How to maximize fat loss and inhibit muscle loss best with clenbuterol and fasting?

[Reno911]

Well this has my vote for oddest thread in the last 6mo at least

Hmmm... Could be a toss up with the diarrhea GH one.

 

[SouthernMuscle]

He changed my name to Sally.

Oh boy, someone doesn‘t know the (fucking obvious) rule that you’re not allowed to edit quoted posts…….

 

[rollerghost]

He changed my name to Sally.

Pardon me It was typing error as I manually quoted texts when I tried to quote multiple different answers on to one post I could not find the 'quote' option to add them automatically. Only reply option to one person at a time.

Edit: Okey, now I saw that the reply option can do that. Next time will use that.

 

[SouthernMuscle]

Pardon me It was typing error as I manually quoted texts when I tried to quote multiple different answers on to one post I could not find the 'quote' option to add them automatically. Only reply option to one person at a time.

Edit: Okey, now I saw that the reply option can do that. Next time will use that.

 

[qbkilla]

I don't think personally excessive fasting has these magic anti cancer properties you have read it does. In my opinion a regular cutting diet or psmf is more healthy than extreme fasting.

 

[pesty4077]

Pardon me It was typing error as I manually quoted texts when I tried to quote multiple different answers on to one post I could not find the 'quote' option to add them automatically. Only reply option to one person at a time.

Edit: Okey, now I saw that the reply option can do that. Next time will use that.

Don't play dumb. You been here too long and should know how things work. You did it on purpose. First and last warning about changing people's names and words in quotes.

 

[rollerghost]

Don't play dumb. You been here too long and should know how things work. You did it on purpose. First and last warning about changing people's names and words in quotes.

Okey, warning taken but I am not sure what you know truly mean. I do not play dumb maybe I am dumb but no I did not know how things work. Yes I figured it now when I tried out and 'reply' button does the job so I was lazy and assumed too much but did not purposedly twist names but used copy paste and wrote names manually on my post.

I mean yes, I have been here long but have not actually been spending time here in the last 5 years and has written last maybe 10 years ago and I am used to forums where there is 'quote' button to add automatically many answers onto one post and I was in hurry when writing, didn't find that button and mistakenly assumed that 'reply' button is only applicable to one person at a time.

I should have taken more time to try it but no, if you are truly now assuming I did it purposedly that is just simply NOT true.

I am sorry about that.

 

[rollerghost]

I don't think personally excessive fasting has these magic anti cancer properties you have read it does. In my opinion a regular cutting diet or psmf is more healthy than extreme fasting.

Right. On the other hand fasting should deplete glucose and glutamine while simultaneously supressing igf-1 and insulin which carry them onto cells. So when most cancers heavily rely on glucose and glutamine preventing their transport should be very effective cancer prevention. That combined with increased autophagy can do very beneficial things and cancer cells in general die much sooner than normal cells when depleted from nutrients. By the time your ego feels like you are starving/dying cancer cells have propably been long gone. They are not so resistant to starvation as normal cells.

Personally I believe (partly on my experience) that on prolonged fast body or muscles/healthy lean tissue becomes very stubborn and resistant and uses adaptive mechanisms to protect itself as it does not want to die. If your mind can handle the stress your muscles can too as body actually does what the mind believes (muscle mind connection and so on).

Also some people report very good results with ketogenic diet regarding cancer treatment/prevention but ketogenic diet still lacks the benefits of increased autophagy and other things that pure fasting can offer.

It has been noted that fasting before and during chemotherapy also very well protects normal cells but allows cancer cells to die more effectively. It offers protection to brains too.

In my experience, regarding this last fast my stomach/esophagus inflammation signifacntly got better which was not obtainable through other routes. Also my blood pressure went onto level 120-130/70-80 and I stopped all my blood pressure medicines. Also other benefits I've noted.

But of course when you continue fast too long eventually also depletion from nutrients starts to weaken immune system and other negative consequences follow. There is certain golden middle way with that too to maximize positive effects it can offer.

 

[Sully1234]

*Accident

 

[Sully1234]

Oh boy, someone doesn‘t know the (fucking obvious) rule that you’re not allowed to edit quoted posts…….

Don't play dumb. You been here too long and should know how things work. You did it on purpose. First and last warning about changing people's names and words in quotes.

Ahh now I feel like a little narc bitch...

