Virtually All Patients With Depression Are Hypothyroid

[haidut]

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

 

[haidut]

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

As one of those studies said, it seems depression is quite likely just brain hypothyroidism. There is a strong link between chronic depression and dementia (Alzheimer). Alzheimer's is now being re-classified as "brain diabetes", which is another condition strongly linked to low thyroid function. This makes the link even more plausible. 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.

 

[aguilaroja]

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.”

 

[haidut]

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.”

Thanks. I also think the fact that MB is so effective for unipolar, bipolar and psychotic depression is further indication of the role of metabolism/thyroid in mental health issues. MB has no other know mechanism (at the doses used in the human trials) except the stimulation of both Krebs cycle and ETC activity.
Even more simplistically, considering that the brain uses about 40% of daily calories and as such is very sensitive to energetic or oxygen deprivation, it seems rather natural to consider energetic abnormality in brain/mental disorders. Thiamine (PDH cofactor and CA inhibitor), niacinamide (NAD precursor) and riboflavin (FAD precursor) are all known to improve depressive and psychotic states, and their primary known role is as energetic cofactors. In light of all this evidence, I have to suspect something other than plain stupidity is responsible for not exploring the metabolic origins of mental health issues more widely in clinical psychiatry.
Acetazolamide Plus Thiamine As Treatment Of Mental Conditions

And I am not even mentioning the fact that all known serotonin antagonists have demonstrated antidepressant effect in animal studies (and many of them in human trials as well). The role of serotonin in suppressing metabolism is well-known even in mainstream medicine, and the SSRI legacy/patents/profits are probably the main reason currently holding psychiatry from progressing and delivering some true cures.

 

[vulture]

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.

Any studies to share on the last?

 

[Elephanto]

MB has no other know mechanism (at the doses used in the human trials) except the stimulation of both Krebs cycle and ETC activity.

Nitric Oxide inhibition ? Considering NO induces mania, and simple Nitric Oxide inhibition produce similar results to NMDA antagonism.

nNOS inhibition promotes effects similar to those observed after NMDA antagonism [13,14].

Additionally, nNOS−/− mice exhibit reduced neurodegeneration after cerebral ischemia, which may be because of reduced glutamate excitotoxicity (15, 16).

 

[Soren]

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

Red light shined on the thyroid has been shown to completely heel the thyroid. Study posted on the forum somewhere showing that people dosing with red light could completely stop their thyroid medication.

 

[haidut]

Nitric Oxide inhibition ? Considering NO induces mania, and simple Nitric Oxide inhibition produce similar results to NMDA antagonism.

True, thanks for pointing it out. I guess it would depend on how much NO reduction MB can achieve in the 1mg-15mg doses used clinically on people with mental health issues.

 

[haidut]

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.

Was looking for the Peat quote on chronic stress causing thyroid failure and found it. Look at the last quote in the thread - the one talking about crocodiles.
Ray Peat The Comedian

 

[cs3000]

Gr8 find ty , so 90% of people with depression don't have enough T3 hormone, t3 is much lower in people with mild depression compared to controls - and moderate / severe depression shows lower t3 than mild depression too. 1 big key

(also you can see TSH is lower than control levels regardless of t3 being crashed, showing tsh alone is not useful)

response to giving people T4 instead of T3 varies because of individual conversion (mild aggravation to moderate improvement seen in 1 study, because t4 can fail to convert to T3 / go to rt3 instead. especially in illness where the body dampens t3 production). the t3 helps reverse depression & t4 if converts well (most people do well on t3:t4 combo it seems) [Administration of thyroid hormones in therapy of psychiatric illnesses] - PubMed
https://www.thieme-connect.com/products/ejournals/pdf/10.4103/1947-489X.210780.pdf


In particular, decreases in serum T4 and rT3 levels are often correlated to antidepressant response, suggesting that an effect on central thyroid hormone metabolism is involved in the as yet unknown mechanism of action of these therapies. Indeed, animal studies have shown that antidepressants do affect deiodinase activities and T3 and T4 concentrations in rat brain. However, the effects are highly area specific .

