[Harpy]

in reply to: T4 to T3 conversion #1178646

beach45 wrote:

Harpy,
Love what you have to say here. Definitely RT3 from what I see is a big factor; my doctors are not into testing it or believe in the theory behind it yet I had it tested on my own along with leptin and TPO antibodies and TSH, FT4 and FT3 in between going to the doctor the end of last year; Definitely a connection between the blood glucose and the leptin. The hormone leptin has been found to be a major regulator of body weight and metabolism. A very small portion of doctors work with leptin resistance yet I believe that is something like RT3 that eventually will be researched further and there will be more awareness in time. My leptin levels are way high along with blood glucose being at the high end in range. Like you said they are associated. In fact glucose was out of range right after RAI and when I went very hypothyroid. My current doctor though said that he has worked with some Graves patients who have struggles with metabolism after treatment as they need what he called a jump start for their metabolism. I am sure in time yet not currently more will be revealed. I see some people have no problems and I know others like myself who struggle with the weight issue. You are definitely on top of the latest! Thanks for sharing….beach

Just a bit more to consider is the research of Leptins role in regulating the immune system, basically:
Low Leptin = increased risk of infectious diseases.
High Leptin = increased risk of autoimmune and chronic inflamatory diseases.
The review below is worth a read, although one must keep in mind it is sometimes hypothesizing based on current available studies and data:

Quote:

REVIEW ARTICLE – Tissue Antigens ISSN 0001-2815
Leptin in autoimmunity: many questions, some answers
G. Matarese, E. H. Leiter & A. La Cava

Abstract
It has recently become apparent that several molecules involved in the control of metabolism also play an important function in the regulation of immune responses. Among those molecules, the adipocyte-derived cytokine leptin has been shown to significantly influence innate and adaptive immune responses both in normal and in pathological conditions. For example, levels of leptin are typically low in infection and high in autoimmunity, both systemically and at the site of inflammation.
Moreover, in addition to its long-known effects on the promotion of T helper 1
immune responses and cell-mediated immunity, leptin has more recently been found capable to constrain proliferation of regulatory T cells. As such, leptin represents not only a link between metabolism and immune responses in general but also a pivotal modulator of the magnitude of selected mechanisms of peripheral immunity in relation to body fat mass. We review here the most recent advances on the role of leptin in the control of immune tolerance and critically discuss how strategies aimed at neutralizing the leptin axis could represent innovative tools for the therapy of autoimmune disorders.

http://onlinelibrary.wiley.com/doi/10.1111/j.1399-0039.2007.00886.x/pdf

Although the targeting of leptin as a therapeutic process, i.e. drugs, is fine as a stop gap measure, I would think it would be more appropriate to determine the cause of abnormal Leptin levels as a greater long term goal.

There are many other questions in the leptin story like the issues of weight gain, which is often quite elusive, it is known that obesity is highly corrolated with systemic inflamation, the question is:
Does obesity cause inflamation or is obesity a desired outcome of an immune response to raise levels of inflamation?
(Note: Inflamation generally just means upregulated immune system processes.)

[Harpy]

in reply to: T4 to T3 conversion #1178642

One of the primary roles of rT3 appears to be in the “Hibernation response” as has been found in other mammals, in addition say for humans it also improves survival rates at times of low nutrition or food availability by down regulating metabolism and this then effectively reduces energy demand within the body.

Outside of thyroid issues, there are many conditions where rT3 is popping up and one of those situations is “weight loss plateaus”. In situations where one is calorie restricting, there is often an early weight reduction, then this plateaus, further calorie restriction may have a small weight loss, but not sustained and this usually results in the individual going into a Hypo type of state. The rT3 response comes first and if calorie restriction is maintained then the thyroid itself is down regulated which results in an effect more akin to the “starvation response”. There are obviously some unanswered questions as to why the body does this while it is still carrying quite a bit of excess fat, for whatever reasons the body is not getting some aspect of nutrition that it needs.

Beach45:

Quote:

We are slowly getting me to where I need to be as far as feeling more myself; weight issues are still there yet I do not have a RT3 problem and I see my leptin levels are too high for me yet that is another concept in itself having to do with metabolism which I will not touch on.

Good to hear you are making progress, fully agreed rT3 is not the entire problem just another clue.
Glad to hear you’re looking at Leptin, my partners level’s are also high, just outside of normal range. Finding out about Leptin was a real eye opener for me, to think that that much maligned adipose tissue (fat) is actually a major endochrine organ that produces Leptin and a variety of other hormones.
As research comes through it appears that Leptin may well play the conductors role in our hormonal orchestra.
Elevated leptin levels are often associated with persistantly elevated blood glucose levels, my partners have consistantly been at the high end of normal range, so we are tackling that to see if leptin levels will normalise.