For the record he didnt change the text of what I said, that very easily could have been a typo - ie jittery fingers from the clen

 

[bbxtreme]

Ahh now I feel like a little narc bitch...

For the record he didnt change the text of what I said, that very easily could have been a typo - ie jittery fingers from the clen

If he did actually “re-type” all of those post… that’s some dedication right there.

 

[rollerghost]

Yes, it was typo accident.

Anyway, I started to think that actually combining low dose (or micro doses) of beta-antagonists with clenbuterol might prevent tolerance build up and extend the time it works effectively. Has anyone tried?

As it is quite universal phenomenon (at least to my limited knowledge) that substances at about 1/10th of their minimal therapeutic dose (either agonist or antagonist) exhibit reverse actions and act opposite to what they are mento to. Like ex. low dose or ultra low dose naltrexone increases opioid receptor sensitivity and pain tolerance and same with flumazenil regarding benzodiazepine receptors. And ex. Morphine if given micro doses actually worsens pain and works more like antagonist. Same principle seems to apply to many other substances or in general biological systems.

Also there is ex. Oxytrex which combains ultra low dose naltrexone with oxycontin and that combination effectively prevents tolerance development and agonist actions of oxy remain constant without need to increase dosage.

So if this is truly some universal phenomenom in biological systems then one could speculate that by using low doses or ultra low doses of beta2-antagonist concomitantly with clenbuterol or other beta-agonist it could possibly prevent tolerance development by sensitizing receptors enough without counteracting the effects of agonist to any significant degree.

I have used bisoprolol and propranolol with clenbuterol now and at least my doses of clen have been the same since I started it and it seems that there is no need to increase dosage because it is still working very well at the same dose after two weeks of use.

Maybe something like 0.1-1mg propranolol used 3-6 times a day could upregulate adrenergic receptors enough to prevent tolerance build up to agonist without inhibiting agonistic actions to any significant degree (like it is with flumazenil or ultra low dose naltrexone combined with agonists/opioids or benzos when they actually enhance the effectiviness of those agonist compounds).

At least beta-antagonists at normal therapeutic doses upregulate receptors in ex. heart tissue so at least in theory one could suppose ultra low doses does that too but without the inhibiting effects to agonistic ligands. Have to try this more and play with different doses of beta-antagonists with clen to find out if this adaptation and sensitazing of the system with ultra low doses truly is the case with adrenergic system too.

 

[SouthernMuscle]

Yes, it was typo accident.

Anyway, I started to think that actually combining low dose (or micro doses) of beta-antagonists with clenbuterol might prevent tolerance build up and extend the time it works effectively. Has anyone tried?

As it is quite universal phenomenon (at least to my limited knowledge) that substances at about 1/10th of their minimal therapeutic dose (either agonist or antagonist) exhibit reverse actions and act opposite to what they are mento to. Like ex. low dose or ultra low dose naltrexone increases opioid receptor sensitivity and pain tolerance and same with flumazenil regarding benzodiazepine receptors. And ex. Morphine if given micro doses actually worsens pain and works more like antagonist. Same principle seems to apply to many other substances or in general biological systems.

Also there is ex. Oxytrex which combains ultra low dose naltrexone with oxycontin and that combination effectively prevents tolerance development and agonist actions of oxy remain constant without need to increase dosage.

So if this is truly some universal phenomenom in biological systems then one could speculate that by using low doses or ultra low doses of beta2-antagonist concomitantly with clenbuterol or other beta-agonist it could possibly prevent tolerance development by sensitizing receptors enough without counteracting the effects of agonist to any significant degree.

I have used bisoprolol and propranolol with clenbuterol now and at least my doses of clen have been the same since I started it and it seems that there is no need to increase dosage because it is still working very well at the same dose after two weeks of use.

Maybe something like 0.1-1mg propranolol used 3-6 times a day could upregulate adrenergic receptors enough to prevent tolerance build up to agonist without inhibiting agonistic actions to any significant degree (like it is with flumazenil or ultra low dose naltrexone combined with agonists/opioids or benzos when they actually enhance the effectiviness of those agonist compounds).

At least beta-antagonists at normal therapeutic doses upregulate receptors in ex. heart tissue so at least in theory one could suppose ultra low doses does that too but without the inhibiting effects to agonistic ligands. Have to try this more and play with different doses of beta-antagonists with clen to find out if this adaptation and sensitazing of the system with ultra low doses truly is the case with adrenergic system too.

