leptin signaling; see the Holtof site for

> > more info) -- and the company is currently in trials to convince the FDA to

> > let them market it for weight loss. Followed, no doubt in my mind, by a form

> > of leptin they are working to produce.

> >

> > If my hypothesis is correct, in two months Symlin will fully restore my

> > amylin/leptin connection, after which I will begin supplementing with

> > UDCA/Actigall. I fully expect to have my letpin resistance restored, my T3

> > problem permanently fixed, and my metabolism completely healed. I also

> > expect to lose the 20 pounds I couldn't before, as well as the 10 I added

> > back when my RT3 began to rise. And I fully expect my insulin sensitivity to

> > grow even better, and my A1c to continue to fall.

> >

> > Knowing now what I know about the brilliance of our intricate hormonal and

> > metabolic systems, and the ability of our brain to rule them *absolutely*

> > despite any of our intentions or actions, I find the advice " To lose weight

> > simply eat less and exercise more " akin to saying " To lose weight bury a

> > chicken bone in the backyard at the full moon and say the following

> > incantation. " Both will be equal in their efficacy. Same thing for " cut out

> > dairy, don't eat grains, count calories, don't count them, eat this, don't

> > eat that, " etc. etc. etc.

> >

> > A person with a perfectly healthy and functioning metabolism will not store

> > excess energy (fat) in the first place. If they feast a day or so they might

> > gain a pound or two, but a week of eating as usual will see that gone

> > without them having to do anything, or eat anything, or not eat anything

> > special. That's how we evolved, and that's how we're still built. Our

> > ancestors never had to 'diet' and neither should we.

> >

> > Abuse or stress my make that metabolism non-functioning, but to cure it

> > requires science, not anecdote or one food over another. My heart aches as I

> > read the same posts over and over on all the various forums dealing with

> > obesity, from calorie-counting forums to low-carb forums. Everywhere is

> > anecdote and useless advice, and science nowhere to be found. I've written

> > this very long post hoping that here at least, with Val and Nick, science

> > will have a place and that their readers will now have a test -- leptin

> > serum level -- to begin, and some solutions to follow.

> >

> > To a Happy and Healthy New Year for us all...

> >

> >

> >

> >

> >

> >

> >

> > ------------------------------------

> >

> >

[Guest guest]

birrdyy@...

my e mail cut off.... without the remainder of the following: " how much

energy "

> > do exactly what it wants, from making cells insulin resistant (thus

storing

> > more fat) to signaling T4 to stop converting into T3 and start

converting to

> > RT3. Or, to conversely, to have it make more T3 and 'turn up the heat' to

> > burn more energy. YOU don't control this. Leptin and your brain does.

> >

> > But leptin does more. It signals the brain about how much energy

what was next??

thanks

C. Hunter

> That's a great question- would love to know. I thought suggests you

> can go off once you are " cured " ?

>

> Bonnie

>

>

>>

>> > I guess the old saying: " It's the exception that proves the rule " is

>> right,

>> > and I'm the exception. ;-)

>> >

>> > When I told back in October that I intended to stay on Iodoral

>> > while doing my T3 therapy, she said she'd be very interested to know

>> if it

>> > worked because she hasn't seen many people for whom that is true.

>> Well, it

>> > worked, so she can now add me to the shortlist. I've continued to

>> take a

>> > single 12.5 mg tab every morning. No HC or Isocort or Iron supplements

>> > either. Nothing but T3, and not all that much required for success. I

>> never

>> > took over 75mcg and that was only for a few days. And my ferritin is

>> only

>> > 47.

>> >

>> > Here are the stats from my latest labs:

>> >

>> > Began 's protocol on November 5, 2009

>> >

>> > After ten days, reached 75mcg per day on November 15 -- became hyper,

>> with

>> > 99+ temps and sweats, pulse in the 90's -- cycled down to zero in a

>> week and

>> > then began again on November 23 using a modified protocol. Modified in

>> this

>> > case means I began with 6.

> 25 mcg and added more T3 very slowly, as Val

>> > recommends, and also that unlike 's recommendation did not take

>> > compounded time-release T3 but Cynomel.

>> >

>> > BLOOD TEST on Dec 4th:

>> > TC and LDL dropped 100 points!

>> > Triglycerides dropped from 67 to 42

>> > HDL rose from 88 to 97

>> > A1c dropped a bit to 5.0

>> > APO B/APO a-1 = .56 -- HALF the *lowest* risk for CHD!

>> >

>> > FT3 = 404 (up from 291)

>> > RT3 = 10 (down from 25).

>> > Ratio = 40.4!!! (up from 11.64)

>> > T4 Total = 3.7 (4.5-12.5)

>> > FT4 = 1.0 (1.4-3.8)

>> > Sodium = 143 (128-145)

>> > Potassium = 4.9 (3.6-5.1)

>> > Ferritn = 47 (20-288)

>> > Iron = 67 (40-160)

>> >

>> > I reached a dose of 50mcg on 12/16. My temps reached 98.6 steady two

>> days

>> > after that. By 12/25 my temps were 99.9 so I reduced my dose to 37.5

>> and

>> > have been there every since. My temps have been rock solid at 98.6 all

>> day,

>> > every day for the last 3 weeks. No hypo symptoms at all, and it's

>> clear from

>> > my blood tests, lack of symptoms and high energy that my T3 is

>> reaching my

>> > cells. I've lost 2 inches from my waist and abs in this time -- mostly

>> due

>> > to the excess cholesterol dump I think, since it binds to fatty acids

>> and is

>> > excreted.

>> >

>> > Even more importantly, I've been doing deep, deep medical research

>> these

>> > last two months and believe I have found the cause of my RT3 problem

>> to

>> > begin with: Leptin Resistance. My blood test for that revealed that I

>> am

>> > severely leptin resistant even though I'm no longer insulin resistant

>> to any

>> > degree! I've decided to write about it here in the hopes that it will

>> ring

>> > some bells for other members and perhaps help them as well.

>> >

>> > Leptin is the King of all the hormones. It manages and gives orders to

>> them

>> > all, including, tellingly, insulin -- yet it takes orders from no

>> hormones.

>> > It reigns supreme. It is created from your adipose fat cells, so the

>> more

>> > stored fat you have, the more leptin you will produce.

>> >

>> > When you begin to eat, your leptin travels up through the bloodstream

>> to

>> > the blood-brain barrier, where with the help of a protein gets folded

>> into a

>> > three-dimensional shape that lets it slip through a precisely shaped

>> keyhole

>> > to reach the hypothalamus. The leptin gives your brain a lot of

>> information

>> > that will be used to determine how to *handle* your ingested energy:

>> burn or

>> > store. And the brain has many tools at its disposal to make your

>> metabolism

>> > do exactly what it wants, from making cells insulin resistant (thus

>> storing

>> > more fat) to signaling T4 to stop converting into T3 and start

>> converting to

>> > RT3. Or, to conversely, to have it make more T3 and 'turn up the heat'

>> to

>> > burn more energy. YOU don't control this. Leptin and your brain does.

>> >

>> > But leptin does more. It signals the brain about how much energy

>> *this*

>> > meal contains versus how much stored fat (the brain only sees 'energy'

>> or

>> > 'not energy') you have. If the brain thinks it has sufficient energy

>> it

>> > raises another hormone to send the signal for you to stop eating.

>> That's

>> > when you get that " Can't eat another bite " feeling and you put down

>> the

>> > fork, no matter how delicious the food. Doggy bags were created to

>> deal with

>> > this hormone. And how it works is important, because that signal

>> makes

>> > glucagon (which controls insulin rise) decrease via a hormone called

>> amylin.

>> >

>> > And leptin does still more. It acts like an A1c test for fat, telling

>> the

>> > brain not only about the meal you're eating now, but about how much

>> energy

>> > you've eaten over the last several days. [Which explains why we see

>> weight

>> > gains on the scale not the day after a binge, but 72 hours later].

>> This is

>> > the crucial information, because the brain doesn't like to make sudden

>> > changes. It gathers the leptin info over the course of a few days and

>> only

>> > then decides what hormones to use to either burn off excess energy or

>> RETAIN

>> > energy by changing your metabolism via your hormones and liver.

>> >

>> > Amazingly, leptin was only discovered in 1994! And it set off a true

>> Gold

>> > Rush among Big Pharma because of how it was discovered: mice bred to

>> be fat

>> > (no matter how little they ate) were discovered to have low levels of

>> this

>> > hormone, yet when it was synthesized and injected into the mice, they

>> > overcame their fat genes and became skinny. Oh! Big Pharma thought --

>> the

>> > Holy Grail! We'll synthesize leptin, patent it, and have the Mother of

>> all

>> > Blockbuster Drugs to sell, one that will reverse obesity with a single

>> pill.

>> >

>> > They poured millions and millions into R & D, but when the first human

>> trials

>> > were done, disaster loomed. Yes, the obese people injected with it did

>> lose

>> > weight. For the first two weeks. Then they stopped losing, gained it

>> all

>> > back, and put on a bit more for good measure. And this was true for

>> all

>> > study subjects.

>> >

>> > Turns out, when they actually examined fat people, they had four to

>> five

>> > times MORE leptin than thin people. WTF???

>> >

>> > At this point, all R & D stopped, and some companies sold their leptin

>> > divisions. One company -- Amylin -- bought out the biggest, and more

>> about

>> > them later.

>> >

>> > So, by 2000, what researchers knew is that obese people are not only

>> often

>> > insulin resistant (which begins in the liver), and not only often

>> thyroid

>> > resistant (which begins in the liver), but are almost all leptin

>> resistant

>> > -- and in all three cases, the result is the same: the correct hormone

>> is

>> > produced, but is blocked from reaching the cells, which in turn means

>> that

>> > the correct signaling cannot get through. The actual process for this

>> is

>> > that the leptin cannot be folded into the proper shape and thus cannot

>> cross

>> > the blood-brain barrier.

>> >

>> > With little or no leptin reaching it, the brain believes the body is

>> in

>> > danger of starvation regardless of actual calories consumed, and takes

>> > immediate steps to slow down the metabolism. So you get fat, which

>> creates

>> > more pooled leptin and you become ever more leptin resistant. It's a

>> vicious

>> > circle because for hormones, the ability to reach the cells with the

>> right

>> > signal is everything.

>> >

>> > This was why, for instance, my cholesterol kept rising until it was

>> > sky-high: T3 carries the signal the liver needs to know there is

>> sufficient

>> > cholesterol in the blood, but RT3 lacks that signal. As soon as

>> cytomel

>> > allowed T3 to once again reach my cells, the correct signal reached

>> the

>> > liver, which immediately dumped excess cholesterol out of my body.

>> >

>> > When leptin doesn't reach the brain, it's much, much worse. What it

>> means,

>> > in essence, is that while I see a still-overweight woman when *I* look

>> in

>> > the mirror, what my *brain* sees is a very thin woman on the edge of

>> > starvation. And it will do everything in its considerable power to

>> conserve

>> > as much ingested and stored energy as possible.

>> >

>> > What this usually means is:

>> >

>> > 1: During a meal, the leptin that normally would go to the brain

>> saying

>> > 'lots of energy here, boss' doesn't get through. So the brain never

>> sends

>> > the hormonal system of 'you're full you idiot, so stop eating!' Thus,

>> leptin

>> > resistant people are usually always hungry and always eating.

>> >

>> > 2: In order to conserve as much energy as possible in the easiest to

>> store

>> > form (fat), the brain sends out a specific hormone that not only tells

>> us to

>> > eat, but to eat lots and lots of carbs, particularly sweets. That's

>> because

>> > the brain knows this will ultimately create insulin resistance, which

>> means

>> > more triglycerides made in the liver, which means more stored fat.

>> This is

>> > why most leptin resistant people say they 'crave' sweets. They do, but

>> only

>> > because they are being ordered by the brain to crave them.

>> >

>> > But what happens when the brain is stored in a body that eats high

>> fat, low

>> > carb, and is thus not only satisfied with less food, but with almost

>> no

>> > sweets? I'll tell you what happens: the thwarted brain simply pulls

>> another

>> > tool from the box for conserving energy: the thyroid hormones. By

>> creating a

>> > RT3 imbalance, energy and fat are stored not burned, and the

>> metabolism is

>> > slowed to such a state that no amount of exercise, no eating this or

>> not

>> > eating that, no calorie reduction will overcome it. In fact, the more

>> you do

>> > to lose weight, the more the leptin-deprived brain conserves energy.

>> This

>> > finally explains the mystery of how morbidly obese patients can be

>> locked

>> > into a hospital metabolic ward, fed 500 calories a day -- and gain

>> weight.

>> > Mysterious no more.

>> >

>> > But what to do about it, that's the question. And for that, someone

>> needed

>> > to show exactly how people become leptin resistant (and diabetic,

>> too!). And

>> > finally, someone has. In a major study done at Boston Children's

>> Hospital

>> > Research Center in 2008 and published in the January 2009 issue of

>> " Cell

>> > Metabolism " as: " Endoplasmic Reticulum Stress Plays a Central Role in

>> > Development of Leptin Resistance " this mechanism was revealed. From

>> the

>> > article:

>> >

>> > " The endoplasmic reticulum (ER) is a sophisticated luminal network in

>> which

>> > protein synthesis, maturation, folding, and transport take place.

>> > Perturbation of these processes in several different pathological

>> states

>> > creates a condition defined as ER stress and leads to activation of a

>> > complex signaling network termed the unfolded protein response

>> > (UPR). Previous studies have demonstrated that ER stress and

>> activation of

>> > UPR signaling pathways play a dominant role in the development of

>> > obesity-induced insulin resistance and type 2 diabetes. Furthermore,

>> > reversal of ER stress with chemical chaperones—agents that have the

>> ability

>> > to increase ER folding machinery—increases insulin sensitivity and

>> reverses

>> > type 2 diabetes in obese mice.

>> >

>> > SUMMARY

>> > Leptin has not evolved as a therapeutic modality for the treatment of

>> > obesity due to the prevalence of leptin resistance in a majority of

>> the

>> > obese population. Nevertheless, the molecular mechanisms of leptin

>> > resistance remain poorly understood. Here, we show that increased

>> > endoplasmic reticulum (ER) stress and activation of the unfolded

>> protein

>> > response (UPR) in the hypothalamus of obese mice inhibits leptin

>> receptor

>> > signaling. The genetic imposition of reduced ER capacity in mice

>> results in

>> > severe leptin resistance and leads to a significant augmentation of

>> obesity.

>> > Moreover, we show that chemical chaperones, 4-phenyl butyric acid

>> (PBA), and

>> > tauroursodeoxycholic acid (TUDCA), which have the ability to decrease

>> ER

>> > stress, act as leptin-sensitizing agents. Taken together, our results

>> may

>> > provide the basis for a novel treatment of obesity. "

>> >

>> > To summarize the summary: the study proved that when something/s

>> (still

>> > unknown but I believe was right about outside stress, like

>> major

>> > surgery in my case, which is when my weight loss stopped after losing

>> 65

>> > pounds but 20 pounds from goal) stresses the ER in the brain, leptin

>> > resistance begins. The ER then activates the UPR (unfolded protein

>> > response), which means the leptin can no longer get through. And then

>> all

>> > metabolic hell ensues.

>> >

>> > What is stunning about the study though, is that the researchers went

>> > further. Once they'd proved the faulty mechanism, they decided to test

>> > whether or not sending along a 'chaperone molecule' with the leptin

>> would

>> > undo the UPR and let the leptin through. And they not only did it,

>> they did

>> > it with two non-toxic drugs already approved by the FDA for treating

>> other

>> > diseases!

>> >

>> > When they gave obese mice a ten-day 'pre-treatment' of 4-PBA the mice

>> > didn't lose weight or fat, but once leptin was added to the

>> injections,

>> > those mice grew thin and *lean* with lots of lost body fat. And the

>> mice

>> > stayed lean. When their hypothalamus' were harvested, it showed that

>> indeed

>> > leptin signaling (leptin sensitivity) had been restored.

>> >

>> > The real eye-opener was with TUDCA though. Just treatment with it

>> alone

>> > caused major weight and fat loss. And when leptin was added, just a

>> fraction

>> > of the amount used with the 4-PBA was needed for even more drastic

>> weight

>> > loss. Which was also stable.

>> >

>> > TUDCA is biologically identical to UDCA (sold as Actigall in this

>> country),

>> > which is used to treat liver diseases. TUDCA was used by the

>> researchers

>> > because it's an inject-able liquid, whereas the UDCA is taken orally.

>> Isn't

>> > it amazing how everything metabolic somehow leads back to the brain's

>> > connection with the liver? And the 'U' in UDCA stands for 'urso' --

>> Bear in

>> > Latin -- because it comes from bear bile. The liver. And it's been

>> used by

>> > Native Americans for centuries to treat illness. It is such an

>> incredible

>> > substance that there are now clinical trials all over the world using

>> TUDCA

>> > to treat Huntington's Disease, Cystic Fibrosis, and Altzheimer's.

>> > Researchers believe they are on the verge of major breakthrough's for

>> all

>> > three, thanks to this simple substance.

>> >

>> > So, armed with this knowledge (and the fact that I had diagnosed my

>> own RT3

>> > and Cholesterol problem, and treated them both of them myself

>> successfully),

>> > I met with my Endo. I was there for two hours. She did most of the

>> > question-asking, and I provided most of the answers.

>> >

>> > When we were done, she agreed that it was indeed likely that my RT3

>> problem

>> > was originally caused by my leptin resistance, and also with my

>> hypothesis

>> > that if I did not treat and cure the original problem (LP), my brain

>> would

>> > continue to be leptin-deprived, continue to think I'm skinny, and

>> would only

>> > pull another metabolic trick out of its hat to retain my weight and

>> fat. I

>> > believe this alone can explain why some people on T3 can lower RT3 and

>> get

>> > T3 back into the cells but not lose weight. And why for many, RT3

>> and/or

>> > hypo symptoms return when they return to dessicated thyroid.

>> >

>> > She agreed to support my being an experiment of one, with help from

>> the

>> > Doctor who is leading the UDCA Cystic Fibrosis study at the University

>> of

>> > Michigan, whom I contacted and spoke to at length.

