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cutejenny77 11-10-2008 12:17 AM

Re: Thyroid Care and Concerns Endocrine Balance Issues
[b]ferritin[/b] - Mine was 33 this summer [I](& I was told [u]normal[/u] by a DORK [SIZE="1"]Dr[/SIZE])[/I] Seriously I raised it to 79 in eight weeks time by eating [u]Cream 0 Wheat / Malt-0-meal[/u] type cereals daily & taking prenatal vitamins. Those cereals contain 60% of daily iron right there :)


Sue, my Ferritin was the same as yours before. I also eat cereal everyday, but I take 100% of iron supplement. After a month, when my blood was drawn. I found it a little bit dark. But I have not had it re-tested yet. Am I overmedicated by iron? BTW, why do you avoid malt? Is it junk food?


mkgb 11-10-2008 05:46 AM

Re: Thyroid Care and Concerns Endocrine Balance Issues

She doesn't avoid Malt-O-Meal. She either eats Malt-O-Meal or Cream O Wheat each morning and supplements with vitamins.

You also can not tell if you are getting too much iron by the color of your blood. You should wait on the actual test results. It being darker is a good sign and is also a sign that the vial seal and vacuum are excellent. Blood turns red with exposure to the O2 in the air. It is quite dark in out veins. ;) I hope that your diet and supplement regime have pulled up your ferritin levels.


mkgb 11-10-2008 11:19 AM

Re: Thyroid Care and Concerns Endocrine Balance Issues
[B]Hypoglycemia/Diabetes/Insulin resistance and the Thyroid how are they linked?
Hypoglycemia(HG) was first discovered in diabetics. It’s the result of too much insulin in an insulin-dependent diabetic. Now it is recognized in non-diabetics and considered a PRE-diabetic state. The endocrine system contributes to the process of metabolizing food into energy and can cause/effect this condition. The main glands of note are the liver, the pancreas, the adrenal glands, the thyroid, and the hypothalamus. A problem in any one of these glands can cause HG and over time diabetes(DB).

First school of thought was HG was simply and only the overproduction of insulin. Now more scientists and doctors have studied this and theorize that there are other common causes of HG, one is a sluggish liver. How the liver works in the processing of sugar is to convert energy stores (glycogen) into glucose for instant energy when blood sugar levels drop below acceptable limits. Chemically glucose and oxygen combine to create energy for the brain and other muscles about the body. When the liver is optimal in health it works quickly to restore flagging glucose levels. In these people there are little to no symptoms of low blood sugar. In patients with suboptimal functioning livers, the process of converting glycogen into glucose is suppressed, this results in HG two to three hours after a meal before returning to a normal insulin and blood sugar level state. It is hard to catch this type of HG with just fasting blood work. You need the full long duration glucose tolerance testing.

Many Mds theorize that HG can be a symptom of hypothyroidism, and that low thyroid function can be caused by a suboptimal functioning liver as well. This can easily be the case in those that do not convert T4 to T3 well. Low levels of T3 in the blood allow for easier detection of a hypothyroid patient due to higher TSH levels. Also give the physical role of T3 in the human metabolism, the low T3 could be the source of the glucose metabolism issues. But we are talking theories here. Proving such mechanisms are factual takes YEARS of targeted research.

Medical theories are considered controversial until proven as fact. Some other “controversial” theories that may explain metabolic the influences on blood sugar are weak adrenal function and poor diet. How can hypoadrenalism of adrenal fatigue effect blood sugar? If there is not proper production of cortisol in the adrenal glands, this affects the process of converting glycogen into glucose. Low cortisol levels lower the conversion rate of glycogen into glucose. Increased cortisol production arises from the fight or flight response and immediately triggers and need for instant energy if a person is unable to create cortisol of respond in such a manner due to hypoadrenalism then this can also cause HG.

How can diet cause it? As a whole most of us eat too many refined carbohydrates. These refined carbs are hard for the body to handle in repetitive long term doses. They cause the blood sugar to get too high and this stimulates the pancreas to secrete an excess amount of insulin which drives the blood sugar too low. The low blood sugar causes excess stimulation of the adrenals and liver. This triggers an unnecessary hunger response and causes a repeat of the cycle. So eating a diet that avoids refined carbohydrates is very important in pre-diabetic states and other states of endocrine dysfunction.