Got any literature to back any of this up?

 

[rollerghost]

Got any literature to back any of this up?

"This upregulation is subtype-specific, i.e., nonselective beta-blockers increase the density of both beta1- and beta2-adrenoceptors whereas beta1-selective antagonists upregulate only the former subtype"

Pharmacology of beta-blockers: classical aspects and recent developments - PubMed

All clinically used beta-blockers share the common feature of being competitive antagonists at beta-adrenoceptors. They differ, however, in additional pharmacological properties, such as beta1/beta2-selectivity ratios, presence or absence of intrinsic sympathomimetic activity (ISA), and/or local...

pubmed.ncbi.nlm.nih.gov

β-blockers Reverse Agonist-Induced β2-AR Downregulation Regardless of Their Signaling Profile

"Treatment with catecholamines causes β2-AR downregulation. To obtain the maximal receptor downregulation, HEK 293 cells stably expressing the N-terminus-FLAG-tagged β2-AR were incubated in the presence of 1 μM isoproterenol, a synthetic β-AR agonist catecholamine, at 37 °C per 3 h according to a previous study [14]. Approximately 40% of β2-ARs were downregulated in response to isoproterenol stimulation, but, upon adding of β-blockers, internalized receptors completely recycled back to the plasma membrane (Figure 2A). All the tested β-blockers showed equal efficacy in restoring receptor density regardless of their ancillary pharmacological properties."

β-blockers Reverse Agonist-Induced β2-AR Downregulation Regardless of Their Signaling Profile

Altered β-adrenergic receptor (β-AR) density has been reported in cells, animals, and humans receiving β-blocker treatment. In some cases, β-AR density is upregulated, but in others, it is unaffected or even reduced. Collectively, ...

www.ncbi.nlm.nih.gov

β-Blockade in Heart Failure: Basic Concepts and Clinical Results


"Although β-blocking agents without ISA would appear to have several advantages, such agents generally lead to an increase in the number and density of β-adrenergic receptors following short-term and long-term use. The significance of such upregulation is unknown. Although early studies suggested that upregulation helped to mediate the benefits of β-blockers in heart failure,[35]recent observations suggest that upregulation may be disadvantageous, because an increase in receptor density may limit the degree of sympathetic antagonism. Furthermore, β-receptor upregulation is believed to be responsible for the rebound phenomena that have been reported following the abrupt withdrawal of β-blockers in patients with ischemic heart disease"

β-Blockade in Heart Failure: Basic Concepts and Clinical Results

Both experimental and clinical observation suggest that activation of the sympathetic nervous system exerts an important deleterious effect in patient…

www.sciencedirect.com

"Propranolol (Prop) antagonized the antidepressant-like effects of clenbuterol (Clen) and dobutamine (Dob), but not that of desipramine (Des), in the forced-swim test in wild-type mice. Propranolol (2.5 mg/kg, i.p.) was given 15 min before clenbuterol (0.5 mg/kg, i.p.)"

https://www.researchgate.net/figure/Propranolol-Prop-antagonized-the-antidepressant-like-effects-of-clenbuterol-Clen-and_fig6_23385337

So about 5x dose of propranolol to clen seems to be approximately enough to antagonize its effects. That would mean 0.2mg of propranolol could antagonize 40ug clen but in my experience it needs to be a little bit higher. But based on studies and my own experiences I would say doses of 0.1-10mg taken at evening _might_ sensitize receptors enough and because of propranolol's short half-life (4-5h) and clenbuterol's long half-life if that low or ultra low dose of propranolol is taken only before bed its antagonizing effects are by morning mostly gone while clen is still high and what remains is that micro dose of antagonist circulating through the day and possibly sensitizing body to effects of clen without dumping its effects.

Or actually propranolol at micro doses might work as a fat burner (by similar logic as how naltrexone works for endorfins/pain or flumazenil to gaba density) by upregulating receptors but allowing adrenaline and other cathecholamines to work even more efficiently during the day. And also benefit is that you can sleep much better with clen with even those very low doses.