[Harpy]

in reply to: T4 to T3 conversion #1178639

Testing for rT3 may shed some more light on the situation.
RT3 is like neutral version of T3, so it takes up receptor sites and blocks active T3 from doing it’s job.
Many Hypo individuals have high rT3 and often low T3 and hence there is a lot of discussion of T3 supplementation in those areas.

When an individual is in the Hyper state, there is the possibility with an accelerated conversion rate as well, they may well show a normal T3 level, but if their rT3 is also very high then they may well show Hypo symptoms, it’s all a case of balance as the rT3 and T3 are in direct competition for the same receptor sites, so you may well be in a situation where your T3 needs to be maintained at a higher level just to balance out the ratio to rT3.

rT3 is a normal part of the metabolism, the body uses it as a way to adjust normal hormonal activities, at this point in time it is thought to simply have a blocking role, but it may well have a specific functionality that we are not aware of yet.

All just more clues in the bigger picture of thyroid disease.

[Harpy]

in reply to: Low Dose Naltrexone #1178601

Far as LDN goes, never looked into it too much, have seen that quite a few people are trying it in many different areas, but results seem to be mixed, there doesn’t seem to be many notations on serious side effects with the low dose, but I’m kind of neutral on it.

I’m not a real big fan of Gardisil and vaccines in general, they definately do have a place in health, but it seems that we have gone over the top with vaccinations just for the sake of it. One example being chicken pox vaccines, where the risks posed by the disease are likely no greater(possibly less) than the risks posed by the vaccine itself, but that’s my opinion.

Regarding the hair loss, not a good place to be, but I tend to agree with Shirley there, if it is a side effect of GD or Hypo, then it will most likely resolve itself as you heal and adding another medication which may present new symptoms and side effects may actually be counter productive.
Hair loss is common with many chronic diseases as the body considers hair to be one of the non essential functions, so it will divert more of it’s energy to other parts of the body that are considered more important. This often happens with Hypo as the metabolism is down regulated and basically there is just less energy to go around.
Hope you stabilise and see some recovery in both your health and hair.

[Harpy]

in reply to: Acetyl L Carnitine for GD Symptom support. #1178052

That particular study has already been widely discussed elswhere and entire study and the conclusions drawn are of dubious value.
It consists of a series of experiments on mice with a defective cholesterol transport gene, poorly controlled human trial one vegan and five omnivores and an small epidemiological study. From these it has used a series of tenuous threads to draw a conclusion, that at best could only be used to propose a hypothesis that needs to be tested with a fully controlled trial.

It does not attempt to answer significant confounders such as the data currently available that show’s the particular bacteria in question is much more prevalent in the GI tract of individuals on grain based diet’s, or the variability of bacterial levels in it’s small cohort, which suggest those outcomes may simply be due to experimental error.

They have also used L Carnitine, which is known to have a lower absorption rate and is more likely to get to lower intestine and be exposed to bacterial fermentation,
where as the natural form found in meats is Acetyl L(Levo) Carnitine is highly absorbed in the small intestine.

They have also ommitted discussion of the fact that Carnitine in it’s various forms is an essential part of everyones metabolism and is used in a wide variety of metabolic processes particularly in the transport of fatty acids across the mitochondrial membrane to provide energy for normal cellular function.

They have also failed to discuss the fact that the overwhelming evidence from previous “clinical” trials in fully controlled studies show a wide variety of benefits and improved health outcomes of carnitine supplimentation.

The one below, a meta analysis of previous trials specifically relating to heart disease, the topic in question, the conclusion being:
http://www.sciencedirect.com/science/article/pii/S0025619613001274

Quote:

Conclusion

Compared with placebo or control, L-carnitine is associated with a 27% reduction in all-cause mortality, a 65% reduction in VAs, and a 40% reduction in anginal symptoms in patients experiencing an acute myocardial infarction. Further study with large randomized controlled trials of this inexpensive and safe therapy in the modern era is warranted.

As for the red meat component, any evidence there from previous studies was primarily epidemiological where the confounders of diet were not adequately controlled as the data was self reported and the consumption of a take away burger or hot dog was included as red meat consumption, somehow it is not considered that the additives or the big fluffy sugary bun may be having an impact on health outcomes.

Press releases and news reports on diet can pretty much be ignored as when taken in totality they cancel out entirely, “everything is good and bad for you”.

[Harpy]

in reply to: Fish oil #1178489

This is the response I got:

Quote:

Thank you for your email and enquiry.