>> >

>> > Starting this week I will begin a 'pre-treatment' of Symlin

>> (pramlintide

>> > acetate) injections with the two sample 'pens' my Endo gave me. Symlin

>> is a

>> > synthetic form of Amylin, a sister hormone of leptin that plays a huge

>> role

>> > in proper insulin use in the body as mentioned above, by signaling the

>> liver

>> > to decrease production of glucagon. Type 1 Diabetics no longer make

>> Amylin,

>> > and it is either low or missing or not working properly in Type 2's --

>> which

>> > is not surprising given that I believe this is their form of leptin

>> > resistance.

>> >

>> > How it works:

>> >

>> > " Symlin, by acting as an amylinomimetic agent, has the following

>> effects:

>> > 1) modulation of gastric emptying; 2) prevention of the postprandial

>> rise in

>> > plasma glucagon; and 3) satiety leading to decreased caloric intake

>> and

>> > potential weight loss. "

>> >

>> > For me, the most important point is reduction of glucagon, which does

>> not

>> > work properly in leptin resistant people.

>> >

>> > Symlin is made by the company Amylin, which was the company I

>> mentioned

>> > earlier, that purchased the R & D and rights to patent leptin back in

>> 2000. In

>> > fact, Symlin has been shown to cause rapid weight and fat loss in type

>> 1 and

>> > type 2 diabetics who take it with their insulin (because I believe

>> based on

>> > my research that it too restores leptin signaling; see the Holtof site

>> for

>> > more info) -- and the company is currently in trials to convince the

>> FDA to

>> > let them market it for weight loss. Followed, no doubt in my mind, by

>> a form

>> > of leptin they are working to produce.

>> >

>> > If my hypothesis is correct, in two months Symlin will fully restore

>> my

>> > amylin/leptin connection, after which I will begin supplementing with

>> > UDCA/Actigall. I fully expect to have my letpin resistance restored,

>> my T3

>> > problem permanently fixed, and my metabolism completely healed. I also

>> > expect to lose the 20 pounds I couldn't before, as well as the 10 I

>> added

>> > back when my RT3 began to rise. And I fully expect my insulin

>> sensitivity to

>> > grow even better, and my A1c to continue to fall.

>> >

>> > Knowing now what I know about the brilliance of our intricate hormonal

>> and

>> > metabolic systems, and the ability of our brain to rule them

>> *absolutely*

>> > despite any of our intentions or actions, I find the advice " To lose

>> weight

>> > simply eat less and exercise more " akin to saying " To lose weight bury

>> a

>> > chicken bone in the backyard at the full moon and say the following

>> > incantation. " Both will be equal in their efficacy. Same thing for

>> " cut out

>> > dairy, don't eat grains, count calories, don't count them, eat this,

>> don't

>> > eat that, " etc. etc. etc.

>> >

>> > A person with a perfectly healthy and functioning metabolism will not

>> store

>> > excess energy (fat) in the first place. If they feast a day or so they

>> might

>> > gain a pound or two, but a week of eating as usual will see that gone

>> > without them having to do anything, or eat anything, or not eat

>> anything

>> > special. That's how we evolved, and that's how we're still built. Our

>> > ancestors never had to 'diet' and neither should we.

>> >

>> > Abuse or stress my make that metabolism non-functioning, but to cure

>> it

>> > requires science, not anecdote or one food over another. My heart

>> aches as I

>> > read the same posts over and over on all the various forums dealing

>> with

>> > obesity, from calorie-counting forums to low-carb forums. Everywhere

>> is

>> > anecdote and useless advice, and science nowhere to be found. I've

>> written

>> > this very long post hoping that here at least, with Val and Nick,

>> science

>> > will have a place and that their readers will now have a test --

>> leptin

>> > serum level -- to begin, and some solutions to follow.

>> >

>> > To a Happy and Healthy New Year for us all...

>> >

>> >

>> >

>> >

>> >

>> >

>> >

>> > ------------------------------------

>> >

>> >

[Guest guest]

birrdyy@...

my e mail cut off.... without the remainder of the following: " how much

energy "

> > do exactly what it wants, from making cells insulin resistant (thus

storing

> > more fat) to signaling T4 to stop converting into T3 and start

converting to

> > RT3. Or, to conversely, to have it make more T3 and 'turn up the heat' to

> > burn more energy. YOU don't control this. Leptin and your brain does.

> >

> > But leptin does more. It signals the brain about how much energy

what was next??

thanks

C. Hunter

> That's a great question- would love to know. I thought suggests you

> can go off once you are " cured " ?

>

> Bonnie

>

>

>>

>> > I guess the old saying: " It's the exception that proves the rule " is

>> right,

>> > and I'm the exception. ;-)

>> >

>> > When I told back in October that I intended to stay on Iodoral

>> > while doing my T3 therapy, she said she'd be very interested to know

>> if it

>> > worked because she hasn't seen many people for whom that is true.

>> Well, it

>> > worked, so she can now add me to the shortlist. I've continued to

>> take a

>> > single 12.5 mg tab every morning. No HC or Isocort or Iron supplements

>> > either. Nothing but T3, and not all that much required for success. I

>> never

>> > took over 75mcg and that was only for a few days. And my ferritin is

>> only

>> > 47.

>> >

>> > Here are the stats from my latest labs:

>> >

>> > Began 's protocol on November 5, 2009

>> >

>> > After ten days, reached 75mcg per day on November 15 -- became hyper,

>> with

>> > 99+ temps and sweats, pulse in the 90's -- cycled down to zero in a

>> week and

>> > then began again on November 23 using a modified protocol. Modified in

>> this

>> > case means I began with 6.

> 25 mcg and added more T3 very slowly, as Val

>> > recommends, and also that unlike 's recommendation did not take

>> > compounded time-release T3 but Cynomel.

>> >

>> > BLOOD TEST on Dec 4th:

>> > TC and LDL dropped 100 points!

>> > Triglycerides dropped from 67 to 42

>> > HDL rose from 88 to 97

>> > A1c dropped a bit to 5.0

>> > APO B/APO a-1 = .56 -- HALF the *lowest* risk for CHD!

>> >

>> > FT3 = 404 (up from 291)

>> > RT3 = 10 (down from 25).

>> > Ratio = 40.4!!! (up from 11.64)

>> > T4 Total = 3.7 (4.5-12.5)

>> > FT4 = 1.0 (1.4-3.8)

>> > Sodium = 143 (128-145)

>> > Potassium = 4.9 (3.6-5.1)

>> > Ferritn = 47 (20-288)

>> > Iron = 67 (40-160)

>> >

>> > I reached a dose of 50mcg on 12/16. My temps reached 98.6 steady two

>> days

>> > after that. By 12/25 my temps were 99.9 so I reduced my dose to 37.5

>> and

>> > have been there every since. My temps have been rock solid at 98.6 all

>> day,

>> > every day for the last 3 weeks. No hypo symptoms at all, and it's

>> clear from

>> > my blood tests, lack of symptoms and high energy that my T3 is

>> reaching my

>> > cells. I've lost 2 inches from my waist and abs in this time -- mostly

>> due

>> > to the excess cholesterol dump I think, since it binds to fatty acids

>> and is

>> > excreted.

>> >

>> > Even more importantly, I've been doing deep, deep medical research

>> these

>> > last two months and believe I have found the cause of my RT3 problem

>> to

>> > begin with: Leptin Resistance. My blood test for that revealed that I

>> am

>> > severely leptin resistant even though I'm no longer insulin resistant

>> to any

>> > degree! I've decided to write about it here in the hopes that it will

>> ring

>> > some bells for other members and perhaps help them as well.

>> >

>> > Leptin is the King of all the hormones. It manages and gives orders to

>> them

>> > all, including, tellingly, insulin -- yet it takes orders from no

>> hormones.

>> > It reigns supreme. It is created from your adipose fat cells, so the

>> more

>> > stored fat you have, the more leptin you will produce.

>> >

>> > When you begin to eat, your leptin travels up through the bloodstream

>> to

>> > the blood-brain barrier, where with the help of a protein gets folded

>> into a

>> > three-dimensional shape that lets it slip through a precisely shaped

>> keyhole

>> > to reach the hypothalamus. The leptin gives your brain a lot of

>> information

>> > that will be used to determine how to *handle* your ingested energy:

>> burn or

>> > store. And the brain has many tools at its disposal to make your

>> metabolism

>> > do exactly what it wants, from making cells insulin resistant (thus

>> storing

>> > more fat) to signaling T4 to stop converting into T3 and start

>> converting to

>> > RT3. Or, to conversely, to have it make more T3 and 'turn up the heat'

>> to

>> > burn more energy. YOU don't control this. Leptin and your brain does.

>> >

>> > But leptin does more. It signals the brain about how much energy

>> *this*

>> > meal contains versus how much stored fat (the brain only sees 'energy'

>> or

>> > 'not energy') you have. If the brain thinks it has sufficient energy

>> it

>> > raises another hormone to send the signal for you to stop eating.

>> That's

>> > when you get that " Can't eat another bite " feeling and you put down

>> the

>> > fork, no matter how delicious the food. Doggy bags were created to

>> deal with

>> > this hormone. And how it works is important, because that signal

>> makes

>> > glucagon (which controls insulin rise) decrease via a hormone called

>> amylin.

>> >

>> > And leptin does still more. It acts like an A1c test for fat, telling

>> the

>> > brain not only about the meal you're eating now, but about how much

>> energy

>> > you've eaten over the last several days. [Which explains why we see

>> weight

>> > gains on the scale not the day after a binge, but 72 hours later].

>> This is

>> > the crucial information, because the brain doesn't like to make sudden

>> > changes. It gathers the leptin info over the course of a few days and

>> only

>> > then decides what hormones to use to either burn off excess energy or

>> RETAIN

>> > energy by changing your metabolism via your hormones and liver.

>> >

>> > Amazingly, leptin was only discovered in 1994! And it set off a true

>> Gold

>> > Rush among Big Pharma because of how it was discovered: mice bred to

>> be fat

>> > (no matter how little they ate) were discovered to have low levels of

>> this

>> > hormone, yet when it was synthesized and injected into the mice, they

>> > overcame their fat genes and became skinny. Oh! Big Pharma thought --

>> the

>> > Holy Grail! We'll synthesize leptin, patent it, and have the Mother of

>> all

>> > Blockbuster Drugs to sell, one that will reverse obesity with a single

>> pill.

>> >

>> > They poured millions and millions into R & D, but when the first human

>> trials

>> > were done, disaster loomed. Yes, the obese people injected with it did

>> lose

>> > weight. For the first two weeks. Then they stopped losing, gained it

>> all

>> > back, and put on a bit more for good measure. And this was true for

>> all

>> > study subjects.

>> >

>> > Turns out, when they actually examined fat people, they had four to

>> five

>> > times MORE leptin than thin people. WTF???

>> >

>> > At this point, all R & D stopped, and some companies sold their leptin

>> > divisions. One company -- Amylin -- bought out the biggest, and more

>> about

>> > them later.

>> >

>> > So, by 2000, what researchers knew is that obese people are not only

>> often

>> > insulin resistant (which begins in the liver), and not only often

>> thyroid

>> > resistant (which begins in the liver), but are almost all leptin

>> resistant

>> > -- and in all three cases, the result is the same: the correct hormone

>> is

>> > produced, but is blocked from reaching the cells, which in turn means

>> that

>> > the correct signaling cannot get through. The actual process for this

>> is

>> > that the leptin cannot be folded into the proper shape and thus cannot

>> cross

>> > the blood-brain barrier.

>> >

>> > With little or no leptin reaching it, the brain believes the body is

>> in

>> > danger of starvation regardless of actual calories consumed, and takes

>> > immediate steps to slow down the metabolism. So you get fat, which

>> creates

>> > more pooled leptin and you become ever more leptin resistant. It's a

>> vicious

>> > circle because for hormones, the ability to reach the cells with the

>> right

>> > signal is everything.

>> >

>> > This was why, for instance, my cholesterol kept rising until it was

>> > sky-high: T3 carries the signal the liver needs to know there is

>> sufficient

>> > cholesterol in the blood, but RT3 lacks that signal. As soon as

>> cytomel

>> > allowed T3 to once again reach my cells, the correct signal reached

>> the

>> > liver, which immediately dumped excess cholesterol out of my body.

>> >

>> > When leptin doesn't reach the brain, it's much, much worse. What it

>> means,

>> > in essence, is that while I see a still-overweight woman when *I* look

>> in

>> > the mirror, what my *brain* sees is a very thin woman on the edge of

>> > starvation. And it will do everything in its considerable power to

>> conserve

>> > as much ingested and stored energy as possible.

>> >

>> > What this usually means is:

>> >

>> > 1: During a meal, the leptin that normally would go to the brain

>> saying

>> > 'lots of energy here, boss' doesn't get through. So the brain never

>> sends

>> > the hormonal system of 'you're full you idiot, so stop eating!' Thus,

>> leptin

>> > resistant people are usually always hungry and always eating.

>> >

>> > 2: In order to conserve as much energy as possible in the easiest to

>> store

>> > form (fat), the brain sends out a specific hormone that not only tells

>> us to

>> > eat, but to eat lots and lots of carbs, particularly sweets. That's

>> because

>> > the brain knows this will ultimately create insulin resistance, which

>> means

>> > more triglycerides made in the liver, which means more stored fat.

>> This is

>> > why most leptin resistant people say they 'crave' sweets. They do, but

>> only

>> > because they are being ordered by the brain to crave them.

>> >

>> > But what happens when the brain is stored in a body that eats high

>> fat, low

>> > carb, and is thus not only satisfied with less food, but with almost

>> no

>> > sweets? I'll tell you what happens: the thwarted brain simply pulls

>> another

>> > tool from the box for conserving energy: the thyroid hormones. By

>> creating a

>> > RT3 imbalance, energy and fat are stored not burned, and the

>> metabolism is

>> > slowed to such a state that no amount of exercise, no eating this or

>> not

>> > eating that, no calorie reduction will overcome it. In fact, the more

>> you do

>> > to lose weight, the more the leptin-deprived brain conserves energy.

>> This

>> > finally explains the mystery of how morbidly obese patients can be

>> locked

>> > into a hospital metabolic ward, fed 500 calories a day -- and gain

>> weight.

>> > Mysterious no more.

>> >

>> > But what to do about it, that's the question. And for that, someone

>> needed

>> > to show exactly how people become leptin resistant (and diabetic,

>> too!). And

>> > finally, someone has. In a major study done at Boston Children's

>> Hospital

>> > Research Center in 2008 and published in the January 2009 issue of

>> " Cell

>> > Metabolism " as: " Endoplasmic Reticulum Stress Plays a Central Role in

>> > Development of Leptin Resistance " this mechanism was revealed. From

>> the

>> > article:

>> >

>> > " The endoplasmic reticulum (ER) is a sophisticated luminal network in

>> which

>> > protein synthesis, maturation, folding, and transport take place.

>> > Perturbation of these processes in several different pathological

>> states

>> > creates a condition defined as ER stress and leads to activation of a

>> > complex signaling network termed the unfolded protein response

>> > (UPR). Previous studies have demonstrated that ER stress and

>> activation of

>> > UPR signaling pathways play a dominant role in the development of

>> > obesity-induced insulin resistance and type 2 diabetes. Furthermore,

>> > reversal of ER stress with chemical chaperones—agents that have the

>> ability

>> > to increase ER folding machinery—increases insulin sensitivity and

>> reverses

>> > type 2 diabetes in obese mice.

>> >

>> > SUMMARY

>> > Leptin has not evolved as a therapeutic modality for the treatment of

>> > obesity due to the prevalence of leptin resistance in a majority of

>> the

>> > obese population. Nevertheless, the molecular mechanisms of leptin

>> > resistance remain poorly understood. Here, we show that increased

>> > endoplasmic reticulum (ER) stress and activation of the unfolded

>> protein

>> > response (UPR) in the hypothalamus of obese mice inhibits leptin

>> receptor

>> > signaling. The genetic imposition of reduced ER capacity in mice

>> results in

>> > severe leptin resistance and leads to a significant augmentation of

>> obesity.

>> > Moreover, we show that chemical chaperones, 4-phenyl butyric acid

>> (PBA), and

>> > tauroursodeoxycholic acid (TUDCA), which have the ability to decrease

>> ER

>> > stress, act as leptin-sensitizing agents. Taken together, our results

>> may

>> > provide the basis for a novel treatment of obesity. "

>> >

>> > To summarize the summary: the study proved that when something/s

>> (still

>> > unknown but I believe was right about outside stress, like

>> major

>> > surgery in my case, which is when my weight loss stopped after losing

>> 65

>> > pounds but 20 pounds from goal) stresses the ER in the brain, leptin

>> > resistance begins. The ER then activates the UPR (unfolded protein

>> > response), which means the leptin can no longer get through. And then

>> all

>> > metabolic hell ensues.

>> >

>> > What is stunning about the study though, is that the researchers went

>> > further. Once they'd proved the faulty mechanism, they decided to test

>> > whether or not sending along a 'chaperone molecule' with the leptin

>> would

>> > undo the UPR and let the leptin through. And they not only did it,

>> they did

>> > it with two non-toxic drugs already approved by the FDA for treating

>> other

>> > diseases!

>> >

>> > When they gave obese mice a ten-day 'pre-treatment' of 4-PBA the mice

>> > didn't lose weight or fat, but once leptin was added to the

>> injections,

>> > those mice grew thin and *lean* with lots of lost body fat. And the

>> mice

>> > stayed lean. When their hypothalamus' were harvested, it showed that

>> indeed

>> > leptin signaling (leptin sensitivity) had been restored.

>> >

>> > The real eye-opener was with TUDCA though. Just treatment with it

>> alone

>> > caused major weight and fat loss. And when leptin was added, just a

>> fraction

>> > of the amount used with the 4-PBA was needed for even more drastic

>> weight

>> > loss. Which was also stable.

>> >

>> > TUDCA is biologically identical to UDCA (sold as Actigall in this

>> country),

>> > which is used to treat liver diseases. TUDCA was used by the

>> researchers

>> > because it's an inject-able liquid, whereas the UDCA is taken orally.

