what a silly study! They look at free T4, the weakest thyroid hormone and found high levels to be associated with dementia. However, they failed to assess free T3, the most biologically active, and reverse T3, inactive. This study was like they intentionally blinded themselves of the body's physiology to study dementia. This is the problem with a lot of research today: they have forgotten their foundation.
Many older adults struggle with poor free T4 to free T3 conversion and high reverse T3 conversion. So, without knowing what these clients were doing in these pathways makes their conclusion obsolete.
nice review of how thyroid disease effects cardiac function. Notice the author of this paper describes "thy- roxine (T4) which is a prohormone and tri-iodothyronine (T3) which acts as the final mediator".
More than 80% of the biologically active hormone triiodothyronine (T3) derives from peripheral conversion of prohormone thyroxine
(T4) secreted by the thyroid gland
Low thyroid hormone concentrations, in particular low serum T3 concentrations, are a common finding in patients with nonthyroidal
illnesses, including cardiac disorders
a direct relationship
between low circulating levels of T3 and adverse prognosis of cardiac patients
The present study clearly shows the existence of a strong association between the reduction of biologically active T3 and
mortality in a large population of cardiac hospitalized patients
highly significant increase in the incidence
of cardiac and cumulative deaths in patients with low T3 compared with patients with normal T3 levels
the relevance of the low T3 state as a strong, independent predictor of mortality in cardiac patients
low T3 concentrations are a strong independent predictive marker of poor prognosis in cardiac patients
low T3 associated with poor prognosis in cardiac patients. Poor prognosis = death. T3 is important in cardiac remodeling, which is inherently important with cardiac disease.
Combined replacement therapy with T4
and T3 (in proportions similar to those secreted by the normal rat thyroid)
completely restored euthyroidism in thyroidectomized rats at much lower
doses of T4 than those needed to normalize T3 in most tissues when T4 alone
was used
which is a major reason for the regaining of lost weight with dieting as well being the mechanism behind stress induced weight gain (it is not due to increased cortisol).
f greater than 10, it demonstrates there is a degree of leptin resistance contributing to an inability to lose weight
that it is difficult to lose weight with leptin resistance. High carbohydrate diets and in particular high-fructose corn syrup is shown to significantly increase leptin resistance and is a likely mechanism that high fructose corn syrup is associated with obesity
it is problem inside the cell that the inactive T4 is not converted to T3 but rather to a mirror image of T3 called reverse T3. The reverse T3 has the opposite effect of T3, blocking the effects of T3 and lowering rather than increasing metabolism.
Studies are showing that stress and dieting (especially yo-yo dieting) can set this hormone into action as well as chronic illness such as diabetes, chronic fatigue syndrome and fibromyalgia.
As soon as the body senses a reduction in calories, the production of reverse T3 is stimulated to lower metabolism
With chronic dieting or stress, the body often stays in this "starvation mode" with elevated levels of reverse T3 and decreased levels of T3, which is a major reason for the regaining of lost weight with dieting as well being the mechanism behind stress induced weight gain (it is not due to increased cortisol).
which is a major reason for the regaining of lost weight with dieting as well being the mechanism behind stress induced weight gain (it is not due to increased cortisol).
which is a major reason for the regaining of lost weight with dieting as well being the mechanism behind stress induced weight gain (it is not due to increased cortisol).
Studies are showing that such standard testing will miss 80% of thyroid dysfunction
Both pregnancy and estrogen administration were associated with increases in serum reverse T3 concentrations presumably because of their ability to augment thyroxine binding globulin synthesis.
it is clear that serum IGF-1 and or IGFBP-3 can be normal in patients with undisputed GHD
Various investigators have reported normal IGF-1 values in 37–70% of GH deficient adults
The co-administration of arginine and GHRH (the combined test) is a powerful stimulus for GH production and has gained increasing acceptance as a useful method of diagnosing GHD [34]. This test has been advocated as a suitable alternative to ITT
The glucagon stimulation test (GST) is a reliable, safe alternative to the ITT in the diagnosis of GHD
An intravenous infusion of arginine (0.5 g/kg body weight) together with an intravenous bolus of GHRH (1 mcg/kg body weight) is administered [30]. Serum samples for GH are then obtained every 15–30 minutes for two hours.
Obesity, particularly marked obesity, is associated with blunted GH secretion in response to provocative stimuli
It has also been suggested that that even mildly increased BMI (25–30 kg/m2) can result in diminished stimulated GH production in 13% of healthy subjects
Corneli et al. have defined BMI-specific cut-off points for diagnosing adult-onset GHD using GHRH + arginine—11.5 ng/mL for those with BMI < 25 kg/m2, 8.0 ng/mL for BMI 25–30 kg/m2, 4.2 ng/mL for those with BMI > 30 kg/m2
GH levels are higher during the luteal phase in comparison with the follicular phase of the cycle
Oral, in contrast to transdermal oestrogen, lowers IGF-1 levels and is associated with increased GH levels
Adequate pituitary replacement with thyroxine and hydrocortisone are needed for optimal GH production
one cannot rely on a low IGF-1 to diagnose GHD in women taking oral oestrogen preparations.
Numerous GH secretagogues are available with the insulin tolerance test being the gold standard and the glucagon stimulation test or the GHRH + arginine as acceptable alternatives
ain et al. found the GST to be at least as good as the ITT in provoking GH secretion
the GST is safe, with almost no contraindications, it causes nausea and sometimes vomiting in 15–20% of subjects
Hashimoto's hypothyroidism is associated with a 44% increase in Heart disease in women under the age o 49. A non-significant change was seen in men. This study found that T4 therapy reduced this risk. A better study would have been if T4 was compared to T4 + T3.
Lipoprotein(a) is a plasma lipoprotein consisting of a cholesterol-rich LDL particle with one molecule of apolipoprotein B100
and an additional protein, apolipoprotein(a)
Elevated Lp(a) levels can potentially increase the risk of CVD (i) via prothrombotic/anti-fibrinolytic effects as apolipoprotein(a)
possesses structural homology with plasminogen and plasmin but has no fibrinolytic activity and (ii) via accelerated atherogenesis
as a result of intimal deposition of Lp(a) cholesterol, or both
evidence suggests that apolipoprotein(a) adducts
extracellularly and covalently to apolipoprotein B100-containing lipoproteins, predominantly LDL
Lp(a) is relatively refractory to both lifestyle and drug intervention.
Other agents reported to decrease Lp(a) to a minor degree (<10%) include aspirin, l-carnitine, ascorbic acid combined with l-lysine, calcium antagonists, angiotensin-converting enzyme inhibitors, androgens, oestrogen, and its replacements (e.g. tibolone),
anti-estrogens (e.g. tamoxifen), and thyroxine replacement in hypothyroid subjects