 

[SouthernMuscle]

"This upregulation is subtype-specific, i.e., nonselective beta-blockers increase the density of both beta1- and beta2-adrenoceptors whereas beta1-selective antagonists upregulate only the former subtype"

Pharmacology of beta-blockers: classical aspects and recent developments - PubMed

All clinically used beta-blockers share the common feature of being competitive antagonists at beta-adrenoceptors. They differ, however, in additional pharmacological properties, such as beta1/beta2-selectivity ratios, presence or absence of intrinsic sympathomimetic activity (ISA), and/or local...

pubmed.ncbi.nlm.nih.gov

β-blockers Reverse Agonist-Induced β2-AR Downregulation Regardless of Their Signaling Profile

"Treatment with catecholamines causes β2-AR downregulation. To obtain the maximal receptor downregulation, HEK 293 cells stably expressing the N-terminus-FLAG-tagged β2-AR were incubated in the presence of 1 μM isoproterenol, a synthetic β-AR agonist catecholamine, at 37 °C per 3 h according to a previous study [14]. Approximately 40% of β2-ARs were downregulated in response to isoproterenol stimulation, but, upon adding of β-blockers, internalized receptors completely recycled back to the plasma membrane (Figure 2A). All the tested β-blockers showed equal efficacy in restoring receptor density regardless of their ancillary pharmacological properties."

β-blockers Reverse Agonist-Induced β2-AR Downregulation Regardless of Their Signaling Profile

Altered β-adrenergic receptor (β-AR) density has been reported in cells, animals, and humans receiving β-blocker treatment. In some cases, β-AR density is upregulated, but in others, it is unaffected or even reduced. Collectively, ...

www.ncbi.nlm.nih.gov

β-Blockade in Heart Failure: Basic Concepts and Clinical Results


"Although β-blocking agents without ISA would appear to have several advantages, such agents generally lead to an increase in the number and density of β-adrenergic receptors following short-term and long-term use. The significance of such upregulation is unknown. Although early studies suggested that upregulation helped to mediate the benefits of β-blockers in heart failure,[35]recent observations suggest that upregulation may be disadvantageous, because an increase in receptor density may limit the degree of sympathetic antagonism. Furthermore, β-receptor upregulation is believed to be responsible for the rebound phenomena that have been reported following the abrupt withdrawal of β-blockers in patients with ischemic heart disease"

β-Blockade in Heart Failure: Basic Concepts and Clinical Results

Both experimental and clinical observation suggest that activation of the sympathetic nervous system exerts an important deleterious effect in patient…

www.sciencedirect.com

"Propranolol (Prop) antagonized the antidepressant-like effects of clenbuterol (Clen) and dobutamine (Dob), but not that of desipramine (Des), in the forced-swim test in wild-type mice. Propranolol (2.5 mg/kg, i.p.) was given 15 min before clenbuterol (0.5 mg/kg, i.p.)"

https://www.researchgate.net/figure/Propranolol-Prop-antagonized-the-antidepressant-like-effects-of-clenbuterol-Clen-and_fig6_23385337

So about 5x dose of propranolol to clen seems to be approximately enough to antagonize its effects. That would mean 0.2mg of propranolol could antagonize 40ug clen but in my experience it needs to be a little bit higher. But based on studies and my own experiences I would say doses of 0.1-10mg taken at evening _might_ sensitize receptors enough and because of propranolol's short half-life (4-5h) and clenbuterol's long half-life if that low or ultra low dose of propranolol is taken only before bed its antagonizing effects are by morning mostly gone while clen is still high and what remains is that micro dose of antagonist circulating through the day and possibly sensitizing body to effects of clen without dumping its effects.

Or actually propranolol at micro doses might work as a fat burner (by similar logic as how naltrexone works for endorfins/pain or flumazenil to gaba density) by upregulating receptors but allowing adrenaline and other cathecholamines to work even more efficiently during the day. And also benefit is that you can sleep much better with clen with even those very low doses.

Anything in there about the 1/10 dose stuff you were talking about

 

[rollerghost]

Anything in there about the 1/10 dose stuff you were talking about

Oh, I will need to check that tomorrow. It was one doctor who spoke about that issue. Now I need to go to sleep; I will find it for you tomorrow.