>> Isn't

>> > it amazing how everything metabolic somehow leads back to the brain's

>> > connection with the liver? And the 'U' in UDCA stands for 'urso' --

>> Bear in

>> > Latin -- because it comes from bear bile. The liver. And it's been

>> used by

>> > Native Americans for centuries to treat illness. It is such an

>> incredible

>> > substance that there are now clinical trials all over the world using

>> TUDCA

>> > to treat Huntington's Disease, Cystic Fibrosis, and Altzheimer's.

>> > Researchers believe they are on the verge of major breakthrough's for

>> all

>> > three, thanks to this simple substance.

>> >

>> > So, armed with this knowledge (and the fact that I had diagnosed my

>> own RT3

>> > and Cholesterol problem, and treated them both of them myself

>> successfully),

>> > I met with my Endo. I was there for two hours. She did most of the

>> > question-asking, and I provided most of the answers.

>> >

>> > When we were done, she agreed that it was indeed likely that my RT3

>> problem

>> > was originally caused by my leptin resistance, and also with my

>> hypothesis

>> > that if I did not treat and cure the original problem (LP), my brain

>> would

>> > continue to be leptin-deprived, continue to think I'm skinny, and

>> would only

>> > pull another metabolic trick out of its hat to retain my weight and

>> fat. I

>> > believe this alone can explain why some people on T3 can lower RT3 and

>> get

>> > T3 back into the cells but not lose weight. And why for many, RT3

>> and/or

>> > hypo symptoms return when they return to dessicated thyroid.

>> >

>> > She agreed to support my being an experiment of one, with help from

>> the

>> > Doctor who is leading the UDCA Cystic Fibrosis study at the University

>> of

>> > Michigan, whom I contacted and spoke to at length.

>> >

>> > Starting this week I will begin a 'pre-treatment' of Symlin

>> (pramlintide

>> > acetate) injections with the two sample 'pens' my Endo gave me. Symlin

>> is a

>> > synthetic form of Amylin, a sister hormone of leptin that plays a huge

>> role

>> > in proper insulin use in the body as mentioned above, by signaling the

>> liver

>> > to decrease production of glucagon. Type 1 Diabetics no longer make

>> Amylin,

>> > and it is either low or missing or not working properly in Type 2's --

>> which

>> > is not surprising given that I believe this is their form of leptin

>> > resistance.

>> >

>> > How it works:

>> >

>> > " Symlin, by acting as an amylinomimetic agent, has the following

>> effects:

>> > 1) modulation of gastric emptying; 2) prevention of the postprandial

>> rise in

>> > plasma glucagon; and 3) satiety leading to decreased caloric intake

>> and

>> > potential weight loss. "

>> >

>> > For me, the most important point is reduction of glucagon, which does

>> not

>> > work properly in leptin resistant people.

>> >

>> > Symlin is made by the company Amylin, which was the company I

>> mentioned

>> > earlier, that purchased the R & D and rights to patent leptin back in

>> 2000. In

>> > fact, Symlin has been shown to cause rapid weight and fat loss in type

>> 1 and

>> > type 2 diabetics who take it with their insulin (because I believe

>> based on

>> > my research that it too restores leptin signaling; see the Holtof site

>> for

>> > more info) -- and the company is currently in trials to convince the

>> FDA to

>> > let them market it for weight loss. Followed, no doubt in my mind, by

>> a form

>> > of leptin they are working to produce.

>> >

>> > If my hypothesis is correct, in two months Symlin will fully restore

>> my

>> > amylin/leptin connection, after which I will begin supplementing with

>> > UDCA/Actigall. I fully expect to have my letpin resistance restored,

>> my T3

>> > problem permanently fixed, and my metabolism completely healed. I also

>> > expect to lose the 20 pounds I couldn't before, as well as the 10 I

>> added

>> > back when my RT3 began to rise. And I fully expect my insulin

>> sensitivity to

>> > grow even better, and my A1c to continue to fall.

>> >

>> > Knowing now what I know about the brilliance of our intricate hormonal

>> and

>> > metabolic systems, and the ability of our brain to rule them

>> *absolutely*

>> > despite any of our intentions or actions, I find the advice " To lose

>> weight

>> > simply eat less and exercise more " akin to saying " To lose weight bury

>> a

>> > chicken bone in the backyard at the full moon and say the following

>> > incantation. " Both will be equal in their efficacy. Same thing for

>> " cut out

>> > dairy, don't eat grains, count calories, don't count them, eat this,

>> don't

>> > eat that, " etc. etc. etc.

>> >

>> > A person with a perfectly healthy and functioning metabolism will not

>> store

>> > excess energy (fat) in the first place. If they feast a day or so they

>> might

>> > gain a pound or two, but a week of eating as usual will see that gone

>> > without them having to do anything, or eat anything, or not eat

>> anything

>> > special. That's how we evolved, and that's how we're still built. Our

>> > ancestors never had to 'diet' and neither should we.

>> >

>> > Abuse or stress my make that metabolism non-functioning, but to cure

>> it

>> > requires science, not anecdote or one food over another. My heart

>> aches as I

>> > read the same posts over and over on all the various forums dealing

>> with

>> > obesity, from calorie-counting forums to low-carb forums. Everywhere

>> is

>> > anecdote and useless advice, and science nowhere to be found. I've

>> written

>> > this very long post hoping that here at least, with Val and Nick,

>> science

>> > will have a place and that their readers will now have a test --

>> leptin

>> > serum level -- to begin, and some solutions to follow.

>> >

>> > To a Happy and Healthy New Year for us all...

>> >

>> >

>> >

>> >

>> >

>> >

>> >

>> > ------------------------------------

>> >

>> >

[Guest guest]

birrdyy@...

my e mail cut off.... without the remainder of the following: " how much

energy "

> > do exactly what it wants, from making cells insulin resistant (thus

storing

> > more fat) to signaling T4 to stop converting into T3 and start

converting to

> > RT3. Or, to conversely, to have it make more T3 and 'turn up the heat' to

> > burn more energy. YOU don't control this. Leptin and your brain does.

> >

> > But leptin does more. It signals the brain about how much energy

what was next??

thanks

C. Hunter

> That's a great question- would love to know. I thought suggests you

> can go off once you are " cured " ?

>

> Bonnie

>

>

>>

>> > I guess the old saying: " It's the exception that proves the rule " is

>> right,

>> > and I'm the exception. ;-)

>> >

>> > When I told back in October that I intended to stay on Iodoral

>> > while doing my T3 therapy, she said she'd be very interested to know

>> if it

>> > worked because she hasn't seen many people for whom that is true.

>> Well, it

>> > worked, so she can now add me to the shortlist. I've continued to

>> take a

>> > single 12.5 mg tab every morning. No HC or Isocort or Iron supplements

>> > either. Nothing but T3, and not all that much required for success. I

>> never

>> > took over 75mcg and that was only for a few days. And my ferritin is

>> only

>> > 47.

>> >

>> > Here are the stats from my latest labs:

>> >

>> > Began 's protocol on November 5, 2009

>> >

>> > After ten days, reached 75mcg per day on November 15 -- became hyper,

>> with

>> > 99+ temps and sweats, pulse in the 90's -- cycled down to zero in a

>> week and

>> > then began again on November 23 using a modified protocol. Modified in

>> this

>> > case means I began with 6.

> 25 mcg and added more T3 very slowly, as Val

>> > recommends, and also that unlike 's recommendation did not take

>> > compounded time-release T3 but Cynomel.

>> >

>> > BLOOD TEST on Dec 4th:

>> > TC and LDL dropped 100 points!

>> > Triglycerides dropped from 67 to 42

>> > HDL rose from 88 to 97

>> > A1c dropped a bit to 5.0

>> > APO B/APO a-1 = .56 -- HALF the *lowest* risk for CHD!

>> >

>> > FT3 = 404 (up from 291)

>> > RT3 = 10 (down from 25).

>> > Ratio = 40.4!!! (up from 11.64)

>> > T4 Total = 3.7 (4.5-12.5)

>> > FT4 = 1.0 (1.4-3.8)

>> > Sodium = 143 (128-145)

>> > Potassium = 4.9 (3.6-5.1)

>> > Ferritn = 47 (20-288)

>> > Iron = 67 (40-160)

>> >

>> > I reached a dose of 50mcg on 12/16. My temps reached 98.6 steady two

>> days

>> > after that. By 12/25 my temps were 99.9 so I reduced my dose to 37.5

>> and

>> > have been there every since. My temps have been rock solid at 98.6 all

>> day,

>> > every day for the last 3 weeks. No hypo symptoms at all, and it's

>> clear from

>> > my blood tests, lack of symptoms and high energy that my T3 is

>> reaching my

>> > cells. I've lost 2 inches from my waist and abs in this time -- mostly

>> due

>> > to the excess cholesterol dump I think, since it binds to fatty acids

>> and is

>> > excreted.

>> >

>> > Even more importantly, I've been doing deep, deep medical research

>> these

>> > last two months and believe I have found the cause of my RT3 problem

>> to

>> > begin with: Leptin Resistance. My blood test for that revealed that I

>> am

>> > severely leptin resistant even though I'm no longer insulin resistant

>> to any

>> > degree! I've decided to write about it here in the hopes that it will

>> ring

>> > some bells for other members and perhaps help them as well.

>> >

>> > Leptin is the King of all the hormones. It manages and gives orders to

>> them

>> > all, including, tellingly, insulin -- yet it takes orders from no

>> hormones.

>> > It reigns supreme. It is created from your adipose fat cells, so the

>> more

>> > stored fat you have, the more leptin you will produce.

>> >

>> > When you begin to eat, your leptin travels up through the bloodstream

>> to

>> > the blood-brain barrier, where with the help of a protein gets folded

>> into a

>> > three-dimensional shape that lets it slip through a precisely shaped

>> keyhole

>> > to reach the hypothalamus. The leptin gives your brain a lot of

>> information

>> > that will be used to determine how to *handle* your ingested energy:

>> burn or

>> > store. And the brain has many tools at its disposal to make your

>> metabolism

>> > do exactly what it wants, from making cells insulin resistant (thus

>> storing

>> > more fat) to signaling T4 to stop converting into T3 and start

>> converting to

>> > RT3. Or, to conversely, to have it make more T3 and 'turn up the heat'

>> to

>> > burn more energy. YOU don't control this. Leptin and your brain does.

>> >

>> > But leptin does more. It signals the brain about how much energy

>> *this*

>> > meal contains versus how much stored fat (the brain only sees 'energy'

>> or

>> > 'not energy') you have. If the brain thinks it has sufficient energy

>> it

>> > raises another hormone to send the signal for you to stop eating.

>> That's

>> > when you get that " Can't eat another bite " feeling and you put down

>> the

>> > fork, no matter how delicious the food. Doggy bags were created to

>> deal with

>> > this hormone. And how it works is important, because that signal

>> makes

>> > glucagon (which controls insulin rise) decrease via a hormone called

>> amylin.

>> >

>> > And leptin does still more. It acts like an A1c test for fat, telling

>> the

>> > brain not only about the meal you're eating now, but about how much

>> energy

>> > you've eaten over the last several days. [Which explains why we see

>> weight

>> > gains on the scale not the day after a binge, but 72 hours later].

>> This is

>> > the crucial information, because the brain doesn't like to make sudden

>> > changes. It gathers the leptin info over the course of a few days and

>> only

>> > then decides what hormones to use to either burn off excess energy or

>> RETAIN

>> > energy by changing your metabolism via your hormones and liver.

>> >

>> > Amazingly, leptin was only discovered in 1994! And it set off a true

>> Gold

>> > Rush among Big Pharma because of how it was discovered: mice bred to

>> be fat

>> > (no matter how little they ate) were discovered to have low levels of

>> this

>> > hormone, yet when it was synthesized and injected into the mice, they

>> > overcame their fat genes and became skinny. Oh! Big Pharma thought --

>> the

>> > Holy Grail! We'll synthesize leptin, patent it, and have the Mother of

>> all

>> > Blockbuster Drugs to sell, one that will reverse obesity with a single

>> pill.

>> >

>> > They poured millions and millions into R & D, but when the first human

>> trials

>> > were done, disaster loomed. Yes, the obese people injected with it did

>> lose

>> > weight. For the first two weeks. Then they stopped losing, gained it

>> all

>> > back, and put on a bit more for good measure. And this was true for

>> all

>> > study subjects.

>> >

>> > Turns out, when they actually examined fat people, they had four to

>> five

>> > times MORE leptin than thin people. WTF???

>> >

>> > At this point, all R & D stopped, and some companies sold their leptin

>> > divisions. One company -- Amylin -- bought out the biggest, and more

>> about

>> > them later.

>> >

>> > So, by 2000, what researchers knew is that obese people are not only

>> often

>> > insulin resistant (which begins in the liver), and not only often

>> thyroid

>> > resistant (which begins in the liver), but are almost all leptin

>> resistant

>> > -- and in all three cases, the result is the same: the correct hormone

>> is

>> > produced, but is blocked from reaching the cells, which in turn means

>> that

>> > the correct signaling cannot get through. The actual process for this

>> is

>> > that the leptin cannot be folded into the proper shape and thus cannot

>> cross

>> > the blood-brain barrier.

>> >

>> > With little or no leptin reaching it, the brain believes the body is

>> in

>> > danger of starvation regardless of actual calories consumed, and takes

>> > immediate steps to slow down the metabolism. So you get fat, which

>> creates

>> > more pooled leptin and you become ever more leptin resistant. It's a

>> vicious

>> > circle because for hormones, the ability to reach the cells with the

>> right

>> > signal is everything.

>> >

>> > This was why, for instance, my cholesterol kept rising until it was

>> > sky-high: T3 carries the signal the liver needs to know there is

>> sufficient

>> > cholesterol in the blood, but RT3 lacks that signal. As soon as

>> cytomel

>> > allowed T3 to once again reach my cells, the correct signal reached

>> the

>> > liver, which immediately dumped excess cholesterol out of my body.

>> >

>> > When leptin doesn't reach the brain, it's much, much worse. What it

>> means,

>> > in essence, is that while I see a still-overweight woman when *I* look

>> in

>> > the mirror, what my *brain* sees is a very thin woman on the edge of

>> > starvation. And it will do everything in its considerable power to

>> conserve

>> > as much ingested and stored energy as possible.

>> >

>> > What this usually means is:

>> >

>> > 1: During a meal, the leptin that normally would go to the brain

>> saying

>> > 'lots of energy here, boss' doesn't get through. So the brain never

>> sends

>> > the hormonal system of 'you're full you idiot, so stop eating!' Thus,

>> leptin

>> > resistant people are usually always hungry and always eating.

>> >

>> > 2: In order to conserve as much energy as possible in the easiest to

>> store

>> > form (fat), the brain sends out a specific hormone that not only tells

>> us to

>> > eat, but to eat lots and lots of carbs, particularly sweets. That's

>> because

>> > the brain knows this will ultimately create insulin resistance, which

>> means

>> > more triglycerides made in the liver, which means more stored fat.

>> This is

>> > why most leptin resistant people say they 'crave' sweets. They do, but

>> only

>> > because they are being ordered by the brain to crave them.

>> >

>> > But what happens when the brain is stored in a body that eats high

>> fat, low

>> > carb, and is thus not only satisfied with less food, but with almost

>> no

>> > sweets? I'll tell you what happens: the thwarted brain simply pulls

>> another

>> > tool from the box for conserving energy: the thyroid hormones. By

>> creating a

>> > RT3 imbalance, energy and fat are stored not burned, and the

>> metabolism is

>> > slowed to such a state that no amount of exercise, no eating this or

>> not

>> > eating that, no calorie reduction will overcome it. In fact, the more

>> you do

>> > to lose weight, the more the leptin-deprived brain conserves energy.

>> This

>> > finally explains the mystery of how morbidly obese patients can be

>> locked

>> > into a hospital metabolic ward, fed 500 calories a day -- and gain

>> weight.

>> > Mysterious no more.

>> >

>> > But what to do about it, that's the question. And for that, someone

>> needed

>> > to show exactly how people become leptin resistant (and diabetic,

>> too!). And

>> > finally, someone has. In a major study done at Boston Children's

>> Hospital

>> > Research Center in 2008 and published in the January 2009 issue of

>> " Cell

>> > Metabolism " as: " Endoplasmic Reticulum Stress Plays a Central Role in

>> > Development of Leptin Resistance " this mechanism was revealed. From

>> the

>> > article:

>> >

>> > " The endoplasmic reticulum (ER) is a sophisticated luminal network in

>> which

>> > protein synthesis, maturation, folding, and transport take place.

>> > Perturbation of these processes in several different pathological

>> states

>> > creates a condition defined as ER stress and leads to activation of a

>> > complex signaling network termed the unfolded protein response

>> > (UPR). Previous studies have demonstrated that ER stress and

>> activation of

>> > UPR signaling pathways play a dominant role in the development of

>> > obesity-induced insulin resistance and type 2 diabetes. Furthermore,

>> > reversal of ER stress with chemical chaperones—agents that have the

>> ability

>> > to increase ER folding machinery—increases insulin sensitivity and

>> reverses

>> > type 2 diabetes in obese mice.

>> >

>> > SUMMARY

>> > Leptin has not evolved as a therapeutic modality for the treatment of

>> > obesity due to the prevalence of leptin resistance in a majority of

>> the

>> > obese population. Nevertheless, the molecular mechanisms of leptin

>> > resistance remain poorly understood. Here, we show that increased

>> > endoplasmic reticulum (ER) stress and activation of the unfolded

>> protein

>> > response (UPR) in the hypothalamus of obese mice inhibits leptin

>> receptor

>> > signaling. The genetic imposition of reduced ER capacity in mice

>> results in

>> > severe leptin resistance and leads to a significant augmentation of

>> obesity.

>> > Moreover, we show that chemical chaperones, 4-phenyl butyric acid

>> (PBA), and

>> > tauroursodeoxycholic acid (TUDCA), which have the ability to decrease

>> ER

>> > stress, act as leptin-sensitizing agents. Taken together, our results

>> may

>> > provide the basis for a novel treatment of obesity. "

>> >

>> > To summarize the summary: the study proved that when something/s

>> (still

>> > unknown but I believe was right about outside stress, like

>> major

>> > surgery in my case, which is when my weight loss stopped after losing

>> 65

>> > pounds but 20 pounds from goal) stresses the ER in the brain, leptin

>> > resistance begins. The ER then activates the UPR (unfolded protein

>> > response), which means the leptin can no longer get through. And then

>> all

>> > metabolic hell ensues.