How does diabetes come from hypoglycemia? Well too much of a good thing is bad for you. By our tendency to overindulge in refined carbs and sugary drinks, we flood the blood with excess sugar causing cyclic spikes and over production of insulin to compensate. This repetitive hammering of the pancreas damages it over time. This wears down the pancreas insulin production capabilities, until it eventually is so damaged it can not meet our physical needs and this results in diabetes. In the US the prevalence of our fast food life style and high caloric intakes resulting from sugary drinks and foods in excess of need are proving to be a major factor. You want numbers? I have some that about knocked me out of my chair. The consumption of sugar in the early part of the century in the US was around 5 pounds per person per year. Now it’s over 120 pounds per person per year. It’s important to read the labels of the food you eat. Doing so, you’ll realize how much sugar is added to foods. Sugar tastes good and the food companies are using it to make EVERYTHING go down easier. Problem with that is our waist size increases correspondingly.

Now hyperthyroidism may have a similar effect on the pancreas. In hyperthyroid patients all metabolic process are heighten/ramped. As a result they work their pancreas harder because they have to eat more to compensate. I know that my Aunt and Great Aunt could eat twice as much as a normal person and still not gain weight with their Graves Disease. If you think about this, they are converting and processing at twice the normal rate. This would mean by the age of 40 they have done 80 years worth of work in theory. If this logic is sound, it only makes since that uncontrolled hyperTs could experience side conditions like diabetes as the wear out their innards. Once again, just a theory!

What are the downsides to HG? Hypoglycemia is almost never fatal; the most serious problem that can result is a low blood sugar induced coma, and this is VERY rare. Under treated or poorly managed HG can result in some intense symptoms can become intense if hypoglycemia is not managed properly. Symptoms that can become unmanageable for some as a result of HG include anxiety, sweating, shakiness, trembling, rapid heart rate, headache, hunger, and overall body/muscle weakness. Long term untreated HG can result in Diabetes.
Now this is where you can make a difference, you have to evaluate your self and study your symptoms given daily routines. Often with HG the patient is in the best position to determine whether he or she is affected. If you have the symptoms listed above, and eating alleviates these symptoms, it’s likely you are affected by a form of hypoglycemia.

1) Testing should include a dietary survey (keep a food log (time, amount, and type of food consumed with symptoms onset comments)

2) Get a GGT(A four or six hour glucose tolerance test, the 2 hour may not catch it). The glucose test should include insulin levels. When the blood sugar goes above 150 at the first or second hour, diabetes is indicated. When you rise to 100 – 150 and then plummet in the 2-4 hours it is indicative of reactive hypoglycemia (pre-diabetes). This ore-diabetes reactive spike and drop are theorized to be indicative of liver dysfunction or adrenal dysfunction. If the blood sugar drops to around 60 after the fourth hour, it usually indicates adrenal dysfunction. A glucose tolerance test that shows high at the first or second hours and low for a couple of hours before normalizing in the fifth hour is called insulin resistant/dysinsulinism. This type of curve would theorized indicate liver and adrenal dysfunction induced insulin resistance/HG. (:D I have this type of curve! It is text book!)

3) Other checks: blood pressure sitting followed by BP upon immediate standing, if the blood pressure drops significantly when the patient stands, it’s usually an indication of adrenal dysfunction, which is frequently a factor in non-diabetic hypoglycemia.

4) Testing patients suffering from HG for hypothyroidism, and adrenal function is beneficial.

Hypothyroidism is typically diagnosed by a blood test, if the MD knows what to look for; HOWEVER, it frequently occurs that a patients displays symptoms of hypothyroidism despite a negative blood tests given the wide spread of NORMAL ranges. Studies have shown that treating such patients for hypothyroidism will often relieve them of their symptoms.
A more reliable way to detect "hidden hypothyroidism" is to measure vital statistics daily: low blood pressure, low basal body temperature first thing in the morning before eating or moving around. Is an early sign of subnormal metabolic management on the thyroids part.

Well that is my take on HG.. working up some more with lots of references. Brace yourselves for the MG WTMI system shock!

osteoblast 11-10-2008 11:32 AM

Re: Thyroid Care and Concerns Endocrine Balance Issues
MG-Interesting info about hypo and diabetes and sugar. Every morning I have my fruit smoothie-cup of orange juice, blueberries, strawberried and banana with a cup of yogurt. Is this fruit drink something that would stress my body--with all the fructose? Is it like having sugar? Over the past 2 yrs. my blood glucose falls in the low 80's on a scale of 70-100. Went to new pcp last week and she said she wanted to look at blood glucose. I don't think I have a problem with glucose now and want to avoid one if possible. She also said with the high antibodies she can see why I have been bouncing around with tsh. She was real keen on getting my ferritin up from 35 to around 100! Hope springs eternal-I think she is going to be a good pcp for me.
P.S.-MG, take a look at my Medical Mystery thread. Would love to hear your comments.
Take care:)

mkgb 12-03-2008 11:19 AM

Re: Thyroid Care and Concerns Endocrine Balance Issues
Since I am looking into endocrine balance and its effects on the thyroid with this thread I feel it is important to talk about Polyglandular Autoimmune Syndrome (PAS). PAS is a rarely documented condition that has many types and many subgroups. Reading the multitude of posts on this board alone and looking at those that have the multitude of issues to result in a PAS classification makes me seriously doubt the 20 in a million diagnosis statistics. I feel in some regards it is another issue stemming from Mds focusing on ONE issue and ignoring the fall out. I hope that this post reaches those that need it and word gets out.