 

[rollerghost]

Anything in there about the 1/10 dose stuff you were talking about

Here is link for Oxytrex which utilizes that kind of principle of using ultra low dose naltrexone with oxycontin. Allthough the naltrexone dose is only 2-4ug when doses that act as an antagonist are usually in mg range but minimal antagonist dose of naltrexone which could cause withdrawals if one is addict is somewhere at 200ug, so that is basically the minimum working dose. So that 2-4ug it would then be more close to 1/50-1/100th of a dose but maybe the scale is more broader than 1/10 and can vary between 1/10 to 1/1000th or something but that doctor maybe generalized it to be usually approximately at about 1/10th.

Oxytrex Minimizes Physical Dependence While Providing Effective Analgesia: A Randomized Controlled Trial in Low Back Pain

Physical dependence or withdrawal is an expected effect of prolonged opioid therapy. Oxytrex (oxycodone + ultralow-dose naltrexone) is an investigatio…

www.sciencedirect.com

 

[SouthernMuscle]

Here is link for Oxytrex which utilizes that kind of principle of using ultra low dose naltrexone with oxycontin. Allthough the naltrexone dose is only 2-4ug when doses that act as an antagonist are usually in mg range but minimal antagonist dose of naltrexone which could cause withdrawals if one is addict is somewhere at 200ug, so that is basically the minimum working dose. So that 2-4ug it would then be more close to 1/50-1/100th of a dose but maybe the scale is more broader than 1/10 and can vary between 1/10 to 1/1000th or something but that doctor maybe generalized it to be usually approximately at about 1/10th.

Oxytrex Minimizes Physical Dependence While Providing Effective Analgesia: A Randomized Controlled Trial in Low Back Pain

Physical dependence or withdrawal is an expected effect of prolonged opioid therapy. Oxytrex (oxycodone + ultralow-dose naltrexone) is an investigatio…

www.sciencedirect.com

Uh ok. Seems like an ultra specific use and moa

 

[Tomgrass]

Thank you for resoponses.



No, I do not believe like that. I know some muscle will be burnt. But I agree walking might not be the best. Maybe only gym couple times a week.

Well you should say that earlier. Now solution is simple as f… 500 mg test plus a lot of protein and carbs low fat. You will regain all you lost so by increasing muscles you will loose bf just by changing ratio of tissue in your body plus regained tissue will speed up metabolism.


.

I am not really obese at all and have not talked&asked about this before. The thing is, that I have history of bodybuilding/strength training and was in my best at quite low body fat at about 240lbs/110kg. Broblem was that at some years ago I got interested in spiritual things but eventually my search and study of God/consciousness caused me quite severe depression for two years. That caused me to stop training totally, lost motivation to eat and do things and was in sickleave. So I lost both muscle and fat very much because of that, little bit more muscle, but in no way I am now obese but I am just a skinnier and little bit fatter version of my old self at about (weight before this fast) 85kg/190lbs and about 15% bodyfat (at 6 feet). So when I started to recover from my depression I got again motivation and energy to start training and eating but after training for a while I just decided I need to loose this extra fat first asap (partly because of health reasons) and then build muscle. I wanted to do it also because I wanted to get rid off sick cells/possible cancer cells and clean my body and lower my blood pressure etc (which actually went down to 120/72 after starting this fast even though I stopped all my three blood pressure medicines except bisoprolol&propranolol at night). But no obesity here.



Good advice. I might change to that in few days.



Yes, I might start that (or PSMF) in few days. What is that more extreme version like?

And thanks for reminding me yohimbine. That might be a good addition. Does topical yohimbine skin cream work? I think I will also increase test dose and see what it does in these conditions. Doesn't testosterone (or AAS in general) increase adrenergic receptor sensitivity in tissues? So increasing dose might boost effectivines of clen and speed up fat loss and inhibit muscle breakdown more and body would be forced to breakdown more other useless tissues including senescent/pathological cells?

 

[rollerghost]

Uh ok. Seems like an ultra specific use and moa

Might be, but on the other hand phenomenom has been noted quite generally with many neurotransmitter systems.

Adrenergic rebound is a known phenomenom after beta-antagonist use and propably involves receptor upregulation/increased sensitivity. Like some of the links I posted on previous message also stated.