>> >

>> > What is stunning about the study though, is that the researchers went

>> > further. Once they'd proved the faulty mechanism, they decided to test

>> > whether or not sending along a 'chaperone molecule' with the leptin

>> would

>> > undo the UPR and let the leptin through. And they not only did it,

>> they did

>> > it with two non-toxic drugs already approved by the FDA for treating

>> other

>> > diseases!

>> >

>> > When they gave obese mice a ten-day 'pre-treatment' of 4-PBA the mice

>> > didn't lose weight or fat, but once leptin was added to the

>> injections,

>> > those mice grew thin and *lean* with lots of lost body fat. And the

>> mice

>> > stayed lean. When their hypothalamus' were harvested, it showed that

>> indeed

>> > leptin signaling (leptin sensitivity) had been restored.

>> >

>> > The real eye-opener was with TUDCA though. Just treatment with it

>> alone

>> > caused major weight and fat loss. And when leptin was added, just a

>> fraction

>> > of the amount used with the 4-PBA was needed for even more drastic

>> weight

>> > loss. Which was also stable.

>> >

>> > TUDCA is biologically identical to UDCA (sold as Actigall in this

>> country),

>> > which is used to treat liver diseases. TUDCA was used by the

>> researchers

>> > because it's an inject-able liquid, whereas the UDCA is taken orally.

>> Isn't

>> > it amazing how everything metabolic somehow leads back to the brain's

>> > connection with the liver? And the 'U' in UDCA stands for 'urso' --

>> Bear in

>> > Latin -- because it comes from bear bile. The liver. And it's been

>> used by

>> > Native Americans for centuries to treat illness. It is such an

>> incredible

>> > substance that there are now clinical trials all over the world using

>> TUDCA

>> > to treat Huntington's Disease, Cystic Fibrosis, and Altzheimer's.

>> > Researchers believe they are on the verge of major breakthrough's for

>> all

>> > three, thanks to this simple substance.

>> >

>> > So, armed with this knowledge (and the fact that I had diagnosed my

>> own RT3

>> > and Cholesterol problem, and treated them both of them myself

>> successfully),

>> > I met with my Endo. I was there for two hours. She did most of the

>> > question-asking, and I provided most of the answers.

>> >

>> > When we were done, she agreed that it was indeed likely that my RT3

>> problem

>> > was originally caused by my leptin resistance, and also with my

>> hypothesis

>> > that if I did not treat and cure the original problem (LP), my brain

>> would

>> > continue to be leptin-deprived, continue to think I'm skinny, and

>> would only

>> > pull another metabolic trick out of its hat to retain my weight and

>> fat. I

>> > believe this alone can explain why some people on T3 can lower RT3 and

>> get

>> > T3 back into the cells but not lose weight. And why for many, RT3

>> and/or

>> > hypo symptoms return when they return to dessicated thyroid.

>> >

>> > She agreed to support my being an experiment of one, with help from

>> the

>> > Doctor who is leading the UDCA Cystic Fibrosis study at the University

>> of

>> > Michigan, whom I contacted and spoke to at length.

>> >

>> > Starting this week I will begin a 'pre-treatment' of Symlin

>> (pramlintide

>> > acetate) injections with the two sample 'pens' my Endo gave me. Symlin

>> is a

>> > synthetic form of Amylin, a sister hormone of leptin that plays a huge

>> role

>> > in proper insulin use in the body as mentioned above, by signaling the

>> liver

>> > to decrease production of glucagon. Type 1 Diabetics no longer make

>> Amylin,

>> > and it is either low or missing or not working properly in Type 2's --

>> which

>> > is not surprising given that I believe this is their form of leptin

>> > resistance.

>> >

>> > How it works:

>> >

>> > " Symlin, by acting as an amylinomimetic agent, has the following

>> effects:

>> > 1) modulation of gastric emptying; 2) prevention of the postprandial

>> rise in

>> > plasma glucagon; and 3) satiety leading to decreased caloric intake

>> and

>> > potential weight loss. "

>> >

>> > For me, the most important point is reduction of glucagon, which does

>> not

>> > work properly in leptin resistant people.

>> >

>> > Symlin is made by the company Amylin, which was the company I

>> mentioned

>> > earlier, that purchased the R & D and rights to patent leptin back in

>> 2000. In

>> > fact, Symlin has been shown to cause rapid weight and fat loss in type

>> 1 and

>> > type 2 diabetics who take it with their insulin (because I believe

>> based on

>> > my research that it too restores leptin signaling; see the Holtof site

>> for

>> > more info) -- and the company is currently in trials to convince the

>> FDA to

>> > let them market it for weight loss. Followed, no doubt in my mind, by

>> a form

>> > of leptin they are working to produce.

>> >

>> > If my hypothesis is correct, in two months Symlin will fully restore

>> my

>> > amylin/leptin connection, after which I will begin supplementing with

>> > UDCA/Actigall. I fully expect to have my letpin resistance restored,

>> my T3

>> > problem permanently fixed, and my metabolism completely healed. I also

>> > expect to lose the 20 pounds I couldn't before, as well as the 10 I

>> added

>> > back when my RT3 began to rise. And I fully expect my insulin

>> sensitivity to

>> > grow even better, and my A1c to continue to fall.

>> >

>> > Knowing now what I know about the brilliance of our intricate hormonal

>> and

>> > metabolic systems, and the ability of our brain to rule them

>> *absolutely*

>> > despite any of our intentions or actions, I find the advice " To lose

>> weight

>> > simply eat less and exercise more " akin to saying " To lose weight bury

>> a

>> > chicken bone in the backyard at the full moon and say the following

>> > incantation. " Both will be equal in their efficacy. Same thing for

>> " cut out

>> > dairy, don't eat grains, count calories, don't count them, eat this,

>> don't

>> > eat that, " etc. etc. etc.

>> >

>> > A person with a perfectly healthy and functioning metabolism will not

>> store

>> > excess energy (fat) in the first place. If they feast a day or so they

>> might

>> > gain a pound or two, but a week of eating as usual will see that gone

>> > without them having to do anything, or eat anything, or not eat

>> anything

>> > special. That's how we evolved, and that's how we're still built. Our

>> > ancestors never had to 'diet' and neither should we.

>> >

>> > Abuse or stress my make that metabolism non-functioning, but to cure

>> it

>> > requires science, not anecdote or one food over another. My heart

>> aches as I

>> > read the same posts over and over on all the various forums dealing

>> with

>> > obesity, from calorie-counting forums to low-carb forums. Everywhere

>> is

>> > anecdote and useless advice, and science nowhere to be found. I've

>> written

>> > this very long post hoping that here at least, with Val and Nick,

>> science

>> > will have a place and that their readers will now have a test --

>> leptin

>> > serum level -- to begin, and some solutions to follow.

>> >

>> > To a Happy and Healthy New Year for us all...

>> >

>> >

>> >

>> >

>> >

>> >

>> >

>> > ------------------------------------

>> >

>> >

[Guest guest]

wrote:

> Very interesting stuff. I have printed it and will reread it several times

> and will surely get tested. Please please let us know how it goes. If you

> could title it something that we would recognize easily that would be

> great.

Birdy, I will do that. I plan to start my first Symlin injection tomorrow.

> Why do you think you were able to tolerate so much T3 with

> such a low ferritin number.

That's a good question. I do have a few ideas, but no proof. First, I've been

eating a very healthy diet for a long time. I get 75% of my calories from fat,

particularly saturated fat (butter, cream, coconut oil, lard, etc). I eat very

modest protein -- about 13% of my calories, or 50 or so grams of animal protein

(I don't count the incomplete protein from veggies or fruit). That's only 7 or 8

ounces a day total from all animal sources including eggs, cream in coffee, etc.

-- far less than most people eat. And I eat just enough carbs to stay out of

ketosis, making sure that includes some glucose foods like potato and rice so

that my body (especially my liver) doesn't need to undergo the stress of

gluconeogenesis by making the glucose it needs for my brain at night from

protein.

Second, I do the right kind of exercise to keep my cardiovascular system in

tip-top shape. That is, I do NO 'cardio' steady state exercise at all (like

walking, treadmill, etc) but instead do the Slow Burn weight lifting outlined in

Body By Science. I work out a total of 15 minutes every ten day to two weeks,

and I not only have biceps you can bounce a nickel off of, my lipids and

C-Reactive Protein tests are so good the Framingham online calculator says my

risk of heart attack in the next ten years is 1%.

Third, of the foods I eat, I make 90% of them myself. I eat very little

processed food. I make my own LC yogurt, fermented mayo, cottage cheese,

mascarpone, creme fraiche, butter, ice-cream, cheesecake, brownies, fudge,

cookies, etc. etc. etc.

I don't believe diet alone can make us healthy if our metabolisms are

compromised, but I do believe the right diet and exercise along with the right

treatment can make a huge difference.

> why do you still have such a (relatively) high FT4 number when you're

> on T3 only.

Do I? My FT4 is 1.0 and the range starts at 1.4. If 1.0 is still high, what

should it be???

> I looked up the prices for Symlin and Actigall and boy is it freckin

> expensive. You are very lucky to get some samples. Convincing a

> doctor on all this would be monumental.

Agreed. But as you've now seen thanks to the recent posts, Actigall is cheap.

According to the Doctor conducting the clinical trials on UDCA and cystic

fibrosis, dosing for me should be 15mg per KG of my weight. That would be about

1200 mg a day for me, or four 300 mg tabs. That's 120 tabs a month. I bet my

insurance/Medco will have a 90-day supply for less than $100 bucks and I'm

hoping a single prescription will do it for me.

Also, if my doc had not given me the samples, I would not have hesitated to

start on Actigall instead.

> Do you plan on staying on T3 indefinitely?

I don't plan on being on any medication at all six months from now. I'm only

staying on the T3 now because it apparently plays very well with Symlin, and

because it will protect me from one of Symlin's side effects: loss of appetite.

I don't eat a lot of food as it is, and if I eat less the T3 will ensure that a

'starvation syndrome' doesn't rear its ugly head. I will probably have to reduce

my dose though. My temps are now going from 98.6 to 98.7-9 -- so clearly lots

more T3 is reaching my cells. Once Symlin begins to let leptin reach my brain

again, my hypothalamus will signal my liver to make even more T3 -- so that

means lowering my T3 dose. By the time I'm done with the Symlin and on to the

Actigall (if needed), I should be off all T3.

Can't wait to start!

[Guest guest]

wrote:

> Very interesting stuff. I have printed it and will reread it several times

> and will surely get tested. Please please let us know how it goes. If you

> could title it something that we would recognize easily that would be

> great.

Birdy, I will do that. I plan to start my first Symlin injection tomorrow.

> Why do you think you were able to tolerate so much T3 with

> such a low ferritin number.

That's a good question. I do have a few ideas, but no proof. First, I've been

eating a very healthy diet for a long time. I get 75% of my calories from fat,

particularly saturated fat (butter, cream, coconut oil, lard, etc). I eat very

modest protein -- about 13% of my calories, or 50 or so grams of animal protein

(I don't count the incomplete protein from veggies or fruit). That's only 7 or 8

ounces a day total from all animal sources including eggs, cream in coffee, etc.

-- far less than most people eat. And I eat just enough carbs to stay out of

ketosis, making sure that includes some glucose foods like potato and rice so

that my body (especially my liver) doesn't need to undergo the stress of

gluconeogenesis by making the glucose it needs for my brain at night from

protein.

Second, I do the right kind of exercise to keep my cardiovascular system in

tip-top shape. That is, I do NO 'cardio' steady state exercise at all (like

walking, treadmill, etc) but instead do the Slow Burn weight lifting outlined in

Body By Science. I work out a total of 15 minutes every ten day to two weeks,

and I not only have biceps you can bounce a nickel off of, my lipids and

C-Reactive Protein tests are so good the Framingham online calculator says my

risk of heart attack in the next ten years is 1%.

Third, of the foods I eat, I make 90% of them myself. I eat very little

processed food. I make my own LC yogurt, fermented mayo, cottage cheese,

mascarpone, creme fraiche, butter, ice-cream, cheesecake, brownies, fudge,

cookies, etc. etc. etc.

I don't believe diet alone can make us healthy if our metabolisms are

compromised, but I do believe the right diet and exercise along with the right

treatment can make a huge difference.

> why do you still have such a (relatively) high FT4 number when you're

> on T3 only.

Do I? My FT4 is 1.0 and the range starts at 1.4. If 1.0 is still high, what

should it be???

> I looked up the prices for Symlin and Actigall and boy is it freckin

> expensive. You are very lucky to get some samples. Convincing a

> doctor on all this would be monumental.

Agreed. But as you've now seen thanks to the recent posts, Actigall is cheap.

According to the Doctor conducting the clinical trials on UDCA and cystic

fibrosis, dosing for me should be 15mg per KG of my weight. That would be about

1200 mg a day for me, or four 300 mg tabs. That's 120 tabs a month. I bet my

insurance/Medco will have a 90-day supply for less than $100 bucks and I'm

hoping a single prescription will do it for me.

Also, if my doc had not given me the samples, I would not have hesitated to

start on Actigall instead.

> Do you plan on staying on T3 indefinitely?

I don't plan on being on any medication at all six months from now. I'm only

staying on the T3 now because it apparently plays very well with Symlin, and

because it will protect me from one of Symlin's side effects: loss of appetite.

I don't eat a lot of food as it is, and if I eat less the T3 will ensure that a

'starvation syndrome' doesn't rear its ugly head. I will probably have to reduce

my dose though. My temps are now going from 98.6 to 98.7-9 -- so clearly lots

more T3 is reaching my cells. Once Symlin begins to let leptin reach my brain

again, my hypothalamus will signal my liver to make even more T3 -- so that

means lowering my T3 dose. By the time I'm done with the Symlin and on to the

Actigall (if needed), I should be off all T3.

Can't wait to start!

[Guest guest]

Wow, you are a brainiac and a healthy eater for that matter.  Very interesting.  Thanks for the explanations.As for the FT4.  I believe the range is .8-1.8.  Unless you have some kind of very strange lab with very strange ranges it doesn't start at 1.4.  On 65 of Cytomel my FT4 is .2.  Almost everyone has such a low number when on T3 only.  I'm very confused about that.  It wasn't a typo on your part was it?

wrote:

> Very interesting stuff.  I have printed it and will reread it several times

> and will surely get tested.  Please please let us know how it goes.  If you

> could title it something that we would recognize easily that would be

> great.

Birdy, I will do that. I plan to start my first Symlin injection tomorrow.

> Why do you think you were able to tolerate so much T3 with

> such a low ferritin number.

That's a good question. I do have a few ideas, but no proof. First, I've been eating a very healthy diet for a long time. I get 75% of my calories from fat, particularly saturated fat (butter, cream, coconut oil, lard, etc). I eat very modest protein -- about 13% of my calories, or 50 or so grams of animal protein (I don't count the incomplete protein from veggies or fruit). That's only 7 or 8 ounces a day total from all animal sources including eggs, cream in coffee, etc. -- far less than most people eat. And I eat just enough carbs to stay out of ketosis, making sure that includes some glucose foods like potato and rice so that my body (especially my liver) doesn't need to undergo the stress of gluconeogenesis by making the glucose it needs for my brain at night from protein.

Second, I do the right kind of exercise to keep my cardiovascular system in tip-top shape. That is, I do NO 'cardio' steady state exercise at all (like walking, treadmill, etc) but instead do the Slow Burn weight lifting outlined in Body By Science. I work out a total of 15 minutes every ten day to two weeks, and I not only have biceps you can bounce a nickel off of, my lipids and C-Reactive Protein tests are so good the Framingham online calculator says my risk of heart attack in the next ten years is 1%.

Third, of the foods I eat, I make 90% of them myself. I eat very little processed food. I make my own LC yogurt, fermented mayo, cottage cheese, mascarpone, creme fraiche, butter, ice-cream, cheesecake, brownies, fudge, cookies, etc. etc. etc.

I don't believe diet alone can make us healthy if our metabolisms are compromised, but I do believe the right diet and exercise along with the right treatment can make a huge difference.

> why do you still have such a (relatively) high FT4 number when you're

> on T3 only.

Do I? My FT4 is 1.0 and the range starts at 1.4. If 1.0 is still high, what should it be???

> I looked up the prices for Symlin and Actigall and boy is it freckin

> expensive.  You are very lucky to get some samples.  Convincing a

> doctor on  all this would be monumental.

Agreed. But as you've now seen thanks to the recent posts, Actigall is cheap. According to the Doctor conducting the clinical trials on UDCA and cystic fibrosis, dosing for me should be 15mg per KG of my weight. That would be about 1200 mg a day for me, or four 300 mg tabs. That's 120 tabs a month. I bet my insurance/Medco will have a 90-day supply for less than $100 bucks and I'm hoping a single prescription will do it for me.

Also, if my doc had not given me the samples, I would not have hesitated to start on Actigall instead.

> Do you plan on staying on T3 indefinitely?

I don't plan on being on any medication at all six months from now. I'm only staying on the T3 now because it apparently plays very well with Symlin, and because it will protect me from one of Symlin's side effects: loss of appetite. I don't eat a lot of food as it is, and if I eat less the T3 will ensure that a 'starvation syndrome' doesn't rear its ugly head. I will probably have to reduce my dose though. My temps are now going from 98.6 to 98.7-9 -- so clearly lots more T3 is reaching my cells. Once Symlin begins to let leptin reach my brain again, my hypothalamus will signal my liver to make even more T3 -- so that means lowering my T3 dose. By the time I'm done with the Symlin and on to the Actigall (if needed), I should be off all T3.

Can't wait to start!

------------------------------------

[Guest guest]

Wow, you are a brainiac and a healthy eater for that matter.  Very interesting.  Thanks for the explanations.As for the FT4.  I believe the range is .8-1.8.  Unless you have some kind of very strange lab with very strange ranges it doesn't start at 1.4.  On 65 of Cytomel my FT4 is .2.  Almost everyone has such a low number when on T3 only.  I'm very confused about that.  It wasn't a typo on your part was it?

wrote:

> Very interesting stuff.  I have printed it and will reread it several times

> and will surely get tested.  Please please let us know how it goes.  If you

> could title it something that we would recognize easily that would be

> great.

