I think the answer was previously posted: we would need t treat depressed subjects with thyroid, or finding such studies
I already posted some such studies.
Virtually All Patients With Depression Are Hypothyroid
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I think the answer was previously posted: we would need t treat depressed subjects with thyroid, or finding such studies
How can you be so convinced of the direction of causality here?
Why does it always have to go from physiological to psychological and not the other way around?
Did you see my response to another user asking the same question?
Virtually All Patients With Depression Are Hypothyroid
...But above all, the links is likely causal since the studies above showed that thyroid administration was beneficial for people with all forms of depression (unipolar, bipolar, psychotic, etc) and all spectrums of severity.
It has been a quiet secret for decades in European and North American medical practice: Some, not all, psychiatrists will consider non-orthodox thyroid prescribing when other specialists will not. Peter Whybrow and colleagues have for decades noted effectiveness of “supra-physiologic” doses of T4 for bipolar disorder. Other psychiatrists will at times prescribe thyroid for depression or other diagnoses. Psychiatry is sometimes given leeway in health care. Other specialists need recourse to send problems somewhere.
This recent (July 2018) Cohen, Sommer &Vuckovic case report & review has some references, and common equivocations:
Psychiatry Online
Antidepressant-Resistant Depression in Patients With Comorbid Subclinical Hypothyroidism or High-Normal TSH Levels
“…even a TSH level in the upper quartile of normal has been reported to be associated with a higher frequency of depressive episodes, more severe symptoms, and poorer response to treatment in people with major depression (27). Pae et al. (28) reported less severe but more treatment- resistant depression in euthyroid perimenopausal women with high-normal TSH levels.”
“Adequate thyroid hormone levels are necessary for most physiologic functions, including normal brain function and response to medications. Unfortunately, the literature is sparse on the specific topic of treating patients who have both high-normal TSH levels, suggesting some degree of thyroid inadequacy, and major depressive disorder. Most studies addressing the use of thyroid hormone supplementation in patients with mild thyroid dysfunction and depression have been small, often called “pilot” and “preliminary” studies by their authors. Such studies have not been followed by large- scale definitive studies, and despite the clinical importance of defining adequate thyroid function in refractory depression, it is unlikely that definitive large-scale studies will be conducted.”
“…mild thyroid abnormalities or inadequate thyroid hormone supplementation are not rare in patients with depression, and a target TSH level below 4.5 mIU/mL, as previously recommended in the literature, would appear to be inadequate for most people, especially those with treatment-resistant depression. In moni-toring supplementation, both blood tests and side effects are followed, but it is likely that the TSH level will need to be below 2.5 mIU/mL, or even below 2 mIU/mL, for most patients to achieve optimal outcomes.”
Any studies to share on the last?What difference does it make? Chicken, egg?
If thyroid supplementation is beneficial, then it should be widely considered as a possible therapy for "treatment-resistant" depression. It would be too much to ask for it to be used as a first-line treatment given the current climate, but this still needs to be taken seriously. I think that is the takeaway here. Arguing the causality is moot if thyroid has been proven time and time again to improve symptoms in depressed patients.
Nitric Oxide inhibition ? Considering NO induces mania, and simple Nitric Oxide inhibition produce similar results to NMDA antagonism.MB has no other know mechanism (at the doses used in the human trials) except the stimulation of both Krebs cycle and ETC activity.
Has anyone you know reversed hypothyroidism without using thyroid hormones? And I'm talking also about stopping DHEA or anything else beside good food and lifestyle and having a good thyroid function
Nitric Oxide inhibition ? Considering NO induces mania, and simple Nitric Oxide inhibition produce similar results to NMDA antagonism.
What would be the most common causes of thyroid damage? Malnutrition? Stress? Drug use? And by damage, do you mean autoimmune type thyroid disorders? I've never read anything of Peat's about permanent physical thyroid damage.
⦁ Thyroid hormones and mitochondria: With a brief look at derivatives and analogues It is now quite widely accepted that thyroid hormones have two types of effects on mitochondria. The first is a rapid stimulation of respiration, which is evident within minutes/hours after hormone treatment, and it is probable that extranuclear/non-genomic mechanisms underlie this effect. The second response occurs one to several days after hormone treatment, and leads to mitochondrial biogenesis and to a change in mitochondrial mass. The hormone signal for the second response involves both T3-responsive nuclear genes and a direct action of T3 at mitochondrial binding sites. T3, by binding to a specific mitochondrial receptor and affecting the transcription apparatus, may thus act in a coordinated manner with the T3 nuclear pathway to regulate mitochondrial biogenesis and turnover.