There may be minute traces of iodine (less than 10 mcg/g) present, most, if not all of it is removed during the manufacturing process.

As the RDA is 150mcg/day of iodine, it is unlikely that this particular product would result in an iodine overload.

My partner has regularly been using 3g/day which would be less than 30mcg iodine.

I suppose it is about the individual gathering enough information and weighing up the pro’s and con’s when it comes to using any form of supplimentation or dietary changes.

[Harpy]

in reply to: symptoms with normal bloods – maybe this will be useful for anyone else in the same situation #1178541

We all have little abberations in our psychology and behaviour, but that’s ok, that’s what makes us individual.
The problem with GD is that some of these things become heightened and exaggerated which may result in a mis diagnosis of mental illness, as your body heals these issues usually fall away, but in some instances, particularly with anxiety, the reinforcement of the behaviour during the GD period is enough that the symptom persists even after GD stabilises, so may require some specific attention to correct it. This may be just simple reaffirmations to oneself to reinforce different behavioural patterns.
Trying a few stress management techniques, to find one that works for you may help minimise some of the psychological symptoms of GD, my partner found yoga and simple self reflection to be helpfull for her.

[Harpy]

in reply to: Fish oil #1178488

That document is a diet in preparation for RAI specifically designed to deplete the body of Iodine levels so that the I131 uptake is most effective, so should be treated with caution.

Even individuals with Hyperthyroid conditions need to have a normal iodine intake, yes they need to be wary of excessive iodine intake, but a normal intake should be fine.

The topic has raised some interesting questions, I have also not been able to locate any specific information on iodine content of fish oil, so to that end have sent an email to the supplier of the product my partner uses to pose this question.

She has used this particular fish oil, an ultra clean version to eliminate any risk of heavy metal contamination, for the entire period of her treatment and has not noticed any ill effects.

With regards to plant based Omega 3 this is Alpha Linoleic Acid (ALA) which is the Parent Omega 3, although most animals, particularly herbivores convert ALA well to eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), humans are not particularly good at converting it, even with a high intake of ALA at best we convert around 18% to EPA and only 5% to DHA, so it is very difficult to maintain adequate EPA & DHA levels.

Although we do use a certain amount of ALA in normal metabolic functions, we also need to consume EPA & particularly DHA through our diet.

[Harpy]

in reply to: Help with lab abbreviations please #1178428

With the TRAB’s there are three different types, stimulating, neutral and blocking.
Not quite sure what the deal is with the neutral guys is, but the stimulating and blocking ones seem to be the bigger issues with GD and other thyroid disease.

Although it is good to know the degree of stimulation by antibodies, the TSI, it is also important to know what total TRAB activity is, some individuals may normalise with the TSI, but then drift into Hypo land because of blocking AB activity, so even with a return of TSH, Thyroid hormone levels fall because the thyroid is being blocked.

This effect may be one of the reasons there has been some good success in the past with Block and Replace, because it effectively removes either situation by supressing the thyroid fully and using replacement hormone to control levels. The primary issue with B & R is the use of higher dose ATD’s.

Point is it’s good to know total TRAB activity as well as TSI if you can get that degree of service.

[Harpy]

in reply to: TRab levels and possibility of remission #1178345

It’s all in probabilities and as always there are confounding factors.
From those studies what I have deduced is:
Those with lower antibodies at diagnosis, and show steady decline during treatment, do not stop ATD’s until AB’s are well into range have the highest chances of lasting remission.

Regarding more difficult cases, like very high AB’s at diagnosis, fluctuating levels during treatment, it may be that they just need to extend treatment for a longer period or there may be other confounding factors aggravating the GD.

Once my partner crossed the two year mark, the Endo effectively said your Thyroid will never return to normal function, because that’s where the her (Endo’s) experience ended, that is their cut off point, and we had a respectful “Agree to Disagree” arrangement from there on.
Another three years of treatment and TSH just kicked in and has been completely normal for 18 months now.
Unfortunately we could not get AB’s tested often enough to determine if there was a pattern, but they were very high at diagnosis, so maybe we were more in the difficult range.

All the studies look at different things, it would be good to see a study put together to use a multipronged approach, taking the best guidelines from a number of studies and puting together a multi faceted approach, but unfortunately that goes against scientific protocol, which is always trying to isolate a singular variable to determine a “Cause & Effect” relationship.
This may be the very weakness of the current state of knowledge re medical treatment of autoimmune diseases, that we are dealing with multiple Causes and Effects that have complex interplays between them, hence there is to many anomolies in treatment protocols and we are left with a state of confusion.