Birdy, I will do that. I plan to start my first Symlin injection tomorrow.

> Why do you think you were able to tolerate so much T3 with

> such a low ferritin number.

That's a good question. I do have a few ideas, but no proof. First, I've been eating a very healthy diet for a long time. I get 75% of my calories from fat, particularly saturated fat (butter, cream, coconut oil, lard, etc). I eat very modest protein -- about 13% of my calories, or 50 or so grams of animal protein (I don't count the incomplete protein from veggies or fruit). That's only 7 or 8 ounces a day total from all animal sources including eggs, cream in coffee, etc. -- far less than most people eat. And I eat just enough carbs to stay out of ketosis, making sure that includes some glucose foods like potato and rice so that my body (especially my liver) doesn't need to undergo the stress of gluconeogenesis by making the glucose it needs for my brain at night from protein.

Second, I do the right kind of exercise to keep my cardiovascular system in tip-top shape. That is, I do NO 'cardio' steady state exercise at all (like walking, treadmill, etc) but instead do the Slow Burn weight lifting outlined in Body By Science. I work out a total of 15 minutes every ten day to two weeks, and I not only have biceps you can bounce a nickel off of, my lipids and C-Reactive Protein tests are so good the Framingham online calculator says my risk of heart attack in the next ten years is 1%.

Third, of the foods I eat, I make 90% of them myself. I eat very little processed food. I make my own LC yogurt, fermented mayo, cottage cheese, mascarpone, creme fraiche, butter, ice-cream, cheesecake, brownies, fudge, cookies, etc. etc. etc.

I don't believe diet alone can make us healthy if our metabolisms are compromised, but I do believe the right diet and exercise along with the right treatment can make a huge difference.

> why do you still have such a (relatively) high FT4 number when you're

> on T3 only.

Do I? My FT4 is 1.0 and the range starts at 1.4. If 1.0 is still high, what should it be???

> I looked up the prices for Symlin and Actigall and boy is it freckin

> expensive.  You are very lucky to get some samples.  Convincing a

> doctor on  all this would be monumental.

Agreed. But as you've now seen thanks to the recent posts, Actigall is cheap. According to the Doctor conducting the clinical trials on UDCA and cystic fibrosis, dosing for me should be 15mg per KG of my weight. That would be about 1200 mg a day for me, or four 300 mg tabs. That's 120 tabs a month. I bet my insurance/Medco will have a 90-day supply for less than $100 bucks and I'm hoping a single prescription will do it for me.

Also, if my doc had not given me the samples, I would not have hesitated to start on Actigall instead.

> Do you plan on staying on T3 indefinitely?

I don't plan on being on any medication at all six months from now. I'm only staying on the T3 now because it apparently plays very well with Symlin, and because it will protect me from one of Symlin's side effects: loss of appetite. I don't eat a lot of food as it is, and if I eat less the T3 will ensure that a 'starvation syndrome' doesn't rear its ugly head. I will probably have to reduce my dose though. My temps are now going from 98.6 to 98.7-9 -- so clearly lots more T3 is reaching my cells. Once Symlin begins to let leptin reach my brain again, my hypothalamus will signal my liver to make even more T3 -- so that means lowering my T3 dose. By the time I'm done with the Symlin and on to the Actigall (if needed), I should be off all T3.

Can't wait to start!

------------------------------------

[Guest guest]

I just reread some of your stuff.  I missed the range on the FT4.  What lab is that?  I have never seen that kind of range for FT4, never.I guess I'm a little confused about the Symlin and Actigall.  It seems like you don't have to do the Symlin first?  Is that what you're saying?  Could you go just to Actigall?  Yes, that stuff is reasonable.  Also, you're saying that a single prescription of either of these can " reset " your system?

Do you think this whole idea is something some doctors might get or is yours just exceptionally smart and accommodating?After all is said and done maybe you need to start your own yahoo group.Your exercise regime sounds fabulous.  Will have to look that one up.  Really, 15 minutes every 10 days.  Wow.

wrote:

> Very interesting stuff.  I have printed it and will reread it several times

> and will surely get tested.  Please please let us know how it goes.  If you

> could title it something that we would recognize easily that would be

> great.

Birdy, I will do that. I plan to start my first Symlin injection tomorrow.

> Why do you think you were able to tolerate so much T3 with

> such a low ferritin number.

That's a good question. I do have a few ideas, but no proof. First, I've been eating a very healthy diet for a long time. I get 75% of my calories from fat, particularly saturated fat (butter, cream, coconut oil, lard, etc). I eat very modest protein -- about 13% of my calories, or 50 or so grams of animal protein (I don't count the incomplete protein from veggies or fruit). That's only 7 or 8 ounces a day total from all animal sources including eggs, cream in coffee, etc. -- far less than most people eat. And I eat just enough carbs to stay out of ketosis, making sure that includes some glucose foods like potato and rice so that my body (especially my liver) doesn't need to undergo the stress of gluconeogenesis by making the glucose it needs for my brain at night from protein.

Second, I do the right kind of exercise to keep my cardiovascular system in tip-top shape. That is, I do NO 'cardio' steady state exercise at all (like walking, treadmill, etc) but instead do the Slow Burn weight lifting outlined in Body By Science. I work out a total of 15 minutes every ten day to two weeks, and I not only have biceps you can bounce a nickel off of, my lipids and C-Reactive Protein tests are so good the Framingham online calculator says my risk of heart attack in the next ten years is 1%.

Third, of the foods I eat, I make 90% of them myself. I eat very little processed food. I make my own LC yogurt, fermented mayo, cottage cheese, mascarpone, creme fraiche, butter, ice-cream, cheesecake, brownies, fudge, cookies, etc. etc. etc.

I don't believe diet alone can make us healthy if our metabolisms are compromised, but I do believe the right diet and exercise along with the right treatment can make a huge difference.

> why do you still have such a (relatively) high FT4 number when you're

> on T3 only.

Do I? My FT4 is 1.0 and the range starts at 1.4. If 1.0 is still high, what should it be???

> I looked up the prices for Symlin and Actigall and boy is it freckin

> expensive.  You are very lucky to get some samples.  Convincing a

> doctor on  all this would be monumental.

Agreed. But as you've now seen thanks to the recent posts, Actigall is cheap. According to the Doctor conducting the clinical trials on UDCA and cystic fibrosis, dosing for me should be 15mg per KG of my weight. That would be about 1200 mg a day for me, or four 300 mg tabs. That's 120 tabs a month. I bet my insurance/Medco will have a 90-day supply for less than $100 bucks and I'm hoping a single prescription will do it for me.

Also, if my doc had not given me the samples, I would not have hesitated to start on Actigall instead.

> Do you plan on staying on T3 indefinitely?

I don't plan on being on any medication at all six months from now. I'm only staying on the T3 now because it apparently plays very well with Symlin, and because it will protect me from one of Symlin's side effects: loss of appetite. I don't eat a lot of food as it is, and if I eat less the T3 will ensure that a 'starvation syndrome' doesn't rear its ugly head. I will probably have to reduce my dose though. My temps are now going from 98.6 to 98.7-9 -- so clearly lots more T3 is reaching my cells. Once Symlin begins to let leptin reach my brain again, my hypothalamus will signal my liver to make even more T3 -- so that means lowering my T3 dose. By the time I'm done with the Symlin and on to the Actigall (if needed), I should be off all T3.

Can't wait to start!

------------------------------------

[Guest guest]

I just reread some of your stuff.  I missed the range on the FT4.  What lab is that?  I have never seen that kind of range for FT4, never.I guess I'm a little confused about the Symlin and Actigall.  It seems like you don't have to do the Symlin first?  Is that what you're saying?  Could you go just to Actigall?  Yes, that stuff is reasonable.  Also, you're saying that a single prescription of either of these can " reset " your system?

Do you think this whole idea is something some doctors might get or is yours just exceptionally smart and accommodating?After all is said and done maybe you need to start your own yahoo group.Your exercise regime sounds fabulous.  Will have to look that one up.  Really, 15 minutes every 10 days.  Wow.

wrote:

> Very interesting stuff.  I have printed it and will reread it several times

> and will surely get tested.  Please please let us know how it goes.  If you

> could title it something that we would recognize easily that would be

> great.

Birdy, I will do that. I plan to start my first Symlin injection tomorrow.

> Why do you think you were able to tolerate so much T3 with

> such a low ferritin number.

That's a good question. I do have a few ideas, but no proof. First, I've been eating a very healthy diet for a long time. I get 75% of my calories from fat, particularly saturated fat (butter, cream, coconut oil, lard, etc). I eat very modest protein -- about 13% of my calories, or 50 or so grams of animal protein (I don't count the incomplete protein from veggies or fruit). That's only 7 or 8 ounces a day total from all animal sources including eggs, cream in coffee, etc. -- far less than most people eat. And I eat just enough carbs to stay out of ketosis, making sure that includes some glucose foods like potato and rice so that my body (especially my liver) doesn't need to undergo the stress of gluconeogenesis by making the glucose it needs for my brain at night from protein.

Second, I do the right kind of exercise to keep my cardiovascular system in tip-top shape. That is, I do NO 'cardio' steady state exercise at all (like walking, treadmill, etc) but instead do the Slow Burn weight lifting outlined in Body By Science. I work out a total of 15 minutes every ten day to two weeks, and I not only have biceps you can bounce a nickel off of, my lipids and C-Reactive Protein tests are so good the Framingham online calculator says my risk of heart attack in the next ten years is 1%.

Third, of the foods I eat, I make 90% of them myself. I eat very little processed food. I make my own LC yogurt, fermented mayo, cottage cheese, mascarpone, creme fraiche, butter, ice-cream, cheesecake, brownies, fudge, cookies, etc. etc. etc.

I don't believe diet alone can make us healthy if our metabolisms are compromised, but I do believe the right diet and exercise along with the right treatment can make a huge difference.

> why do you still have such a (relatively) high FT4 number when you're

> on T3 only.

Do I? My FT4 is 1.0 and the range starts at 1.4. If 1.0 is still high, what should it be???

> I looked up the prices for Symlin and Actigall and boy is it freckin

> expensive.  You are very lucky to get some samples.  Convincing a

> doctor on  all this would be monumental.

Agreed. But as you've now seen thanks to the recent posts, Actigall is cheap. According to the Doctor conducting the clinical trials on UDCA and cystic fibrosis, dosing for me should be 15mg per KG of my weight. That would be about 1200 mg a day for me, or four 300 mg tabs. That's 120 tabs a month. I bet my insurance/Medco will have a 90-day supply for less than $100 bucks and I'm hoping a single prescription will do it for me.

Also, if my doc had not given me the samples, I would not have hesitated to start on Actigall instead.

> Do you plan on staying on T3 indefinitely?

I don't plan on being on any medication at all six months from now. I'm only staying on the T3 now because it apparently plays very well with Symlin, and because it will protect me from one of Symlin's side effects: loss of appetite. I don't eat a lot of food as it is, and if I eat less the T3 will ensure that a 'starvation syndrome' doesn't rear its ugly head. I will probably have to reduce my dose though. My temps are now going from 98.6 to 98.7-9 -- so clearly lots more T3 is reaching my cells. Once Symlin begins to let leptin reach my brain again, my hypothalamus will signal my liver to make even more T3 -- so that means lowering my T3 dose. By the time I'm done with the Symlin and on to the Actigall (if needed), I should be off all T3.

Can't wait to start!

------------------------------------

[Guest guest]

birrdyy wrote:

> I missed the range on the FT4. What lab is that?

The Endo takes the blood at her office and sends it to Quest -- but often

different ones for different tests. My ranges never seem to be the same twice.

But still, FT4 of 1.0 is okay?

> I guess I'm a little confused about the Symlin and Actigall. It seems like

> you don't have to do the Symlin first? Is that what you're saying?

My best answer would be: I'm not sure but I believe based on my research that

it's true. After all, the researchers at Boston Hospital who conducted the tests

of 4-PBA and TUDCA on the mice did not use Symlin at all. And the TUDCA treated

mice lost 30% of their total bodyweight and fat in weeks, not months.

> Could you go just to Actigall?

I believe you could and if I had not been *given* the Symlin, would have done

just that. But since I do have the pens and won't see the Endo again till

February, I'm going to use it.

> Also, you're saying that a single prescription of either of these can " reset "

> your system?

I don't see why not. Let's look at the process itself. My adipose fat makes

leptin. The more fat, the more leptin. If my leptin *were* reaching my

hypothalamus (which would no doubt scream in horror if so!), it would

immediately single my liver to make more T3 to burn all the excess off. The body

has no vested interested in being fat. We've evolved to be lean and mean and run

down our food or run away from anything that wants to make us food. [it's why

Body By Science works, btw -- it develops exactly the powerful explosive muscle

that lets you escape that saber-tooth tiger eyeing you for a snack]

But my leptin isn't getting through. My hypothalamus believes I'm skinny. If I

were to take Actigall tomorrow in the proper dose -- it would either work to

accompany leptin up from my liver to my brain and have it fold properly to cross

the blood-brain barrier -- or it wouldn't work.

If it worked, and I see no reason as to why it would not, then my brain would

get the first real look at the state of my body (hence the scream) and

immediately send the signal to DUMP, DUMP, DUMP [FAT]. There's no need to 'build

up' to anything. The signal goes through, or it doesn't go through.

That said, the researcher said to take the Actigall slowly at first so as to not

get diarrhea, but that ramping up to full dose would only take a week or so.

After that it's full steam ahead. And sure, the weight would not leave my body

overnight, but I expect to lose a fair bit in the first month, and maybe a bit

more slowly each week after that. Remember, the body loves stasis above all, so

it tends to pause and reset after a large weight loss or gain before proceeding

again.

Once the leptin has broken through, and the weight/fat dump begins, I will in

fact produce less and less leptin. That too will slow the weight loss down. At

some point I will reach equilibrium, and my metabolism should work just fine

from that point on unless something in my life causes such major stress again (I

will need another hip surgery) that things get out of whack. But if that does

happen, I will know all the signs, and will take prompt action.

> Do you think this whole idea is something some doctors might get or is

> yours just exceptionally smart and accommodating?

She is one of the few doctors I know that actually has any intellectual

curiosity left. The rest are bought off by Big Pharma reps and utterly useless

IMHO. But I didn't find her by accident. I searched long and hard and talked to

lots of people and read reviews about her online.

For those who cannot do this, I would suggest creating a letter that lays out

your beliefs in the lipid system, eating low carb and high fat, and T3/RT3 and

Leptin Resistance. I would then send the letter to ten Endos in your area and

say that if they are of the same mind -- or willing at least to have an open

mind -- to have their receptionist call you for an appointment.

If they don't respond, you don't want them anyway -- and you can move on to the

next ten. Will only cost you paper and postage.

> After all is said and done maybe you need to start your own yahoo

> group.

Never say I don't take good advice. I just started one:

http://health.groups.yahoo.com/group/Leptin_Resistance

Please join! And by all means bring your great questions (about this and BBS

workouts) with you!

[Guest guest]

birrdyy wrote:

> I missed the range on the FT4. What lab is that?

The Endo takes the blood at her office and sends it to Quest -- but often

different ones for different tests. My ranges never seem to be the same twice.

But still, FT4 of 1.0 is okay?

> I guess I'm a little confused about the Symlin and Actigall. It seems like

> you don't have to do the Symlin first? Is that what you're saying?

My best answer would be: I'm not sure but I believe based on my research that

it's true. After all, the researchers at Boston Hospital who conducted the tests

of 4-PBA and TUDCA on the mice did not use Symlin at all. And the TUDCA treated

mice lost 30% of their total bodyweight and fat in weeks, not months.

> Could you go just to Actigall?

I believe you could and if I had not been *given* the Symlin, would have done

just that. But since I do have the pens and won't see the Endo again till

February, I'm going to use it.

> Also, you're saying that a single prescription of either of these can " reset "

> your system?

I don't see why not. Let's look at the process itself. My adipose fat makes

leptin. The more fat, the more leptin. If my leptin *were* reaching my

hypothalamus (which would no doubt scream in horror if so!), it would

immediately single my liver to make more T3 to burn all the excess off. The body

has no vested interested in being fat. We've evolved to be lean and mean and run

down our food or run away from anything that wants to make us food. [it's why

Body By Science works, btw -- it develops exactly the powerful explosive muscle

that lets you escape that saber-tooth tiger eyeing you for a snack]

But my leptin isn't getting through. My hypothalamus believes I'm skinny. If I

were to take Actigall tomorrow in the proper dose -- it would either work to

accompany leptin up from my liver to my brain and have it fold properly to cross

the blood-brain barrier -- or it wouldn't work.

If it worked, and I see no reason as to why it would not, then my brain would

get the first real look at the state of my body (hence the scream) and

immediately send the signal to DUMP, DUMP, DUMP [FAT]. There's no need to 'build

up' to anything. The signal goes through, or it doesn't go through.

That said, the researcher said to take the Actigall slowly at first so as to not

get diarrhea, but that ramping up to full dose would only take a week or so.

After that it's full steam ahead. And sure, the weight would not leave my body

overnight, but I expect to lose a fair bit in the first month, and maybe a bit

more slowly each week after that. Remember, the body loves stasis above all, so

it tends to pause and reset after a large weight loss or gain before proceeding

again.

Once the leptin has broken through, and the weight/fat dump begins, I will in

fact produce less and less leptin. That too will slow the weight loss down. At

some point I will reach equilibrium, and my metabolism should work just fine

from that point on unless something in my life causes such major stress again (I

will need another hip surgery) that things get out of whack. But if that does

happen, I will know all the signs, and will take prompt action.

> Do you think this whole idea is something some doctors might get or is

> yours just exceptionally smart and accommodating?

She is one of the few doctors I know that actually has any intellectual

curiosity left. The rest are bought off by Big Pharma reps and utterly useless

IMHO. But I didn't find her by accident. I searched long and hard and talked to

lots of people and read reviews about her online.

For those who cannot do this, I would suggest creating a letter that lays out

your beliefs in the lipid system, eating low carb and high fat, and T3/RT3 and

Leptin Resistance. I would then send the letter to ten Endos in your area and

say that if they are of the same mind -- or willing at least to have an open

mind -- to have their receptionist call you for an appointment.

If they don't respond, you don't want them anyway -- and you can move on to the

next ten. Will only cost you paper and postage.

