Lithium Supplementation

@Tim If you don’t feel comfortable taking something, it’s best not to take it. It’s all a personal choice. No worries. :slight_smile:

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Opinion piece by two neurologists at King’s College London: Lithium: balancing mental and renal health (full text here):

However, the effect of lithium on eGFR showed high inter-individual variation, and this pattern appears only significant for people taking lithium for >10 years. Of few CKD cases, 42% were definitively caused by lithium, with 25% partially attributable and 34% not attributable. Of the latter, half had not been exposed to lithium, and half of those exposed had lithium incorrectly recorded as CKD cause on medical records. Wrongful attribution of CKD as lithium-induced is concerning, as this appears to occur routinely, albeit infrequently.
Wrongful attribution of CKD as lithium-induced is concerning, as this appears to occur routinely, albeit infrequently.
The result about lithium exposure duration is important in helping to explain previously conflicting findings. Altogether, caution is warranted around long-term lithium use at ‘therapeutic’ levels.
As well as lithium’s potential to treat dementia (at low doses), there appears a clear case for low-dose lithium as a preventative intervention e.g., against cognitive decline8 (suicide and mood disorders are other examples).
The biological and clinical potential of trace (<~5mg/day) and micro (~5-20mg/day elemental lithium) doses require systematic investigation to verify the above claims in human studies. Prolonged exposure to low dose lithium could be one of several routes towards identifying how this environmental, bioavailable mineral could impart its magic effectively while averting chronic renal problems.

There are 3 levels of lithium levels (per this source):

  • Low lithium levels (<0.5 mEq/L)
  • Maintenance lithium levels (0.5–0.8 mEq/L)
  • Antimanic lithium levels (>0.8 mEq/L)

These two 2015 papers say:

  • Long-term effect of lithium maintenance therapy on estimated glomerular filtration rate in patients with affective disorders: a population-based cohort study: “Our analysis suggests no effect of stable lithium maintenance therapy (lithium levels in therapeutic range) on the rate of change in eGFR over time. Our results therefore contradict the idea that long-term lithium therapy is associated with nephrotoxicity in the absence of episodes of acute intoxication and that duration of therapy and cumulative dose are the major determinants of toxicity.”
  • Use of Lithium and Anticonvulsants and the Rate of Chronic Kidney Disease: A Nationwide Population-Based Study: “The conclusion from our study is in accordance with the Swedish case-control study concluding that modern lithium treatment within recommended serum levels between 0.6 and 0.8 mEq/L (to convert to millimoles per liter, multiply by 1.0) has eliminated the risk of lithium-induced end-stage renal disease, supporting the continued use of lithium as a safe drug for the long-term treatment of mood disorders. […] Our results indicate that bipolar disorder is associated with CKD independent of drug treatment. Additionally, in patients with bipolar disorder, CKD is associated not only with lithium but also with anticonvulsants, with the latter in fact being associated with increased end-stage CKD. In contrast, long-term maintenance treatment with lithium as practiced in Denmark during 2 recent decades with initial and regular monitoring of the serum creatinine level every 3 to 6 months and aiming for a serum lithium level of 0.6 to 0.8 mEq/L is not associated with end-stage CKD. It cannot be excluded that at least part of the associations between medication and CKD is a result of bias.”

So, I understand that according to at least one RCT and several longitudinal studies, there is no kidney risk with long-term use of low-dose lithium as long as you’re below 0.5 mEq/L (which requires 150 mg to 450 mg of lithium per day!). Even better, based on animal and experimental models, at these low doses, lithium might offer kidney protection.

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Caveat: not safe for pregnant women? Higher lithium levels in drinking water may raise autism risk | UCLA Health

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It seems there is some confusion here. Lithium citrate and hydroxycitric acid (HCA) are completely different compounds. Garcinia cambogia supplements are standardized to contain a high percentage of HCA, which is extracted from the fruit rind. HCA is considered to be the major active ingredient responsible for garcinia cambogia’s effects. I could not find any reputable sources indicating that lithium citrate is present in or extracted from Garcinia cambogia fruit. Lithium citrate is a pharmaceutical salt used in medications for bipolar disorder - it has no connection to garcinia cambogia. The paper you found claiming lithium citrate is the active ingredient of garcinia cambogia seems to be incorrect. All evidence points to HCA as the key active compound, not lithium.
Bottom line: Garcinia cambogia does not naturally contain or have added lithium.

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Thanks, I mean what made you chose telmisartan over other BP meds?

See the conversation I linked to and also this one for the rationale: Angiotensin II receptor blocker (ARB) experiences? - #25 by adssx

Let’s stick to lithium here.

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You are probably right. I simply thought having found something that was potentially vaguely relevant I should provide the link, but if it is a rubbish paper then I am happy to delele my post. Alternatively the post can remain, but with your comment and mine remaining as well.