Adrenergic hypersensitivity after beta-blocker withdrawal

Adrenergic hypersensitivity after beta-blocker withdrawal - PubMed

We investigated the possibility of a rebound increase in sympathetic response after stopping beta-blocker treatment by measuring heart rate under conditions of increased sympathetic drive, as provided by standing with vasodilatation, or the Valsalva manoeuvure. Significant rebound increases in...

pubmed.ncbi.nlm.nih.gov

Adrenergic hypersensitivity after beta-blocker withdrawal in hypertrophic cardiomyopathy

Adrenergic hypersensitivity after beta-blocker withdrawal in hypertrophic cardiomyopathy

Withdrawal of β-blocker therapy has been associated with the development of adrenergic hypersensitivity and adverse clinical effects in patients with …

www.sciencedirect.com

That law applies to many if not most systems like PPI:s (proton pump inhibitors), antihistamines, serotonin/dopamine/gaba/opioid antagonists and so on.

Ex.

Feasibility of reversing benzodiazepine tolerance with flumazenil

Feasibility of reversing benzodiazepine tolerance with flumazenil - PubMed

To examine whether the benzodiazepine antagonist flumazenil can reverse tolerance to benzodiazepines but without precipitating withdrawal seizures, the antiepileptic effect of flumazenil itself and its ability to reverse tolerance at a dose that would leave sufficient receptors free for the...

pubmed.ncbi.nlm.nih.gov

Intravenous flumazenil versus oxazepam tapering in the treatment of benzodiazepine withdrawal: a randomized, placebo-controlled study

Intravenous flumazenil versus oxazepam tapering in the treatment of benzodiazepine withdrawal: a randomized, placebo-controlled study - PubMed

Flumazenil (FLU), a benzodiazepine (BZD) partial agonist with a weak intrinsic activity, was previously found unable to precipitate withdrawal in tolerant subjects submitted to long-lasting BZD treatment. The potential use of FLU to treat BZD withdrawal symptoms has also been evaluated...

pubmed.ncbi.nlm.nih.gov

Also dopaminergic system is known to compensate and upregulate after antagonist use by creating eventually hyperdopaminergic state.

"Long-term administration of antipsychotics, through D2 receptor blockade, increases D2 receptor density in the striatum."

Antipsychotic-Induced Dopamine Supersensitivity Psychosis: Pharmacology, Criteria, and Therapy

Abstract. The first-line treatment for psychotic disorders remains antipsychotic drugs with receptor antagonist properties at D2-like dopamine receptors. However, long-term administration of antipsychotics can upregulate D2 receptors and produce receptor supersensitivity manifested by behavioral...

karger.com

Of course one cannot extrapolate this phenomenom to concern all possible receptor systems and it might be inverse agonists that are actually more helpful for reversing tolerance/upregulating receptors&sensitivity in general more than pure antagonists. As naltrexone is also partially inverse agonist and low dose naltrexone has been proven to be quite beneficial treatment by upregulating opioid system and decreasing inflammmation.

Also propranolol is inverse agonist like carvedilol so one could expect it to have receptor upregulating/sensitizing effects like other inverse agonists.

"A β-blocker does not simply “block” the receptor, but further inactivates receptor activity beyond its baseline value, depending on its degree of inverse agonist activity. Antagonists (at both β1-ARs and β2-ARs), such as metoprolol, carvedilol, propranolol, nebivolol, and bisoprolol, have shown inverse agonist activity."

Inverse agonism and its therapeutic significance

Inverse agonism and its therapeutic significance

A large number of G-protein-coupled receptors (GPCRs) show varying degrees of basal or constitutive activity. This constitutive activity is usually minimal in natural receptors but is markedly observed in wild type and mutated (naturally or induced) receptors. ...

www.ncbi.nlm.nih.gov

"Inverse agonist activity is of importance for β-AR regulation also. In chronic heart failure, β-ARs are downregulated due to chronic sympathetic activation. Inactivation of β-ARs by inverse agonists inhibits phosphorylation of receptors, and thus desensitization and downregulation. Strong inverse agonist, such as metoprolol, but not the weak inverse agonist carvedilol, leads to upregulation of ventricular β-AR density"

Propranolol is stronger inverse agonist than carvedilol.

I just feel like propranolol also might reduce tolerance development now as I've used it with clen (low doses only before bed). 10-15mg is enough to abolish the effects of 20ug of clen so it is too much for tolerance prevention purposes only. So that is why I said that 0.1-1mg could be a dose that upregulates receptors/sensitivity without preventing agonist activity to any significant degree at any timepoint and it was based on that doc's general statement (1/10th of a dose) which I yet could not find and partly on my own experience as 10mg is too much.