> After all is said and done maybe you need to start your own yahoo

> group.

Never say I don't take good advice. I just started one:

http://health.groups.yahoo.com/group/Leptin_Resistance

Please join! And by all means bring your great questions (about this and BBS

workouts) with you!

[Guest guest]

this is very long...just skim it. its great info about lepitin.

Subject: Another Success Story - long but hopefully worth it.To: RT3_T3 Date: Saturday, January 2, 2010, 2:55 PM

I guess the old saying:"It's the exception that proves the rule" is right, and I'm the exception. ;-)When I told back in October that I intended to stay on Iodoral while doing my T3 therapy, she said she'd be very interested to know if it worked because she hasn't seen many people for whom that is true. Well, it worked, so she can now add me to the shortlist. I've continued to take a single 12.5 mg tab every morning. No HC or Isocort or Iron supplements either. Nothing but T3, and not all that much required for success. I never took over 75mcg and that was only for a few days. And my ferritin is only 47. Here are the stats from my latest labs:Began 's protocol on November 5, 2009 After ten days, reached 75mcg per day on November 15 -- became hyper, with 99+ temps and sweats, pulse in the 90's -- cycled down to zero in a week and then began again on November 23 using a modified

protocol. Modified in this case means I began with 6.25 mcg and added more T3 very slowly, as Val recommends, and also that unlike 's recommendation did not take compounded time-release T3 but Cynomel.BLOOD TEST on Dec 4th: TC and LDL dropped 100 points!Triglycerides dropped from 67 to 42HDL rose from 88 to 97A1c dropped a bit to 5.0APO B/APO a-1 = .56 -- HALF the *lowest* risk for CHD!FT3 = 404 (up from 291)RT3 = 10 (down from 25). Ratio = 40.4!!! (up from 11.64)T4 Total = 3.7 (4.5-12.5)FT4 = 1.0 (1.4-3.8)Sodium = 143 (128-145)Potassium = 4.9 (3.6-5.1)Ferritn = 47 (20-288)Iron = 67 (40-160)I reached a dose of 50mcg on 12/16. My temps reached 98.6 steady two days after that. By 12/25 my temps were 99.9 so I reduced my dose to 37.5 and have been there every since. My temps have been rock solid at 98.6 all day, every day for the last 3 weeks. No hypo symptoms at all, and

it's clear from my blood tests, lack of symptoms and high energy that my T3 is reaching my cells. I've lost 2 inches from my waist and abs in this time -- mostly due to the excess cholesterol dump I think, since it binds to fatty acids and is excreted.Even more importantly, I've been doing deep, deep medical research these last two months and believe I have found the cause of my RT3 problem to begin with: Leptin Resistance. My blood test for that revealed that I am severely leptin resistant even though I'm no longer insulin resistant to any degree! I've decided to write about it here in the hopes that it will ring some bells for other members and perhaps help them as well.Leptin is the King of all the hormones. It manages and gives orders to them all, including, tellingly, insulin -- yet it takes orders from no hormones. It reigns supreme. It is created from your adipose fat cells, so the more stored fat you have, the more leptin you

will produce. When you begin to eat, your leptin travels up through the bloodstream to the blood-brain barrier, where with the help of a protein gets folded into a three-dimensional shape that lets it slip through a precisely shaped keyhole to reach the hypothalamus. The leptin gives your brain a lot of information that will be used to determine how to *handle* your ingested energy: burn or store. And the brain has many tools at its disposal to make your metabolism do exactly what it wants, from making cells insulin resistant (thus storing more fat) to signaling T4 to stop converting into T3 and start converting to RT3. Or, to conversely, to have it make more T3 and 'turn up the heat' to burn more energy. YOU don't control this. Leptin and your brain does.But leptin does more. It signals the brain about how much energy *this* meal contains versus how much stored fat (the brain only sees 'energy' or 'not energy') you have. If the brain

thinks it has sufficient energy it raises another hormone to send the signal for you to stop eating. That's when you get that "Can't eat another bite" feeling and you put down the fork, no matter how delicious the food. Doggy bags were created to deal with this hormone. And how it works is important, because that signal makes glucagon (which controls insulin rise) decrease via a hormone called amylin.And leptin does still more. It acts like an A1c test for fat, telling the brain not only about the meal you're eating now, but about how much energy you've eaten over the last several days. [Which explains why we see weight gains on the scale not the day after a binge, but 72 hours later]. This is the crucial information, because the brain doesn't like to make sudden changes. It gathers the leptin info over the course of a few days and only then decides what hormones to use to either burn off excess energy or RETAIN energy by changing your

metabolism via your hormones and liver.Amazingly, leptin was only discovered in 1994! And it set off a true Gold Rush among Big Pharma because of how it was discovered: mice bred to be fat (no matter how little they ate) were discovered to have low levels of this hormone, yet when it was synthesized and injected into the mice, they overcame their fat genes and became skinny. Oh! Big Pharma thought -- the Holy Grail! We'll synthesize leptin, patent it, and have the Mother of all Blockbuster Drugs to sell, one that will reverse obesity with a single pill.They poured millions and millions into R & D, but when the first human trials were done, disaster loomed. Yes, the obese people injected with it did lose weight. For the first two weeks. Then they stopped losing, gained it all back, and put on a bit more for good measure. And this was true for all study subjects.Turns out, when they actually examined fat people, they had four to

five times MORE leptin than thin people. WTF???At this point, all R & D stopped, and some companies sold their leptin divisions. One company -- Amylin -- bought out the biggest, and more about them later.So, by 2000, what researchers knew is that obese people are not only often insulin resistant (which begins in the liver), and not only often thyroid resistant (which begins in the liver), but are almost all leptin resistant -- and in all three cases, the result is the same: the correct hormone is produced, but is blocked from reaching the cells, which in turn means that the correct signaling cannot get through. The actual process for this is that the leptin cannot be folded into the proper shape and thus cannot cross the blood-brain barrier. With little or no leptin reaching it, the brain believes the body is in danger of starvation regardless of actual calories consumed, and takes immediate steps to slow down the metabolism.

So you get fat, which creates more pooled leptin and you become ever more leptin resistant. It's a vicious circle because for hormones, the ability to reach the cells with the right signal is everything.This was why, for instance, my cholesterol kept rising until it was sky-high: T3 carries the signal the liver needs to know there is sufficient cholesterol in the blood, but RT3 lacks that signal. As soon as cytomel allowed T3 to once again reach my cells, the correct signal reached the liver, which immediately dumped excess cholesterol out of my body. When leptin doesn't reach the brain, it's much, much worse. What it means, in essence, is that while I see a still-overweight woman when *I* look in the mirror, what my *brain* sees is a very thin woman on the edge of starvation. And it will do everything in its considerable power to conserve as much ingested and stored energy as possible.What this usually means is:1: During

a meal, the leptin that normally would go to the brain saying 'lots of energy here, boss' doesn't get through. So the brain never sends the hormonal system of 'you're full you idiot, so stop eating!' Thus, leptin resistant people are usually always hungry and always eating.2: In order to conserve as much energy as possible in the easiest to store form (fat), the brain sends out a specific hormone that not only tells us to eat, but to eat lots and lots of carbs, particularly sweets. That's because the brain knows this will ultimately create insulin resistance, which means more triglycerides made in the liver, which means more stored fat. This is why most leptin resistant people say they 'crave' sweets. They do, but only because they are being ordered by the brain to crave them.But what happens when the brain is stored in a body that eats high fat, low carb, and is thus not only satisfied with less food, but with almost no sweets? I'll

tell you what happens: the thwarted brain simply pulls another tool from the box for conserving energy: the thyroid hormones. By creating a RT3 imbalance, energy and fat are stored not burned, and the metabolism is slowed to such a state that no amount of exercise, no eating this or not eating that, no calorie reduction will overcome it. In fact, the more you do to lose weight, the more the leptin-deprived brain conserves energy. This finally explains the mystery of how morbidly obese patients can be locked into a hospital metabolic ward, fed 500 calories a day -- and gain weight. Mysterious no more.But what to do about it, that's the question. And for that, someone needed to show exactly how people become leptin resistant (and diabetic, too!). And finally, someone has. In a major study done at Boston Children's Hospital Research Center in 2008 and published in the January 2009 issue of "Cell Metabolism" as: "Endoplasmic Reticulum Stress Plays a

Central Role in Development of Leptin Resistance" this mechanism was revealed. From the article:"The endoplasmic reticulum (ER) is a sophisticated luminal network in which protein synthesis, maturation, folding, and transport take place. Perturbation of these processes in several different pathological states creates a condition defined as ER stress and leads to activation of a complex signaling network termed the unfolded protein response(UPR). Previous studies have demonstrated that ER stress and activation of UPR signaling pathways play a dominant role in the development ofobesity-induced insulin resistance and type 2 diabetes. Furthermore, reversal of ER stress with chemical chaperones—agents that have the ability to increase ER folding machinery—increases insulin sensitivity and reverses type 2 diabetes in obese mice.SUMMARYLeptin has not evolved as a therapeutic modality for the treatment of obesity due to the

prevalence of leptin resistance in a majority of the obese population. Nevertheless, the molecular mechanisms of leptin resistance remain poorly understood. Here, we show that increased endoplasmic reticulum (ER) stress and activation of the unfolded protein response (UPR) in the hypothalamus of obese mice inhibits leptin receptor signaling. The genetic imposition of reduced ER capacity in mice results in severe leptin resistance and leads to a significant augmentation of obesity. Moreover, we show that chemical chaperones, 4-phenyl butyric acid (PBA), and tauroursodeoxycholic acid (TUDCA), which have the ability to decrease ER stress, act as leptin-sensitizing agents. Taken together, our results may provide the basis for a novel treatment of obesity."To summarize the summary: the study proved that when something/s (still unknown but I believe was right about outside stress, like major surgery in my case, which is when my weight loss

stopped after losing 65 pounds but 20 pounds from goal) stresses the ER in the brain, leptin resistance begins. The ER then activates the UPR (unfolded protein response), which means the leptin can no longer get through. And then all metabolic hell ensues. What is stunning about the study though, is that the researchers went further. Once they'd proved the faulty mechanism, they decided to test whether or not sending along a 'chaperone molecule' with the leptin would undo the UPR and let the leptin through. And they not only did it, they did it with two non-toxic drugs already approved by the FDA for treating other diseases!When they gave obese mice a ten-day 'pre-treatment' of 4-PBA the mice didn't lose weight or fat, but once leptin was added to the injections, those mice grew thin and *lean* with lots of lost body fat. And the mice stayed lean. When their hypothalamus' were harvested, it showed that indeed leptin signaling (leptin

sensitivity) had been restored.The real eye-opener was with TUDCA though. Just treatment with it alone caused major weight and fat loss. And when leptin was added, just a fraction of the amount used with the 4-PBA was needed for even more drastic weight loss. Which was also stable. TUDCA is biologically identical to UDCA (sold as Actigall in this country), which is used to treat liver diseases. TUDCA was used by the researchers because it's an inject-able liquid, whereas the UDCA is taken orally. Isn't it amazing how everything metabolic somehow leads back to the brain's connection with the liver? And the 'U' in UDCA stands for 'urso' -- Bear in Latin -- because it comes from bear bile. The liver. And it's been used by Native Americans for centuries to treat illness. It is such an incredible substance that there are now clinical trials all over the world using TUDCA to treat Huntington's Disease, Cystic Fibrosis, and Altzheimer's.

Researchers believe they are on the verge of major breakthrough's for all three, thanks to this simple substance.So, armed with this knowledge (and the fact that I had diagnosed my own RT3 and Cholesterol problem, and treated them both of them myself successfully), I met with my Endo. I was there for two hours. She did most of the question-asking, and I provided most of the answers. When we were done, she agreed that it was indeed likely that my RT3 problem was originally caused by my leptin resistance, and also with my hypothesis that if I did not treat and cure the original problem (LP), my brain would continue to be leptin-deprived, continue to think I'm skinny, and would only pull another metabolic trick out of its hat to retain my weight and fat. I believe this alone can explain why some people on T3 can lower RT3 and get T3 back into the cells but not lose weight. And why for many, RT3 and/or hypo symptoms return when they return

to dessicated thyroid. She agreed to support my being an experiment of one, with help from the Doctor who is leading the UDCA Cystic Fibrosis study at the University of Michigan, whom I contacted and spoke to at length. Starting this week I will begin a 'pre-treatment' of Symlin (pramlintide acetate) injections with the two sample 'pens' my Endo gave me. Symlin is a synthetic form of Amylin, a sister hormone of leptin that plays a huge role in proper insulin use in the body as mentioned above, by signaling the liver to decrease production of glucagon. Type 1 Diabetics no longer make Amylin, and it is either low or missing or not working properly in Type 2's -- which is not surprising given that I believe this is their form of leptin resistance. How it works:"Symlin, by acting as an amylinomimetic agent, has the following effects: 1) modulation of gastric emptying; 2) prevention of the postprandial rise in plasma glucagon;

and 3) satiety leading to decreased caloric intake and potential weight loss."For me, the most important point is reduction of glucagon, which does not work properly in leptin resistant people.Symlin is made by the company Amylin, which was the company I mentioned earlier, that purchased the R & D and rights to patent leptin back in 2000. In fact, Symlin has been shown to cause rapid weight and fat loss in type 1 and type 2 diabetics who take it with their insulin (because I believe based on my research that it too restores leptin signaling; see the Holtof site for more info) -- and the company is currently in trials to convince the FDA to let them market it for weight loss. Followed, no doubt in my mind, by a form of leptin they are working to produce. If my hypothesis is correct, in two months Symlin will fully restore my amylin/leptin connection, after which I will begin supplementing with UDCA/Actigall. I fully expect to

have my letpin resistance restored, my T3 problem permanently fixed, and my metabolism completely healed. I also expect to lose the 20 pounds I couldn't before, as well as the 10 I added back when my RT3 began to rise. And I fully expect my insulin sensitivity to grow even better, and my A1c to continue to fall. Knowing now what I know about the brilliance of our intricate hormonal and metabolic systems, and the ability of our brain to rule them *absolutely* despite any of our intentions or actions, I find the advice "To lose weight simply eat less and exercise more" akin to saying "To lose weight bury a chicken bone in the backyard at the full moon and say the following incantation." Both will be equal in their efficacy. Same thing for "cut out dairy, don't eat grains, count calories, don't count them, eat this, don't eat that," etc. etc. etc. A person with a perfectly healthy and functioning metabolism will not store excess energy

(fat) in the first place. If they feast a day or so they might gain a pound or two, but a week of eating as usual will see that gone without them having to do anything, or eat anything, or not eat anything special. That's how we evolved, and that's how we're still built. Our ancestors never had to 'diet' and neither should we.Abuse or stress my make that metabolism non-functioning, but to cure it requires science, not anecdote or one food over another. My heart aches as I read the same posts over and over on all the various forums dealing with obesity, from calorie-counting forums to low-carb forums. Everywhere is anecdote and useless advice, and science nowhere to be found. I've written this very long post hoping that here at least, with Val and Nick, science will have a place and that their readers will now have a test -- leptin serum level -- to begin, and some solutions to follow. To a Happy and Healthy New Year for us

all...------------------------------------

[Guest guest]

this is very long...just skim it. its great info about lepitin.

Subject: Another Success Story - long but hopefully worth it.To: RT3_T3 Date: Saturday, January 2, 2010, 2:55 PM

I guess the old saying:"It's the exception that proves the rule" is right, and I'm the exception. ;-)When I told back in October that I intended to stay on Iodoral while doing my T3 therapy, she said she'd be very interested to know if it worked because she hasn't seen many people for whom that is true. Well, it worked, so she can now add me to the shortlist. I've continued to take a single 12.5 mg tab every morning. No HC or Isocort or Iron supplements either. Nothing but T3, and not all that much required for success. I never took over 75mcg and that was only for a few days. And my ferritin is only 47. Here are the stats from my latest labs:Began 's protocol on November 5, 2009 After ten days, reached 75mcg per day on November 15 -- became hyper, with 99+ temps and sweats, pulse in the 90's -- cycled down to zero in a week and then began again on November 23 using a modified

protocol. Modified in this case means I began with 6.25 mcg and added more T3 very slowly, as Val recommends, and also that unlike 's recommendation did not take compounded time-release T3 but Cynomel.BLOOD TEST on Dec 4th: TC and LDL dropped 100 points!Triglycerides dropped from 67 to 42HDL rose from 88 to 97A1c dropped a bit to 5.0APO B/APO a-1 = .56 -- HALF the *lowest* risk for CHD!FT3 = 404 (up from 291)RT3 = 10 (down from 25). Ratio = 40.4!!! (up from 11.64)T4 Total = 3.7 (4.5-12.5)FT4 = 1.0 (1.4-3.8)Sodium = 143 (128-145)Potassium = 4.9 (3.6-5.1)Ferritn = 47 (20-288)Iron = 67 (40-160)I reached a dose of 50mcg on 12/16. My temps reached 98.6 steady two days after that. By 12/25 my temps were 99.9 so I reduced my dose to 37.5 and have been there every since. My temps have been rock solid at 98.6 all day, every day for the last 3 weeks. No hypo symptoms at all, and

it's clear from my blood tests, lack of symptoms and high energy that my T3 is reaching my cells. I've lost 2 inches from my waist and abs in this time -- mostly due to the excess cholesterol dump I think, since it binds to fatty acids and is excreted.Even more importantly, I've been doing deep, deep medical research these last two months and believe I have found the cause of my RT3 problem to begin with: Leptin Resistance. My blood test for that revealed that I am severely leptin resistant even though I'm no longer insulin resistant to any degree! I've decided to write about it here in the hopes that it will ring some bells for other members and perhaps help them as well.Leptin is the King of all the hormones. It manages and gives orders to them all, including, tellingly, insulin -- yet it takes orders from no hormones. It reigns supreme. It is created from your adipose fat cells, so the more stored fat you have, the more leptin you

will produce. When you begin to eat, your leptin travels up through the bloodstream to the blood-brain barrier, where with the help of a protein gets folded into a three-dimensional shape that lets it slip through a precisely shaped keyhole to reach the hypothalamus. The leptin gives your brain a lot of information that will be used to determine how to *handle* your ingested energy: burn or store. And the brain has many tools at its disposal to make your metabolism do exactly what it wants, from making cells insulin resistant (thus storing more fat) to signaling T4 to stop converting into T3 and start converting to RT3. Or, to conversely, to have it make more T3 and 'turn up the heat' to burn more energy. YOU don't control this. Leptin and your brain does.But leptin does more. It signals the brain about how much energy *this* meal contains versus how much stored fat (the brain only sees 'energy' or 'not energy') you have. If the brain

thinks it has sufficient energy it raises another hormone to send the signal for you to stop eating. That's when you get that "Can't eat another bite" feeling and you put down the fork, no matter how delicious the food. Doggy bags were created to deal with this hormone. And how it works is important, because that signal makes glucagon (which controls insulin rise) decrease via a hormone called amylin.And leptin does still more. It acts like an A1c test for fat, telling the brain not only about the meal you're eating now, but about how much energy you've eaten over the last several days. [Which explains why we see weight gains on the scale not the day after a binge, but 72 hours later]. This is the crucial information, because the brain doesn't like to make sudden changes. It gathers the leptin info over the course of a few days and only then decides what hormones to use to either burn off excess energy or RETAIN energy by changing your

metabolism via your hormones and liver.Amazingly, leptin was only discovered in 1994! And it set off a true Gold Rush among Big Pharma because of how it was discovered: mice bred to be fat (no matter how little they ate) were discovered to have low levels of this hormone, yet when it was synthesized and injected into the mice, they overcame their fat genes and became skinny. Oh! Big Pharma thought -- the Holy Grail! We'll synthesize leptin, patent it, and have the Mother of all Blockbuster Drugs to sell, one that will reverse obesity with a single pill.They poured millions and millions into R & D, but when the first human trials were done, disaster loomed. Yes, the obese people injected with it did lose weight. For the first two weeks. Then they stopped losing, gained it all back, and put on a bit more for good measure. And this was true for all study subjects.Turns out, when they actually examined fat people, they had four to

five times MORE leptin than thin people. WTF???At this point, all R & D stopped, and some companies sold their leptin divisions. One company -- Amylin -- bought out the biggest, and more about them later.So, by 2000, what researchers knew is that obese people are not only often insulin resistant (which begins in the liver), and not only often thyroid resistant (which begins in the liver), but are almost all leptin resistant -- and in all three cases, the result is the same: the correct hormone is produced, but is blocked from reaching the cells, which in turn means that the correct signaling cannot get through. The actual process for this is that the leptin cannot be folded into the proper shape and thus cannot cross the blood-brain barrier. With little or no leptin reaching it, the brain believes the body is in danger of starvation regardless of actual calories consumed, and takes immediate steps to slow down the metabolism.

