Is that at the massively higher dosages used for bipolar and schizophrenia - or also for the doses we are talking here for longevity which people are feeling and significantly lower - more like the impact of living higher lithium in drinking water from tap areas…?
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why are you taking telmisartan?
is the kidney injury dose dependent?
@Tim. Please read the following articles. The daily dose they discuss is 900 mg of Lithium daily. And they say at that level you need to worry about lithium toxicity.
I do believe that 5 mg daily should not cause lithium toxicity.
FDA administration guide below.
The orotate form contains much less lithium than the chemically processed versions and it is thought that is why it does not produce the same harsh reactions as lithium carbonate.1
Drug-free Lithium Alternatives | Learn about nutritional lithium orotate.
So 5 mg of orotate vs 300 mg of carbonate, the orotate seems perfectly safe.
In order to screen for kidney disease, they said to monitor creatinine and make sure it doesn’t go above 1.6. my creatinine is lower than the lowest bound (barely) so I may have super kidneys. 
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I think the kidney disease is caused by inhibition of the citrate transporter (probably SLC13A2 or SLC13A3). That’s why you want to keep the serum level really low.
As everyone else told you: this is for medical lithium (the first link you shared starts with: “Lithium is a common medicine used to help calm mood for treating people with mental disorders.”). So about 1g per day. Compared to 1,000 times less for what most people take as a supplement. Yes, one thousand.
@Jonas for hypertension. See: Optimal Blood Pressure we Should Target? Systolic Under 110 or 100? - #222 by adssx
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It is however, the serum level that drives the effect. For mental health the targeted level is about 1mmol/L which is on the threshold of toxic effects. 2mmol/L is probably toxic for most people. I am personally aiming for under 50 micromoles per litre which is about 20th of the serum concentration. I think people taking 1mg probably get around at a guess 20 micromoles which is about a 50th of the concentration.
the IC50 for SLC13 inhibition is I think around 2 millimolar.
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@Neo
I’m fairly sure that the studies involved therapeutic doses; i.e., higher than what posters here are taking. But if the substance accumulates, then long-term usage may be risky too. And if a person already had stage 3 or stage 4 kidney disease, then even modest doses would be contraindicated.
@Jonas
The papers I read didn’t say that the toxic effects are dose dependent, but it’s reasonable to assume that they are. But just the whisper, just the hint, of an association between the two was enough to give me pause.
@DeStrider
I’m probably being hyper-cautious, but I know how even small amounts of caffeine or alcohol can spike my BP and precipitate a sharp decline in my GFR. As it says on my medical chart, “Patient has a history of Acute Kidney Injury.”
@adssx
But the paper in Psychiatrist.com does say that “The lithium group presented more overall adverse events (P = .045), particularly interfering in daily activities (P < .001).”
Your second group of papers is intriguing: “In contrast, in experimental models of acute kidney injury and glomerular disease, lithium has antiproteinuric, kidney protective, and reparative effects.” I will need to study the question further. Thank you for digging.
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Looks like it’s not the case: Long-Term, Low-Dose Lithium Treatment Does Not Impair Renal Function in the Elderly: A 2-Year Randomized, Placebo-Controlled Trial Followed by Single-Blind Extension 2014.
Their definition of “low-dose” is still way higher than what people take here:
Patients received low doses of lithium salts (from 150 mg to 450 mg of lithium salts daily) to achieve sub-therapeutic lithium levels (target serum lithium level of 0,25 - 0,5 mEq/L). Lithium doses were administered twice a day. Lithium doses were titrated to achieve the target serum lithium levels within the first two weeks after study recruitment. After achieving the target serum lithium level, lithium salts doses remained stable until the end of the study.
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Interesting (not a great journal though): “In experimental AKI, lithium at small doses is able to ameliorate AKI and promote kidney repair.” (Rationale and Design of Assessing the Effectiveness of Short-Term Low-Dose Lithium Therapy in Averting Cardiac Surgery-Associated Acute Kidney Injury: A Randomized, Double Blinded, Placebo Controlled Pilot Trial 2021)
But they cite good journals:
- Delayed Administration of a Single Dose of Lithium Promotes Recovery from AKI 2014
- What we need to know about the effect of lithium on the kidney 2016: “In contrast, in experimental models of acute kidney injury and glomerular disease, lithium has antiproteinuric, kidney protective, and reparative effects. This paradox may be partially explained by lower lithium doses and short duration of therapy. While long-term exposure to higher psychiatric doses of lithium may be nephrotoxic, short-term low dose of lithium may be beneficial and ameliorate kidney and podocyte injury. […] Future studies are warranted to discover the exact “kidney-protective dose” of lithium and test the effects of low-dose lithium on acute and chronic kidney disease in humans.”
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@Tim If you don’t feel comfortable taking something, it’s best not to take it. It’s all a personal choice. No worries. 
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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 
) 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
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Do you want me to delete the post?