hypothyroid help

**ironaddict69** · 10-10-2006, 03:53 PM

i have all the hypothyroid symptoms.

these are my tests after 90 mg of armour for a few weeks (they didnt change from the first test)

T4- 6.8 (5.1-14.1)
T3 uptake- 37.6 (24.0-39.0%)

i just started lions T3 today and did 60 mcg. not feelin much diferent tho.
any help wud be appreciated.

**gymrocken** · 10-11-2006, 10:14 AM

DO NOT USE LIONS STUFF.
if you truley have hypothyroidism then use pills from your doctor or buy some from somewhere else.
his liquid is not made to support a predeposition.
cheers

**oswaldosalcedo** · 10-11-2006, 12:19 PM

Originally Posted by ironaddict69

i have all the hypothyroid symptoms.

these are my tests after 90 mg of armour for a few weeks (they didnt change from the first test)

T4- 6.8 (5.1-14.1)
T3 uptake- 37.6 (24.0-39.0%)

i just started lions T3 today and did 60 mcg. not feelin much diferent tho.
any help wud be appreciated.

but you have it over 5.1 (6.8)
first you have to see,if is secondary or primary hypo.
and you have to take is t4 not t3!

by me at cuttingedgemuscle.com
http://www.cuttingedgemuscle.com/For...threadid=16935

Water retention by androgens
Oswaldo Salcedo (my ruminations)

HYPOPITUITARISM -> HYPOADRENALISM ->HYPONATREMIA
......................... -> HYPOTHYROIDISM ->HYPONATREMIA

one of the main mechanisms responsible for water retention is induced Hypopituitarism (reduced output of any pituitary hormone) by displaced Glucocorticoids (GC) through Androgens at the GC receptors, acting by antagonist mode, therefore decreasing Corticotropin (ACTH) w/wo decreased Thyrotropin (TSH) release. Subsequent to the ACTH decreased secretion, inhibits cortisol segregation at adrenals (Central Hypoadrenalism - Secondary Adrenal Insufficiency). The cortisol suppression produces in the hypothalamus, vasopressin (AVP) release, also known like anti diuretic hormone (ADH), this way GC insufficiency increases AVP mRNA expression, elevating abnormally, AVP levels, gives an increase in free water retention, decreased sodium pump activity, shift of extracellular sodium into cells and decreased delivery of filtrate to diluting segments of the nephron as a result of decreased glomerular filtration rate and effective renal plasma flow . GC inhibit AVP secretion by impairing AVP gene transcription.
The possible decreased TSH produces a central hypothyroidism ( trophoprivic, suprathyroid hypothyroidism) , which can contribute more to edema by augmented AVP release at the hypothalamus, decreased atrial natriuretic hormone (ANH), and decreased renin-angiotensin-aldosterone system (RAAS), diminished salt delivery to the loop of Henle, and hialuronic acid (D-glucoronic acid and N-acetyl-D-glucosamine) and chondroitin sulfate b (L-iduronic acid and N-acetyl-D-galactosamine sulfate) hydrophilic deposits,this two mucopolysaccharides (Glycosaminoglycans, GAGs) which attract water strongly, results in more total body water. Characteristic of hypothyroidism too, is myxedema megacolon; a distended and hanging colon, facial edema and others.

and:

Nephrol Dial Transplant. 2001 Sep;16(9):1799-806.

Thyroxine treatment induces upregulation of renin-angiotensin-aldosterone system due to decreasing effective plasma volume in patients with primary myxoedema.
Park CW, Shin YS, Ahn SJ, Kim SY, Choi EJ, Chang YS, Bang BK.

Division of Nephrology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, #62 Yoido-Dong, Youngdungpo-Ku, Seoul 150-713, Korea.

BACKGROUND: In experimental animals and humans, hypothyroidism is associated with fluid retention and generalized oedema, increased antidiuretic hormone (ADH), decreased atrial natriuretic hormone (ANH), and decreased renin-angiotensin-aldosterone system (RAAS), which subsequently can be corrected by thyroid hormone replacement. The purpose of this study was to determine the effect of thyroxine therapy on RAAS and neurohormones affecting water and electrolyte metabolism and the reason for these changes in patients with primary myxoedema. METHODS: We measured changes in the plasma renin activity (PRA), serum aldosterone (Aldo), ADH, ANH levels, serum and 24 h urinary electrolytes and osmolalities, and cardiac function in 22 female patients with primary myxoedema before and after correction of hypothyroidism. We also evaluated age-, sex-, and BMI-matched 15 healthy control subjects (Cont). RESULTS: It took an average of 4.3 months (range, 3-9 months) to normalize thyroid function. The mean reductions of body weight and estimated plasma volume were 1.8+/-1.0 kg (P=0.002) and 8.5% (P<0.001), respectively. In addition, serum Na+ and osmolality and the haematocrit were significantly elevated after correction of hypothyroidism (P<0.01 and P<0.001, respectively). Increased F(E)Na and C(OSM) (P<0.05) levels in patients with hypothyroidism (Ho) compared with those in Cont did not change after thyroxine therapy (Eu). However, C(H(2)O), U(E)K, F(E)K, and TTKG levels as well as creatinine clearance (Ccr) were markedly increased in Eu compared with Ho and Cont (P<0.01, respectively). Increased plasma ADH concentration and decreased plasma ANH concentration were normalized compared to Cont after thyroxine therapy (P<0.001 and P<0.01, respectively). Low PRA and serum Aldo concentration in Ho were significantly increased in Eu (P<0.001 and P<0.01, respectively). In addition, increased left ventricular mass index and decreased cardiac output in Ho were normalized compared to Cont after thyroxine therapy (P<0.01, respectively) CONCLUSIONS: These findings suggest that the exaggerated upregulation of RAAS after correction of hypothyroidism in patients with primary myxoedema is associated with an increase in Ccr and a decrease in plasma volume resulting from water diuresis, natriuresis, osmotic diuresis and inappropriate changes in plasma ADH and ANH levels. The improved renal function coincided with an amelioration of cardiac function. These changes seem to be an adaptive response for preventing excessive plasma volume and weight loss after thyroxine therapy.

--------------------------------

if the hypo is androgen induced,it will cease later after roid discotinuation.

**stupidhippo** · 10-11-2006, 01:37 PM

good post ossie...

**oswaldosalcedo** · 10-12-2006, 12:51 PM

Originally Posted by stupidhippo

good post ossie...

thanks!

**ironaddict69** · 10-12-2006, 06:53 PM

okay but im on HRT, theres no coming off, and my feet are usually cold and have been since about 2 years ago. plus i have all the sides

**oswaldosalcedo** · 10-13-2006, 10:32 AM

Originally Posted by ironaddict69

okay but im on HRT, theres no coming off, and my feet are usually cold and have been since about 2 years ago. plus i have all the sides

ok. your feet cool look like raynaud disease,a symptom in hypothyroidism.

The solution is t4,but i will like to see your values tsh,t4 free,t3 free, in u/ml or picograms or nanomols.
take a cortisol am and pm test and acth test to discard adrenal insufficiency.
normally the use of 50-100 mcg of t4 (first thing in the morning,you have to maintain tablets in the refrigerator at the low part) is enough to ward of symptoms,have to take values monthly, later more separated.

t4: synthroid