So you get fat, which creates more pooled leptin and you become ever more leptin resistant. It's a vicious circle because for hormones, the ability to reach the cells with the right signal is everything.This was why, for instance, my cholesterol kept rising until it was sky-high: T3 carries the signal the liver needs to know there is sufficient cholesterol in the blood, but RT3 lacks that signal. As soon as cytomel allowed T3 to once again reach my cells, the correct signal reached the liver, which immediately dumped excess cholesterol out of my body. When leptin doesn't reach the brain, it's much, much worse. What it means, in essence, is that while I see a still-overweight woman when *I* look in the mirror, what my *brain* sees is a very thin woman on the edge of starvation. And it will do everything in its considerable power to conserve as much ingested and stored energy as possible.What this usually means is:1: During

a meal, the leptin that normally would go to the brain saying 'lots of energy here, boss' doesn't get through. So the brain never sends the hormonal system of 'you're full you idiot, so stop eating!' Thus, leptin resistant people are usually always hungry and always eating.2: In order to conserve as much energy as possible in the easiest to store form (fat), the brain sends out a specific hormone that not only tells us to eat, but to eat lots and lots of carbs, particularly sweets. That's because the brain knows this will ultimately create insulin resistance, which means more triglycerides made in the liver, which means more stored fat. This is why most leptin resistant people say they 'crave' sweets. They do, but only because they are being ordered by the brain to crave them.But what happens when the brain is stored in a body that eats high fat, low carb, and is thus not only satisfied with less food, but with almost no sweets? I'll

tell you what happens: the thwarted brain simply pulls another tool from the box for conserving energy: the thyroid hormones. By creating a RT3 imbalance, energy and fat are stored not burned, and the metabolism is slowed to such a state that no amount of exercise, no eating this or not eating that, no calorie reduction will overcome it. In fact, the more you do to lose weight, the more the leptin-deprived brain conserves energy. This finally explains the mystery of how morbidly obese patients can be locked into a hospital metabolic ward, fed 500 calories a day -- and gain weight. Mysterious no more.But what to do about it, that's the question. And for that, someone needed to show exactly how people become leptin resistant (and diabetic, too!). And finally, someone has. In a major study done at Boston Children's Hospital Research Center in 2008 and published in the January 2009 issue of "Cell Metabolism" as: "Endoplasmic Reticulum Stress Plays a

Central Role in Development of Leptin Resistance" this mechanism was revealed. From the article:"The endoplasmic reticulum (ER) is a sophisticated luminal network in which protein synthesis, maturation, folding, and transport take place. Perturbation of these processes in several different pathological states creates a condition defined as ER stress and leads to activation of a complex signaling network termed the unfolded protein response(UPR). Previous studies have demonstrated that ER stress and activation of UPR signaling pathways play a dominant role in the development ofobesity-induced insulin resistance and type 2 diabetes. Furthermore, reversal of ER stress with chemical chaperones—agents that have the ability to increase ER folding machinery—increases insulin sensitivity and reverses type 2 diabetes in obese mice.SUMMARYLeptin has not evolved as a therapeutic modality for the treatment of obesity due to the

prevalence of leptin resistance in a majority of the obese population. Nevertheless, the molecular mechanisms of leptin resistance remain poorly understood. Here, we show that increased endoplasmic reticulum (ER) stress and activation of the unfolded protein response (UPR) in the hypothalamus of obese mice inhibits leptin receptor signaling. The genetic imposition of reduced ER capacity in mice results in severe leptin resistance and leads to a significant augmentation of obesity. Moreover, we show that chemical chaperones, 4-phenyl butyric acid (PBA), and tauroursodeoxycholic acid (TUDCA), which have the ability to decrease ER stress, act as leptin-sensitizing agents. Taken together, our results may provide the basis for a novel treatment of obesity."To summarize the summary: the study proved that when something/s (still unknown but I believe was right about outside stress, like major surgery in my case, which is when my weight loss

stopped after losing 65 pounds but 20 pounds from goal) stresses the ER in the brain, leptin resistance begins. The ER then activates the UPR (unfolded protein response), which means the leptin can no longer get through. And then all metabolic hell ensues. What is stunning about the study though, is that the researchers went further. Once they'd proved the faulty mechanism, they decided to test whether or not sending along a 'chaperone molecule' with the leptin would undo the UPR and let the leptin through. And they not only did it, they did it with two non-toxic drugs already approved by the FDA for treating other diseases!When they gave obese mice a ten-day 'pre-treatment' of 4-PBA the mice didn't lose weight or fat, but once leptin was added to the injections, those mice grew thin and *lean* with lots of lost body fat. And the mice stayed lean. When their hypothalamus' were harvested, it showed that indeed leptin signaling (leptin

sensitivity) had been restored.The real eye-opener was with TUDCA though. Just treatment with it alone caused major weight and fat loss. And when leptin was added, just a fraction of the amount used with the 4-PBA was needed for even more drastic weight loss. Which was also stable. TUDCA is biologically identical to UDCA (sold as Actigall in this country), which is used to treat liver diseases. TUDCA was used by the researchers because it's an inject-able liquid, whereas the UDCA is taken orally. Isn't it amazing how everything metabolic somehow leads back to the brain's connection with the liver? And the 'U' in UDCA stands for 'urso' -- Bear in Latin -- because it comes from bear bile. The liver. And it's been used by Native Americans for centuries to treat illness. It is such an incredible substance that there are now clinical trials all over the world using TUDCA to treat Huntington's Disease, Cystic Fibrosis, and Altzheimer's.

Researchers believe they are on the verge of major breakthrough's for all three, thanks to this simple substance.So, armed with this knowledge (and the fact that I had diagnosed my own RT3 and Cholesterol problem, and treated them both of them myself successfully), I met with my Endo. I was there for two hours. She did most of the question-asking, and I provided most of the answers. When we were done, she agreed that it was indeed likely that my RT3 problem was originally caused by my leptin resistance, and also with my hypothesis that if I did not treat and cure the original problem (LP), my brain would continue to be leptin-deprived, continue to think I'm skinny, and would only pull another metabolic trick out of its hat to retain my weight and fat. I believe this alone can explain why some people on T3 can lower RT3 and get T3 back into the cells but not lose weight. And why for many, RT3 and/or hypo symptoms return when they return

to dessicated thyroid. She agreed to support my being an experiment of one, with help from the Doctor who is leading the UDCA Cystic Fibrosis study at the University of Michigan, whom I contacted and spoke to at length. Starting this week I will begin a 'pre-treatment' of Symlin (pramlintide acetate) injections with the two sample 'pens' my Endo gave me. Symlin is a synthetic form of Amylin, a sister hormone of leptin that plays a huge role in proper insulin use in the body as mentioned above, by signaling the liver to decrease production of glucagon. Type 1 Diabetics no longer make Amylin, and it is either low or missing or not working properly in Type 2's -- which is not surprising given that I believe this is their form of leptin resistance. How it works:"Symlin, by acting as an amylinomimetic agent, has the following effects: 1) modulation of gastric emptying; 2) prevention of the postprandial rise in plasma glucagon;

and 3) satiety leading to decreased caloric intake and potential weight loss."For me, the most important point is reduction of glucagon, which does not work properly in leptin resistant people.Symlin is made by the company Amylin, which was the company I mentioned earlier, that purchased the R & D and rights to patent leptin back in 2000. In fact, Symlin has been shown to cause rapid weight and fat loss in type 1 and type 2 diabetics who take it with their insulin (because I believe based on my research that it too restores leptin signaling; see the Holtof site for more info) -- and the company is currently in trials to convince the FDA to let them market it for weight loss. Followed, no doubt in my mind, by a form of leptin they are working to produce. If my hypothesis is correct, in two months Symlin will fully restore my amylin/leptin connection, after which I will begin supplementing with UDCA/Actigall. I fully expect to

have my letpin resistance restored, my T3 problem permanently fixed, and my metabolism completely healed. I also expect to lose the 20 pounds I couldn't before, as well as the 10 I added back when my RT3 began to rise. And I fully expect my insulin sensitivity to grow even better, and my A1c to continue to fall. Knowing now what I know about the brilliance of our intricate hormonal and metabolic systems, and the ability of our brain to rule them *absolutely* despite any of our intentions or actions, I find the advice "To lose weight simply eat less and exercise more" akin to saying "To lose weight bury a chicken bone in the backyard at the full moon and say the following incantation." Both will be equal in their efficacy. Same thing for "cut out dairy, don't eat grains, count calories, don't count them, eat this, don't eat that," etc. etc. etc. A person with a perfectly healthy and functioning metabolism will not store excess energy

(fat) in the first place. If they feast a day or so they might gain a pound or two, but a week of eating as usual will see that gone without them having to do anything, or eat anything, or not eat anything special. That's how we evolved, and that's how we're still built. Our ancestors never had to 'diet' and neither should we.Abuse or stress my make that metabolism non-functioning, but to cure it requires science, not anecdote or one food over another. My heart aches as I read the same posts over and over on all the various forums dealing with obesity, from calorie-counting forums to low-carb forums. Everywhere is anecdote and useless advice, and science nowhere to be found. I've written this very long post hoping that here at least, with Val and Nick, science will have a place and that their readers will now have a test -- leptin serum level -- to begin, and some solutions to follow. To a Happy and Healthy New Year for us

all...------------------------------------

[Guest guest]

Fabulous.  I am joining your group and I'm dying to get testing done.  I hope you don't mind helping interrupt those test for us?  I can't believe how well versed you are on this topic.  Yes, indeed you have done some heavy research.

As for the FT4.  I am no even more confused because quest never had such a range.  My sister just last week went to quest and the .8-1.4 is what she got.  I think you can even go online to see what their ranges are.  I would seriously give the lab a call to clarify.  If it's correct then I believe that's okay.  If the range is not correct then I don't know what to say.  That would be very strange to have such a high (if the range was indeed .8 and up) result with on T3 only.  Val always says she like T4 at 1.4 when on NDT so you see you're not far from that and yet not on NDT.  Do you have an actual copy of the results or did they read them to you?

birrdyy wrote:

> I missed the range on the FT4.  What lab is that?

The Endo takes the blood at her office and sends it to Quest -- but often different ones for different tests. My ranges never seem to be the same twice. But still, FT4 of 1.0 is okay?

> I guess I'm a little confused about the Symlin and Actigall.  It seems like

> you don't have to do the Symlin first? Is that what you're saying?

My best answer would be: I'm not sure but I believe based on my research that it's true. After all, the researchers at Boston Hospital who conducted the tests of 4-PBA and TUDCA on the mice did not use Symlin at all. And the TUDCA treated mice lost 30% of their total bodyweight and fat in weeks, not months.

> Could you go just to Actigall?

I believe you could and if I had not been *given* the Symlin, would have done just that. But since I do have the pens and won't see the Endo again till February, I'm going to use it.

> Also, you're saying that a single prescription of either of these can " reset "

> your system?

I don't see why not. Let's look at the process itself. My adipose fat makes leptin. The more fat, the more leptin. If my leptin *were* reaching my hypothalamus (which would no doubt scream in horror if so!), it would immediately single my liver to make more T3 to burn all the excess off. The body has no vested interested in being fat. We've evolved to be lean and mean and run down our food or run away from anything that wants to make us food. [it's why Body By Science works, btw -- it develops exactly the powerful explosive muscle that lets you escape that saber-tooth tiger eyeing you for a snack]

But my leptin isn't getting through. My hypothalamus believes I'm skinny. If I were to take Actigall tomorrow in the proper dose -- it would either work to accompany leptin up from my liver to my brain and have it fold properly to cross the blood-brain barrier -- or it wouldn't work.

If it worked, and I see no reason as to why it would not, then my brain would get the first real look at the state of my body (hence the scream) and immediately send the signal to DUMP, DUMP, DUMP [FAT]. There's no need to 'build up' to anything. The signal goes through, or it doesn't go through.

That said, the researcher said to take the Actigall slowly at first so as to not get diarrhea, but that ramping up to full dose would only take a week or so. After that it's full steam ahead. And sure, the weight would not leave my body overnight, but I expect to lose a fair bit in the first month, and maybe a bit more slowly each week after that. Remember, the body loves stasis above all, so it tends to pause and reset after a large weight loss or gain before proceeding again.

Once the leptin has broken through, and the weight/fat dump begins, I will in fact produce less and less leptin. That too will slow the weight loss down. At some point I will reach equilibrium, and my metabolism should work just fine from that point on unless something in my life causes such major stress again (I will need another hip surgery) that things get out of whack. But if that does happen, I will know all the signs, and will take prompt action.

> Do you think this whole idea is something some doctors might get or is

> yours just exceptionally smart and accommodating?

She is one of the few doctors I know that actually has any intellectual curiosity left. The rest are bought off by Big Pharma reps and utterly useless IMHO. But I didn't find her by accident. I searched long and hard and talked to lots of people and read reviews about her online.

For those who cannot do this, I would suggest creating a letter that lays out your beliefs in the lipid system, eating low carb and high fat, and T3/RT3 and Leptin Resistance. I would then send the letter to ten Endos in your area and say that if they are of the same mind -- or willing at least to have an open mind -- to have their receptionist call you for an appointment.

If they don't respond, you don't want them anyway -- and you can move on to the next ten. Will only cost you paper and postage.

> After all is said and done maybe you need to start your own yahoo

> group.

Never say I don't take good advice. I just started one:

http://health.groups.yahoo.com/group/Leptin_Resistance

Please join! And by all means bring your great questions (about this and BBS workouts) with you!

------------------------------------

[Guest guest]

birrdyy wrote:

> I am joining your group and I'm dying to get testing done.

Birrdyy, you're now a member!

> I hope you don't mind helping interrupt those test for us?

I will happily do so on the new group. I don't think it would be fair to hijack

this one, and certainly have no intention to do so. And of course, everyone here

is welcome there as well. All I ask is that when you apply for membership you

say you're from this group -- and give your name! I hate it when folks apply to

join a moderated group and don't say who they are. It means you have to say

" Dear ??? " ))

> I can't believe how well versed you are on this topic. Yes, indeed you

> have done some heavy research.

I believe I have perfected the art of tracking down articles in medical journals

I can't afford, and flattering them enough to have them send me the articles for

free. LOL

> As for the FT4. I am no even more confused because quest never had

> such a range. My sister just last week went to quest and the .8-1.4 is

> what she got.

Hmm. Wonder if I wrote the range down wrong. There were a LOT of numbers. I'll

go look later. I never allow anyone to 'tell me' my results. I insist on a full

copy and keep them all. I can trace every test back five years, so I can

compare.

In any event, 1.0 isn't that far off from .8 -- and it is lower than the 1.4 I

had at my former blood test in June. It's lower, and that's good. Also, remember

I'd only been on T3 for a month before the test. It's clear from everything else

though that T3 IS getting into my cells nicely now -- and my RT3 falling my more

than half while my FT3 rose beautifully is proof as well.

Looking forward to 'meeting' you on Leptin Resistance!

[Guest guest]

birrdyy wrote:

> I am joining your group and I'm dying to get testing done.

Birrdyy, you're now a member!

> I hope you don't mind helping interrupt those test for us?

I will happily do so on the new group. I don't think it would be fair to hijack

this one, and certainly have no intention to do so. And of course, everyone here

is welcome there as well. All I ask is that when you apply for membership you

say you're from this group -- and give your name! I hate it when folks apply to

join a moderated group and don't say who they are. It means you have to say

" Dear ??? " ))

> I can't believe how well versed you are on this topic. Yes, indeed you

> have done some heavy research.

I believe I have perfected the art of tracking down articles in medical journals

I can't afford, and flattering them enough to have them send me the articles for

free. LOL

> As for the FT4. I am no even more confused because quest never had

> such a range. My sister just last week went to quest and the .8-1.4 is

> what she got.