Supplementation of T3 Recovers Hypothyroid Rat Liver Cells from Oxidatively Damaged Inner Mitochondrial Membrane Leading to Apoptosis. Supplementation of T3 Recovers Hypothyroid Rat Liver Cells from Oxidatively Damaged Inner Mitochondrial Membrane Leading to Apoptosis
In order to check whether the effects caused by hypothyroidism are reversed by T3, the above parameters were evaluated in a subset of T3-treated hypothyroid rats. Complex I activity was inhibited in hypothyroid SMP, whereas T3 supplementation upregulated electron transport chain complexes. Higher mitochondrial H2O2 levels in hypothyroidism due to reduced matrix GPx activity culminated in severe oxidative damage to membrane lipids.
SMP and matrix proteins were stabilised in hypothyroidism but exhibited increased carbonylation after T3 administration. Glutathione content was higher in both. Hepatocyte apoptosis was evident in hypothyroid liver sections; T3 administration, on the other hand, exerted antiapoptotic and proproliferative effects. Hence, thyroid hormone level critically regulates functional integrity of hepatic mitochondria; hypothyroidism injures mitochondrial membrane lipids leading to hepatocyte apoptosis, which is substantially recovered upon T3 supplementation.
myelin is lower in people with depression Myelination of the brain in Major Depressive Disorder: An in vivo quantitative magnetic resonance imaging study - Scientific Reports along with the neuron loss seenHypothyroidism is a well-described cause of hypomyelination. In addition, thyroid hormone (T3) has recently been shown to enhance remyelination in various animal models of CNS demyelination
The human brain consumes 20% of our total energy expenditure compared to 13% in monkeys and 2-8% in other vertebrates. This striking shift in resource use was made possible by important evolutionary adaptations in lipid and energy metabolism. Compared to other species, these adaptations made it possible to devote a greater proportion (approximately 25%) of our brain’s mass to myelin and thus achieve the information processing capacity that defines the human species
The “connectivity” provided by myelination consists of increased action potential transmission speed (over 100-fold) and decreased refractory time (34-fold) which increases the number of action potentials that can be transmitted per unit time (in Internet terminology this would represent expanded “bandwidth”).
Myelination thus potentially increases the information processing capacity of our brain’s “Internet” by over 3,000 fold, making human myelination indispensable for developing our species’ elaborate cognitive functions
From the perspective of the exceptionally myelinated human species, the development and maintenance/repair of myelin’s functional integrity may be the single most important and vulnerable element for acquiring and maintaining optimal cognitive and behavioral function.
Mechanisms at play in recurrant depression - REM sleep & Myelin
I was wondering why REM sleep is so skewed in depression. where REM onset hits abnormally fast instead of a delay and gets overactive, similar to narcolepsy. where both conditions come with daytime exhaustion. why would this be happening During REM sleep myelin repair goes up (oligodendrocyte...raypeatforum.com
⦁ In critical illness, (diodinase 3) can deplete T3 to very low levels within days. Unfortunately, as T3 levels become lower, the body becomes weaker and sicker. Research says that the lower T3 goes, the greater is the chance a sick person will die.
The idea that the "free hormone" is the active form has been tested in a few situations, and in the case of the thyroid hormone, it is clearly not true for the brain, and some other organs. The protein-bound hormone is, in these cases, the active form; the associations between the "free hormone" and the biological processes and diseases will be completely false, if they are ignoring the active forms of the hormone in favor of the less active forms. The conclusions will be false, as they are when T4 is measured, and T3 ignored. Thyroid-dependent processes will appear to be independent of the level of thyroid hormone; hypothyroidism could be caller hyperthyroidism.
Alcohol use lowers thiamine, thiamine deficiency damages thyroid function. The thyroid needs thiamine to have the energy to do its job. Thiamine deficiency and thyroid deficiency (hypothyroidism) share many symptoms.Would alcohol use really damage thyroid?
Life interventions like environmental toxins, such as heavy metals, permanently damage the thyroid gland too.I think this applies to people who have had medical interventions like radiation, chemo or surgery that has permanently damaged the thyroid gland requiring life long thyroid hormone replacement.