When we look at simple pathogenic infections, they very much behave in a singular cause and effect, although there are some anomolies there too, but neverthless in most cases it is possible to treat very simply with a singular protocol.
Autoimmune and other Chronic diseases seem to confound the singular isolated hypothesis and maybe we need to be looking at these conditions in a more holistic sense, i.e. whole body treatment tailered to a particular individuals conditions, using a variety of protocols in unison.

[Harpy]

in reply to: TRab levels and possibility of remission #1178342

You may well be right on your last point, here in Aus there is a reluctance to test for AB’s during treatment, only considered as part of initial diagnosis.

As for the AB levels and remission, seems it is related to both the level of AB’s at start of treatment as well as the pattern during treatment, a consistant decline, rather than fluctuating AB’s level improved rates of remission.

This thread from last year had some discussion and links on the AB’s, extended ATD treatment and the Block and Replace protocol:
http://www.gdatf.org/forum/topic/42708/

[Harpy]

in reply to: Anyone else experience all this, or am i just a baby? #1177792

Everyone has an Agenda, whether they care to admit it or not.

The medical system has an Agenda and two of the primary drivers of that are patient care and cost, which unfortunately most of the time are pulling in opposite directions.

I’m sure that most doctors would like to give the best care possible to their patients, but the constraints of the system mean they need to make compromises, this is evident in public debate regarding budgetary measures and within the doctors office with the short duration of consultations.

So with these constraints, it then falls back to the patient to do adequate research if they want the best health outcome possible, so that they can make informed decisions.

Each treatment for thyroid conditions comes with it’s own set of risks, and different options will suit different individuals. From what I read here and elswhere the medical system in general does not have a good handle when it comes to applying any of the three treatment protocols although they all do have their place when applied properly, in my opinion most doctors are behind on current research, primarily because they are time poor, I don’t think they are bad people, but this means that they may not be in the best position to give the most up to date advice.

There are global discrepancies on the way treatment protocols are applied, but there is only one set of scientific data and with this day and age of information at your fingertips, one would imagine that there should be a treatment consensus based on the science available, hence the only way I can explain these discrepancies is that different Agenda’s are driving the preferential approaches in different countries.

If there was global medical consensus based on the current level on scientific information we would not be having this discussion.

[Harpy]

in reply to: Anyone else experience all this, or am i just a baby? #1177787

There really is no benefit to RAI or Surgery,
All three treatment options carry ther own set of risk factors,

To evaluate what is best for you, you need to do plenty of research, searching all over, using all resources at your disposal so that you can make a fully informed decision.

From what I have seen over the years, there is more at work with GD than just the simple thyroid antibodies hypothesis and there are plenty of people that have had RAI or Surgery and still deal with lingering symptoms many years later, that by itself tells anyone that the thyroid itself is not the issue.

A statement I read recently stated simply:
“If your doc’s can’t get your dosage right now, with a thyroid, do you really think they will be any better at regulating your dose when when they have removed/ablated your thyroid’

I think you are right with the Hypo thing, there are 10 times as many Hypothyroid individuals VS GD patients, this should be a big enough pool for the medical profession to perfect their practices, yet Hypo discussion groups are everywhere, because people just don’t feel well and hence feel the need to look elswhere.

Another thing to consider as well is just the simple fact, may be a rare event and not be pertinent to everyone but it is a fact, without a functioning thyroid you rely on an external dose for support, if you go travelling, trecking, get marooned, lost etc and don’t have med’s, then it’s gonna end pretty bad, think it’s 6 weeks before your body runs out of what’s in the system.

[Harpy]

in reply to: Goodbye and so much good luck to all. #1178128

Thank you brondack,
I do not agree fully with everything you have stated, but I’m not into nit picking, so let’s move on as you said.

I do think that Kimberly does a good job within the constraints that are placed on her, but in saying that I do not always agree with her, maybe it’s her or maybe it’s the guidelines speaking, sometimes I will object other times I just let it roll through.

I am not privy to the actual PM’s that transpired and whether they were innocent attempts to help or whether they could be considered harrasament, I was just surprised to see the disharmony when I logged on after being away on a trip.

[Harpy]

in reply to: What Triggers GD?? #1178086

Sorry Kimberly, I feel the need to qualify your statement:

Quote:

For the most part, Graves’ is not a condition that can be improved by diet

It should read something like:

Quote:

There have been no studies carried out, that we are aware of, to show that Graves Disease can be improved by diet.

I personally believe that diet does have a major impact on not only remission rates but also on the initial manifestation of the disease it self.
I do not think it is the only factor at play, but it is a significant factor in my opinion.
I do not have any scientific studies to support this view currently, it is just my personal experience and general reading in a variety of areas that have led me to this conclusion.

[Author]

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