Hmm. Wonder if I wrote the range down wrong. There were a LOT of numbers. I'll

go look later. I never allow anyone to 'tell me' my results. I insist on a full

copy and keep them all. I can trace every test back five years, so I can

compare.

In any event, 1.0 isn't that far off from .8 -- and it is lower than the 1.4 I

had at my former blood test in June. It's lower, and that's good. Also, remember

I'd only been on T3 for a month before the test. It's clear from everything else

though that T3 IS getting into my cells nicely now -- and my RT3 falling my more

than half while my FT3 rose beautifully is proof as well.

Looking forward to 'meeting' you on Leptin Resistance!

[Guest guest]

birrdyy wrote:

> I am joining your group and I'm dying to get testing done.

Birrdyy, you're now a member!

> I hope you don't mind helping interrupt those test for us?

I will happily do so on the new group. I don't think it would be fair to hijack

this one, and certainly have no intention to do so. And of course, everyone here

is welcome there as well. All I ask is that when you apply for membership you

say you're from this group -- and give your name! I hate it when folks apply to

join a moderated group and don't say who they are. It means you have to say

" Dear ??? " ))

> I can't believe how well versed you are on this topic. Yes, indeed you

> have done some heavy research.

I believe I have perfected the art of tracking down articles in medical journals

I can't afford, and flattering them enough to have them send me the articles for

free. LOL

> As for the FT4. I am no even more confused because quest never had

> such a range. My sister just last week went to quest and the .8-1.4 is

> what she got.

Hmm. Wonder if I wrote the range down wrong. There were a LOT of numbers. I'll

go look later. I never allow anyone to 'tell me' my results. I insist on a full

copy and keep them all. I can trace every test back five years, so I can

compare.

In any event, 1.0 isn't that far off from .8 -- and it is lower than the 1.4 I

had at my former blood test in June. It's lower, and that's good. Also, remember

I'd only been on T3 for a month before the test. It's clear from everything else

though that T3 IS getting into my cells nicely now -- and my RT3 falling my more

than half while my FT3 rose beautifully is proof as well.

Looking forward to 'meeting' you on Leptin Resistance!

[Guest guest]

Wow - I am so interested in this.

I was diagnosed as hypo when I was a kid & have spent a lifetime dealing with

weight issues. I currently am at an alarming weight & its frustrating to no

end. One day I gained 8lbs (in a single day!) & I didn't eat more than 1600

calls that day.

Could you give me an idea of a typical day's menu of your diet?

And some links to any info that I can research - to follow in your footsteps.

If you do start a Yahoo group, I want to join too.

Thanks,

C

>

> > Very interesting stuff. I have printed it and will reread it several times

> > and will surely get tested. Please please let us know how it goes. If you

> > could title it something that we would recognize easily that would be

> > great.

>

> Birdy, I will do that. I plan to start my first Symlin injection tomorrow.

>

> > Why do you think you were able to tolerate so much T3 with

> > such a low ferritin number.

>

> That's a good question. I do have a few ideas, but no proof. First, I've been

eating a very healthy diet for a long time. I get 75% of my calories from fat,

particularly saturated fat (butter, cream, coconut oil, lard, etc). I eat very

modest protein -- about 13% of my calories, or 50 or so grams of animal protein

(I don't count the incomplete protein from veggies or fruit). That's only 7 or 8

ounces a day total from all animal sources including eggs, cream in coffee, etc.

-- far less than most people eat. And I eat just enough carbs to stay out of

ketosis, making sure that includes some glucose foods like potato and rice so

that my body (especially my liver) doesn't need to undergo the stress of

gluconeogenesis by making the glucose it needs for my brain at night from

protein.

>

> Second, I do the right kind of exercise to keep my cardiovascular system in

tip-top shape. That is, I do NO 'cardio' steady state exercise at all (like

walking, treadmill, etc) but instead do the Slow Burn weight lifting outlined in

Body By Science. I work out a total of 15 minutes every ten day to two weeks,

and I not only have biceps you can bounce a nickel off of, my lipids and

C-Reactive Protein tests are so good the Framingham online calculator says my

risk of heart attack in the next ten years is 1%.

>

> Third, of the foods I eat, I make 90% of them myself. I eat very little

processed food. I make my own LC yogurt, fermented mayo, cottage cheese,

mascarpone, creme fraiche, butter, ice-cream, cheesecake, brownies, fudge,

cookies, etc. etc. etc.

>

> I don't believe diet alone can make us healthy if our metabolisms are

compromised, but I do believe the right diet and exercise along with the right

treatment can make a huge difference.

>

> > why do you still have such a (relatively) high FT4 number when you're

> > on T3 only.

>

> Do I? My FT4 is 1.0 and the range starts at 1.4. If 1.0 is still high, what

should it be???

>

> > I looked up the prices for Symlin and Actigall and boy is it freckin

> > expensive. You are very lucky to get some samples. Convincing a

> > doctor on all this would be monumental.

>

> Agreed. But as you've now seen thanks to the recent posts, Actigall is cheap.

According to the Doctor conducting the clinical trials on UDCA and cystic

fibrosis, dosing for me should be 15mg per KG of my weight. That would be about

1200 mg a day for me, or four 300 mg tabs. That's 120 tabs a month. I bet my

insurance/Medco will have a 90-day supply for less than $100 bucks and I'm

hoping a single prescription will do it for me.

>

> Also, if my doc had not given me the samples, I would not have hesitated to

start on Actigall instead.

>

> > Do you plan on staying on T3 indefinitely?

>

> I don't plan on being on any medication at all six months from now. I'm only

staying on the T3 now because it apparently plays very well with Symlin, and

because it will protect me from one of Symlin's side effects: loss of appetite.

I don't eat a lot of food as it is, and if I eat less the T3 will ensure that a

'starvation syndrome' doesn't rear its ugly head. I will probably have to reduce

my dose though. My temps are now going from 98.6 to 98.7-9 -- so clearly lots

more T3 is reaching my cells. Once Symlin begins to let leptin reach my brain

again, my hypothalamus will signal my liver to make even more T3 -- so that

means lowering my T3 dose. By the time I'm done with the Symlin and on to the

Actigall (if needed), I should be off all T3.

>

> Can't wait to start!

>

>

>

[Guest guest]

Wow - I am so interested in this.

I was diagnosed as hypo when I was a kid & have spent a lifetime dealing with

weight issues. I currently am at an alarming weight & its frustrating to no

end. One day I gained 8lbs (in a single day!) & I didn't eat more than 1600

calls that day.

Could you give me an idea of a typical day's menu of your diet?

And some links to any info that I can research - to follow in your footsteps.

If you do start a Yahoo group, I want to join too.

Thanks,

C

>

> > Very interesting stuff. I have printed it and will reread it several times

> > and will surely get tested. Please please let us know how it goes. If you

> > could title it something that we would recognize easily that would be

> > great.

>

> Birdy, I will do that. I plan to start my first Symlin injection tomorrow.

>

> > Why do you think you were able to tolerate so much T3 with

> > such a low ferritin number.

>

> That's a good question. I do have a few ideas, but no proof. First, I've been

eating a very healthy diet for a long time. I get 75% of my calories from fat,

particularly saturated fat (butter, cream, coconut oil, lard, etc). I eat very

modest protein -- about 13% of my calories, or 50 or so grams of animal protein

(I don't count the incomplete protein from veggies or fruit). That's only 7 or 8

ounces a day total from all animal sources including eggs, cream in coffee, etc.

-- far less than most people eat. And I eat just enough carbs to stay out of

ketosis, making sure that includes some glucose foods like potato and rice so

that my body (especially my liver) doesn't need to undergo the stress of

gluconeogenesis by making the glucose it needs for my brain at night from

protein.

>

> Second, I do the right kind of exercise to keep my cardiovascular system in

tip-top shape. That is, I do NO 'cardio' steady state exercise at all (like

walking, treadmill, etc) but instead do the Slow Burn weight lifting outlined in

Body By Science. I work out a total of 15 minutes every ten day to two weeks,

and I not only have biceps you can bounce a nickel off of, my lipids and

C-Reactive Protein tests are so good the Framingham online calculator says my

risk of heart attack in the next ten years is 1%.

>

> Third, of the foods I eat, I make 90% of them myself. I eat very little

processed food. I make my own LC yogurt, fermented mayo, cottage cheese,

mascarpone, creme fraiche, butter, ice-cream, cheesecake, brownies, fudge,

cookies, etc. etc. etc.

>

> I don't believe diet alone can make us healthy if our metabolisms are

compromised, but I do believe the right diet and exercise along with the right

treatment can make a huge difference.

>

> > why do you still have such a (relatively) high FT4 number when you're

> > on T3 only.

>

> Do I? My FT4 is 1.0 and the range starts at 1.4. If 1.0 is still high, what

should it be???

>

> > I looked up the prices for Symlin and Actigall and boy is it freckin

> > expensive. You are very lucky to get some samples. Convincing a

> > doctor on all this would be monumental.

>

> Agreed. But as you've now seen thanks to the recent posts, Actigall is cheap.

According to the Doctor conducting the clinical trials on UDCA and cystic

fibrosis, dosing for me should be 15mg per KG of my weight. That would be about

1200 mg a day for me, or four 300 mg tabs. That's 120 tabs a month. I bet my

insurance/Medco will have a 90-day supply for less than $100 bucks and I'm

hoping a single prescription will do it for me.

>

> Also, if my doc had not given me the samples, I would not have hesitated to

start on Actigall instead.

>

> > Do you plan on staying on T3 indefinitely?

>

> I don't plan on being on any medication at all six months from now. I'm only

staying on the T3 now because it apparently plays very well with Symlin, and

because it will protect me from one of Symlin's side effects: loss of appetite.

I don't eat a lot of food as it is, and if I eat less the T3 will ensure that a

'starvation syndrome' doesn't rear its ugly head. I will probably have to reduce

my dose though. My temps are now going from 98.6 to 98.7-9 -- so clearly lots

more T3 is reaching my cells. Once Symlin begins to let leptin reach my brain

again, my hypothalamus will signal my liver to make even more T3 -- so that

means lowering my T3 dose. By the time I'm done with the Symlin and on to the

Actigall (if needed), I should be off all T3.

>

> Can't wait to start!

>

>

>

[Guest guest]

Wow - I am so interested in this.

I was diagnosed as hypo when I was a kid & have spent a lifetime dealing with

weight issues. I currently am at an alarming weight & its frustrating to no

end. One day I gained 8lbs (in a single day!) & I didn't eat more than 1600

calls that day.

Could you give me an idea of a typical day's menu of your diet?

And some links to any info that I can research - to follow in your footsteps.

If you do start a Yahoo group, I want to join too.

Thanks,

C

>

> > Very interesting stuff. I have printed it and will reread it several times

> > and will surely get tested. Please please let us know how it goes. If you

> > could title it something that we would recognize easily that would be

> > great.

>

> Birdy, I will do that. I plan to start my first Symlin injection tomorrow.

>

> > Why do you think you were able to tolerate so much T3 with

> > such a low ferritin number.

>

> That's a good question. I do have a few ideas, but no proof. First, I've been

eating a very healthy diet for a long time. I get 75% of my calories from fat,

particularly saturated fat (butter, cream, coconut oil, lard, etc). I eat very

modest protein -- about 13% of my calories, or 50 or so grams of animal protein

(I don't count the incomplete protein from veggies or fruit). That's only 7 or 8

ounces a day total from all animal sources including eggs, cream in coffee, etc.

-- far less than most people eat. And I eat just enough carbs to stay out of

ketosis, making sure that includes some glucose foods like potato and rice so

that my body (especially my liver) doesn't need to undergo the stress of

gluconeogenesis by making the glucose it needs for my brain at night from

protein.

>

> Second, I do the right kind of exercise to keep my cardiovascular system in

tip-top shape. That is, I do NO 'cardio' steady state exercise at all (like

walking, treadmill, etc) but instead do the Slow Burn weight lifting outlined in

Body By Science. I work out a total of 15 minutes every ten day to two weeks,

and I not only have biceps you can bounce a nickel off of, my lipids and

C-Reactive Protein tests are so good the Framingham online calculator says my

risk of heart attack in the next ten years is 1%.

>

> Third, of the foods I eat, I make 90% of them myself. I eat very little

processed food. I make my own LC yogurt, fermented mayo, cottage cheese,

mascarpone, creme fraiche, butter, ice-cream, cheesecake, brownies, fudge,

cookies, etc. etc. etc.

>

> I don't believe diet alone can make us healthy if our metabolisms are

compromised, but I do believe the right diet and exercise along with the right

treatment can make a huge difference.

>

> > why do you still have such a (relatively) high FT4 number when you're

> > on T3 only.

>

> Do I? My FT4 is 1.0 and the range starts at 1.4. If 1.0 is still high, what

should it be???

>

> > I looked up the prices for Symlin and Actigall and boy is it freckin

> > expensive. You are very lucky to get some samples. Convincing a

> > doctor on all this would be monumental.

>

> Agreed. But as you've now seen thanks to the recent posts, Actigall is cheap.

According to the Doctor conducting the clinical trials on UDCA and cystic

fibrosis, dosing for me should be 15mg per KG of my weight. That would be about

1200 mg a day for me, or four 300 mg tabs. That's 120 tabs a month. I bet my

insurance/Medco will have a 90-day supply for less than $100 bucks and I'm

hoping a single prescription will do it for me.

>

> Also, if my doc had not given me the samples, I would not have hesitated to

start on Actigall instead.

>

> > Do you plan on staying on T3 indefinitely?

>

> I don't plan on being on any medication at all six months from now. I'm only

staying on the T3 now because it apparently plays very well with Symlin, and

because it will protect me from one of Symlin's side effects: loss of appetite.

I don't eat a lot of food as it is, and if I eat less the T3 will ensure that a

'starvation syndrome' doesn't rear its ugly head. I will probably have to reduce

my dose though. My temps are now going from 98.6 to 98.7-9 -- so clearly lots

more T3 is reaching my cells. Once Symlin begins to let leptin reach my brain

again, my hypothalamus will signal my liver to make even more T3 -- so that

means lowering my T3 dose. By the time I'm done with the Symlin and on to the

Actigall (if needed), I should be off all T3.

>

> Can't wait to start!

>

>

>

[Guest guest]

Wow, I'm so glad now I decided to go to the Holtorf center!

This is a GREAT post.

But my question is in regard to the Iodoral: why did you decide to stay on it?

What benefits did you think it had in restoring your health? I am particularly

curious because iodine stimulates the thyroid to make t4 and since your was

converting to t3, I wondered why you chose to stay on it.

I took Iodoral for a while and initially seemed to feel better, but eventually

went even more hypo since my t4 doesn't convert. All that rt3 really taxed my

poor adrenals, too. :-( So I quit it, but my D.O.M. is always trying to get me

to go back on, which I haven't!

Thanks!

Kathleen

>

> I guess the old saying: " It's the exception that proves the rule " is right, and

I'm the exception. ;-)

>

> When I told back in October that I intended to stay on Iodoral while

doing my T3 therapy, she said she'd be very interested to know if it worked

because she hasn't seen many people for whom that is true. Well, it worked, so

she can now add me to the shortlist. I've continued to take a single 12.5 mg

tab every morning.

[Guest guest]

Wow, I'm so glad now I decided to go to the Holtorf center!

This is a GREAT post.

But my question is in regard to the Iodoral: why did you decide to stay on it?

What benefits did you think it had in restoring your health? I am particularly

curious because iodine stimulates the thyroid to make t4 and since your was

converting to t3, I wondered why you chose to stay on it.

I took Iodoral for a while and initially seemed to feel better, but eventually

went even more hypo since my t4 doesn't convert. All that rt3 really taxed my

poor adrenals, too. :-( So I quit it, but my D.O.M. is always trying to get me

to go back on, which I haven't!

Thanks!

Kathleen

>

> I guess the old saying: " It's the exception that proves the rule " is right, and

I'm the exception. ;-)

>

> When I told back in October that I intended to stay on Iodoral while

doing my T3 therapy, she said she'd be very interested to know if it worked

because she hasn't seen many people for whom that is true. Well, it worked, so

she can now add me to the shortlist. I've continued to take a single 12.5 mg

tab every morning.

[Guest guest]

Wow, I'm so glad now I decided to go to the Holtorf center!

This is a GREAT post.

But my question is in regard to the Iodoral: why did you decide to stay on it?

What benefits did you think it had in restoring your health? I am particularly

curious because iodine stimulates the thyroid to make t4 and since your was

converting to t3, I wondered why you chose to stay on it.

I took Iodoral for a while and initially seemed to feel better, but eventually

went even more hypo since my t4 doesn't convert. All that rt3 really taxed my

poor adrenals, too. :-( So I quit it, but my D.O.M. is always trying to get me

to go back on, which I haven't!

Thanks!

Kathleen

>

> I guess the old saying: " It's the exception that proves the rule " is right, and

I'm the exception. ;-)

>

> When I told back in October that I intended to stay on Iodoral while

doing my T3 therapy, she said she'd be very interested to know if it worked

because she hasn't seen many people for whom that is true. Well, it worked, so

she can now add me to the shortlist. I've continued to take a single 12.5 mg

tab every morning.

[Guest guest]

Sorry, but another question! You were on sr t3, then switched to Cynomel? Any

particular reason? I was on Cytomel, but am now seeing a Holtorf doc and they do

prefer the time release, although he did tell me I could continue to take

Cytomel spread out if I wanted, albeit a pain in the butt.

I have decided to at least try their protocol, but I am not sure about this SR.

They want me to take it all in one dose in the AM. Is that what you did with the

SR?

When you switched to Cynomel, did you take multiple doses. I think s said

you have to take at least 6 -- basically every 3 hours and then bedtime, when he

used to use regular t3.

Thanks again!

Kathleen

> After ten days, reached 75mcg per day on November 15 -- became hyper, with 99+

temps and sweats, pulse in the 90's -- cycled down to zero in a week and then

began again on November 23 using a modified protocol. Modified in this case

means I began with 6.25 mcg and added more T3 very slowly, as Val recommends,

and also that unlike 's recommendation did not take compounded

time-release T3 but Cynomel.