... Thyroid hormone regulates hippocampal subgranular zone (SGZ) progenitor survival and neuronal cell fate acquisition Adult neural stem cell fate is determined by thyroid hormone activation of mitochondrial metabolism prolonged hypothyroidism reduced not only neuroblast numbers but also their mitochondrial activity.
myelin + neurogenesis + mitochondria effect of thyroid increasing brain function?


thyroid hormone stimulates cellular energy production right away:

Thyroid hormone T3 creates immediate change in mitochondria function (respiration) , key for mitochondria producing cellular energy well. (thyroid function is key for mitochondria)
⦁ Transthyretin, carrying the thyroid hormone, enters the cell's mitochondria and nucleus (Azimova, et al., 1984, 1985). In the nucleus, it immediately causes generalized changes in the structure of chromosomes, as if preparing the cell for major adaptive changes. Respiratory activation is immediate in the mitochondria, but as respiration is stimulated, everything in the cell responds, including the genes that support respiratory metabolism.

⦁ 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.

Thyroid / igf-1 plays a role in myelin in the brain and neuroprotection / neurogenesis
which is another reason why thyroid helps with depression alongside the mitochondria boost

Hypothyroidism 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

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 seen

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

Found this womans articles on T3 well written:
Our tips and guides

⦁ 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.

--- what ive got to fix hypothyroid:
- pineapple juice daily https://www.researchgate.net/public...d_gland_and_attenuates_hyperlipidemia_in_rats
- 200g+ carbs
- 2400 calories 2000+
- Limit pufa intake to a few grams daily (<5g? need a couple) https://www.researchgate.net/public...FECTS_OF_PUFAS_POLYUNSATURATED_FATS_AND_HERBS
- ensure iron is good , heme iron polypeptide x2 spread 7hrs if not or infusion
- thyroid hormone product for initial 2 weeks to get thyroid & body functioning well: before sleep take 1:2 ratio T3:T4 6mcg t3. on wakeup 6-9 mcg t3 solo (or combo again). midday 1:2 T3:T4 6mcg t3. (test temperature under the tongue ~2 hours after dosing the morning & afternoon doses, see if good lvl). & after 2 weeks lower & stop , see if natty takes over from there
- ensure the baseline iodide & selneium needed is covered daily. 100mcg of iodide intake. and some selenium (80mcg?)
- eat coconut oil if salicylates tolerated (small temp boost, & increases expression of t3 receptors)

⦁ Since T3 has a short half life, it should be taken frequently. If the liver isn't producing a noticeable amount of T3, it is usually helpful to take a few micorgrams per hour. Since it restores respiration and metabolic efficiency very quickly, it isn't usually necessary to take it every hour or two, but until normal temperature and pulse have been achieved and stabilized, sometimes it's necessary to take it four or more times during the day. T4 acts by being changed to T3, so it tends to accumulate in the body, and on a given dose, usually reaches a steady concentration after about two weeks.
⦁ An effective way to use supplements is to take a combination T4-T3 dose, e.g., 40 mcg of T4 and 10 mcg of T3 once a day, and to use a few mcg of T3 at other times in the day. Keeping a 14-day chart of pulse rate and temperature allows you to see whether the dose is producing the desired response. If the figures aren't increasing at all after a few days, the dose can be increased, until a gradual daily increment can be seen
⦁ Coconut oil decreases the expression of prolactin receptors, and promote the expression of the T3 (thyroid) receptor .

ray peat has article on thyroid Thyroid: Therapies, Confusion, and Fraud
* actually ray said bound T3 is active so fT3 isnt the only count that counts

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.

 

[mostlylurking]

Would alcohol use really damage thyroid?

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.

 

[mostlylurking]

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.

Life interventions like environmental toxins, such as heavy metals, permanently damage the thyroid gland too.

 

[Blossom]

@mostlylurking