I don’t mean to beat this to death, but based on the available evidence I could find, lithium citrate does not appear to be present in or extracted from Garcinia cambogia fruit.
The papers below analyze Garcinia cambogia fruit and its extract but do not mention lithium.
It is improbable that anyone could get significant amounts of lithium from Garcinia cambogia fruit.
I have looked at many papers (because I didn’t have anything better to do this morning :slightly_smiling_face:) concerning
Garcinia cambogia. I could not find one that mentioned lithium.
Phytochemical studies have revealed the presence of many elements in Garcinia cambogia, including:
Phenolic compounds
Saponins
Tannins
CaXanthones, such as carbogiol
Benzophenones, such as garcinol
Organic acids, such as HCA
Amino acids, such as gamma aminobutyric acid
Alkaloids
Flavanoids
rbohydrates
Proteins

https://www.sciencedirect.com/science/article/pii/S1878535221000708#:~:text=Among%20macro%20elements%2C%20K%20and%20Ca%20showed,>%20Ni60%2C%20and%20among%20essential%20trace%20elements

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Do you want me to delete the post?

@John_Hemming I think you should delete your post. :slight_smile:

This has now been done. ____________

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@adssx
I think it may be worth experimenting with. I don’t think 1-5 mg would hurt. @DeStrider found an immediate upside at 5 mg, while others are more comfortable with 1 mg. @desertshores is a longtime user and advocate. Of all the lithium salts out there, ororate may have the longest half-life, allowing low doses to accumulate in the brain. And it seems to have a significant number of life-enhancing properties. I’ll continue with my routine blood tests, but my physician probably won’t be involved in this experiment.

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This thread has been a fascinating read, thanks to @John_Hemming for starting it!

Leaving aside the mood and mental health benefits for a moment the protection of the brain and specifically dopaminergic neurons is incredibly exciting from a longevity perspective. Loss of dopaminergic neurons is a key limiter on longevity (not just for unlucky Parkinson’s sufferers) and if we can slow that it would be a huge benefit.

EDIT: Was trying to find the original article I read on dopaminergic neuron loss and aging years ago but couldn’t! An extract from this was similar though:

https://www.sciencedirect.com/science/article/abs/pii/S0047637499000640

"Dopamine neurons in the substantia nigra of human brains are known to be selectively vulnerable and neuronal loss with advancing age was estimated to be more than one third between the age of 20 and 90 years (McGeer et al., 1988). There is a linear fallout of dopamine neurons with aging at a rate of 5–10% per decade (Fearnley and Lees, 1991), and the limited number of the cells causes dysfunction in cognition and motor movement. "

The point of the article was that since we have this consistant loss of dopaminergic neurons with age if we live long enough all of us will develop Parkinson’s. If you think about all the effort people here go to to avoid CVD (rightly!) there should be equal effort to preserve dopaminergic neurons in order to preserve our cognitive and motor function into old age.

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Thanksz. Any other things with this goal for general dopa/neurological longevity you think we should consider for our playbook?

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can you expand on that? and studies?

I’m far from an expert so take what I say with a grain of salt but a good book on general brain health and nutrition is Brain Food by Lisa Mosconi who is fairly unique in having qualifications in both neuroscience and nutrition. It is non-technical and easy reading with practical advice.

Regarding specific chemicals caffeine appears to have strong protective effects on dopaminergic neurons and appears to help with Parkinson’s also:

Low dose lithium is protective as mentioned here as are anti-inflammatory drugs generally although I’m not saying you should chronically take anti-inflammatory drugs!

There are quite a few drugs in development which I am even further from being qualified to talk about but many drugs developed for preventing or slowing parkinson’s will target the dopaminergic neurons.

There are mixed opinions on rapamycin helping but I have hopes everolimus could have positive effects but I am very much wait and see on that…

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Some argue low dose selegiline is the way. I’m skeptical.

GLP1RA work but are they pro longevity as they increase insulin? SGLTi and telmisartan seem very promising (see the first paper here for instance: Parkinson's disease - #109 by adssx ). Then of course coffee (and smoking, if you don’t mind lung cancer…). There are also papers around glutathione but I’m skeptical and, if true, GlyNAC might do the job better. Many people are hopeful that immunosuppressants/immuno-modulators could work (there’s an ongoing RCT finishing soon). And autophagy enhancere (ongoing trials of Ambroxol, soon Urolithin A…). See more: Parkinson's disease - #108 by adssx I think that’s all we know so far… (other than healthy diet, good sleep hygiene, stress management, physical exercise, etc.)

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@Jonas,

See all the papers posted by @adssx.

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I’ve been taking 300 micrograms of lithium chloride drops for a few weeks now and haven’t really noticed anything. It should be similar to lithium from other sources like orotate right? I was happy to find 50 microgram drops so I could adjust my dose up slowly and make sure there’s no issues and I didn’t want to jump straight to 1 mg which was lowest regular dose I could find.

Is that a measurement of LiCl or elemental Li? li atomic mass is about 1/5 of cl.