So what is PAS and how is it defined? Well PAS is diagnosed when a patient has a multitude or certain grouping of autoimmune disorders of the endocrine glands. In most cases the AIS result in failure of the glands to produce their hormones (Hashimoto's, Diabetes, Addison's.. enough said).

It is a proven fact that is commonly ignored by the YOU KNOW WHO'S.. glandular abnormalities of the endocrine system tend to occur in clusters. When one thing goes you tend to deal with an endocrine domino run. Another fact that makes me question the 20:1000000 diagnosis ratio is that statistics show up to a forth of patients with evidence of hypofunction (hypothyroidism, hypoadrenalism...etc) in one gland have evidence of other endocrine issues/diseases. BUT many Mdon'ts do not continue to consider other glandular hypofunction when evaluating patients with any type of endocrine hypofunction. I personally think this is a crock..because the risk of multiple glandular involvement is quite significant in my opinion. If we want to watch ourselves and see we get thorough care and testing we are going to have to fight for it and lead or MD through the obstical course of our thyroid/endocrine issues.

Now for those of you wondering why THOSE THAT I WILL NOT NAME have not looked into or followed PAS in those at risk.. well here are some facts. It is not due to PAS being a NEW FANGLED disorder. NOPE! The concept of polyglandular failure is not new at all. As a matter of fact it achieved recognition in the 19th century. The exact date and MD you wonder? 1853 - Thomas Addison (yeah * snort * the name is significant) Addison was the first to describe the clinical and pathological features of adrenocortical failure in patients( Addison's Disease ;) ) who also appeared to have pernicious anemia (PA- low B12 based anemia)... earliest recognition of PAS. More issues/PAS combonations were noted in 1908(common pathologies of PAS), 1926(thyroiditis and adrenal cortex failure linked), and 1964(PAS including insulin dependent Diabetes). So why isn't it being taken seriously? Are we above having these issues in this modern age? NOPE, * sigh * just chalk it up to ignorance and laziness.

Now some MDs and scientist have been furthering the early research into PAS.
1980 - Neufeld and Blizzard developed the first classification of PAS by breaking it into 2 broad categories, PAS type I and PAS type II (PAS I and PAS II). An additional group, PAS type III (PAS III), was subsequently described... but tends to be a precursor to PAS I or PAS II. PAS III differs from PAS I and II because it does not involve the adrenal cortex. In PAS III, Hashimoto's/autoimmune thyroiditis occurs with another organ-specific autoimmune disease, but the syndrome cannot be classified as PAS I or II.

I am going to work backward because PAS III may apply to more of you than the other catergories. PAS III is broken down into 3 subcategories (A, B, C):
PAS IIIA - Autoimmune thyroiditis with immune-mediated diabetes (IMD) mellitus(Type 1)
PAS IIIB - Autoimmune thyroiditis with Pernicious Anemia
PAS IIIC - Autoimmune thyroiditis with vitiligo / alopecia / other organ-specific autoimmune disease(excluding Adrenal AIs)

Other organ-specific AIDs is a broad term. The main diseases that fall into this catergory are Celiac's, hypogonadism, Myasthenia gravis. Non organ specific qualifying conditions for type IIIC: Sarcoidosis, Sjogren's, Rheumatoid arthritis.. there are more but this gets the bulk of the wow factor out of the way.

Cases of PAS III are not well documented as far as I can tell. Why? Not going to waste my finger energy. So what can cause PAS III- autoimmunity, environmental factors, and genetic factors are the 3 major factors that should be considered in the source of PAS III. All in all they can not tell you what was the cause unless you have a clear genetic marker indicating it is your fault. ;)

Now I do find that the main autoimmunity source is interesting and noteworthy. It is known that an autoimmune disease affecting a single endocrine gland is frequently followed by impairment of other glands. When multiple glands are impaired and the issues are not treated the end result is multiple endocrine gland failure. The first and still MAIN autoimmune source of these disorders was noted in the mid-20th century... * typed with a DRY tone * 1956. COME ON MDS. * sigh * I will not vent. In 1956 guess what was discovered circulating about in patients... precipitating autoantibodies to thyroglobulin (TGAB) in patients with Hashimoto thyroiditis. * DING WE HAVE A WINNER * This was the first evidence and test pointing to an autoimmune source/link to PAS. Just food for thought. What do you think?

PAS II and PAS I discussion to come. Man was that a lot of typing...

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