Talk to me about raising testosterone levels in women?

[Nebula]

I don't feel the thyromix at all when I use it.

That could possibly be from high free fatty acids blocking thyroid’s entry into the cell. Small 20-30 mg doses of niacinamide every few hours along with carbs might be something worth trying. I’ve noticed a huge reduction in stress hormones from this and much better response from thyroid and progesterone. Large doses had the opposite effect.

 

[Blossom]

I’m No One (sorry I’m not able to tag you),
I’m a 52 y/o female-definitely post menopausal for about 5 years. I’ve used testosterone base for the past 3-4 years in microgram doses. At your age I’d definitely try to boost it by natural methods and balancing other hormones if possible. I was in a bad place and needed to desperately strengthen my uretogenital system and it worked. I still use it maybe once or twice a week. I literally only tried it out as a last ditch effort to avoid surgery which I’m glad to report I have done successfully so far. If I had ovaries still producing hormones though I probably would not have chosen to replace it directly. I only really had one bad day with it when I used too much of my husband’s androgel on accident before I obtained the base powder. I don’t know enough about it’s use in women to give any guidance but just wanted to share a bit of my experience.

 

[I'm.No.One]

That could possibly be from high free fatty acids blocking thyroid’s entry into the cell. Small 20-30 mg doses of niacinamide every few hours along with carbs might be something worth trying. I’ve noticed a huge reduction in stress hormones from this and much better response from thyroid and progesterone. Large doses had the opposite effect.

Thanks I'll dig into that.

I’m No One (sorry I’m not able to tag you),
I’m a 52 y/o female-definitely post menopausal for about 5 years. I’ve used testosterone base for the past 3-4 years in microgram doses. At your age I’d definitely try to boost it by natural methods and balancing other hormones if possible. I was in a bad place and needed to desperately strengthen my uretogenital system and it worked. I still use it maybe once or twice a week. I literally only tried it out as a last ditch effort to avoid surgery which I’m glad to report I have done successfully so far. If I had ovaries still producing hormones though I probably would not have chosen to replace it directly. I only really had one bad day with it when I used too much of my husband’s androgel on accident before I obtained the base powder. I don’t know enough about it’s use in women to give any guidance but just wanted to share a bit of my experience.

Thank you for sharing, yeah I figure actually taking testosterone should be the last thing I attempt after all else fails.

 

[sunny]

@Blossom , how do you take the Testosterone base powder?

 

[PeskyPeater]

Losartan or candesartan seems to have good restorative effect of the HPA. And niacinamide is the alternative for aspirin
Angiotensin II Inhibition Reduces Stress Sensitivity of Hypothalamo-Pituitary-Adrenal Axis in Spontaneously Hypertensive Rats

Angiotensin II type 1 (AT1) receptors are expressed within organs of the hypothalamo-pituitary-adrenal (HPA) axis and seem to be important for its stress responsiveness. Secretion of CRH, ACTH, and corticosterone (CORT) is increased by stimulation of AT1 receptors. In the present study, we tested whether a blockade of the angiotensin II system attenuates the HPA axis reactivity in spontaneously hypertensive rats. Spontaneously hypertensive rats were treated with candesartan (2 mg/kg), ramipril (1 mg/kg), or mibefradil (12 mg/kg) for 5 wk. In addition to baseline levels, CORT and ACTH responses to injection of CRH (100 μg/kg) were monitored over 4 h. mRNA of CRH, proopiomelanocortin, AT1A, AT1B, and AT2 receptors was quantified by real-time PCR. All treatments induced equivalent reductions of blood pressure and had no effect on baseline levels of CORT and ACTH. However, both candesartan and ramipril significantly reduced CRH-stimulated plasma levels of ACTH (−26 and −15%) and CORT (−36 and −18%) and lowered hypothalamic CRH mRNA (−25 and −29%). Mibefradil did not affect any of these parameters. Gene expression of AT1A, AT1B, and AT2 receptors within the HPA axis was not altered by any drug. We show for the first time that antihypertensive treatment by inhibition of AT1 receptors or angiotensin-converting enzyme attenuates HPA axis reactivity independently of blood pressure reduction. This action is solely evident after CRH stimulation but not under baseline conditions. Both a reduced pituitary sensitivity to CRH and a down-regulation of hypothalamic CRH expression have the potential to reduce HPA axis activity during chronic AT1 blockade or angiotensin-converting enzyme inhibition.

 

[Blossom]

@Blossom , how do you take the Testosterone base powder?

I use it topically diluted in dmso.

 

[I'm.No.One]

Losartan or candesartan seems to have good restorative effect of the HPA. And niacinamide is the alternative for aspirin
Angiotensin II Inhibition Reduces Stress Sensitivity of Hypothalamo-Pituitary-Adrenal Axis in Spontaneously Hypertensive Rats

Angiotensin II type 1 (AT1) receptors are expressed within organs of the hypothalamo-pituitary-adrenal (HPA) axis and seem to be important for its stress responsiveness. Secretion of CRH, ACTH, and corticosterone (CORT) is increased by stimulation of AT1 receptors. In the present study, we tested whether a blockade of the angiotensin II system attenuates the HPA axis reactivity in spontaneously hypertensive rats. Spontaneously hypertensive rats were treated with candesartan (2 mg/kg), ramipril (1 mg/kg), or mibefradil (12 mg/kg) for 5 wk. In addition to baseline levels, CORT and ACTH responses to injection of CRH (100 μg/kg) were monitored over 4 h. mRNA of CRH, proopiomelanocortin, AT1A, AT1B, and AT2 receptors was quantified by real-time PCR. All treatments induced equivalent reductions of blood pressure and had no effect on baseline levels of CORT and ACTH. However, both candesartan and ramipril significantly reduced CRH-stimulated plasma levels of ACTH (−26 and −15%) and CORT (−36 and −18%) and lowered hypothalamic CRH mRNA (−25 and −29%). Mibefradil did not affect any of these parameters. Gene expression of AT1A, AT1B, and AT2 receptors within the HPA axis was not altered by any drug. We show for the first time that antihypertensive treatment by inhibition of AT1 receptors or angiotensin-converting enzyme attenuates HPA axis reactivity independently of blood pressure reduction. This action is solely evident after CRH stimulation but not under baseline conditions. Both a reduced pituitary sensitivity to CRH and a down-regulation of hypothalamic CRH expression have the potential to reduce HPA axis activity during chronic AT1 blockade or angiotensin-converting enzyme inhibition.

Thank you so much for this!

I wonder though can niacinamide be used alongside aspirin safely?

Aspirin has been so insanely effective at reducing my serotonin levels I'd almost be nervous not to use it at this point.

 

[PeskyPeater]

Thank you so much for this!

I wonder though can niacinamide be used alongside aspirin safely?

Aspirin has been so insanely effective at reducing my serotonin levels I'd almost be nervous not to use it at this point.

I'm not sure. There is some risk with niacinamide at higher dosage of 50mg affecting the enzymes that breakdown catecholamines and serotonin but I don't know if this affects aspirin effects. Eventually the body becomes better at breaking down serotonin.
I suppose it's oke with normal use of aspirin. It is great at inhibiting prostaglandins and inflammation too, I know. I couldn't live without it when I was heavily affected by PUFA release. Ginger root is also good for that and against serotonin.

 

[I'm.No.One]

I'm not sure. There is some risk with niacinamide at higher dosage of 50mg affecting the enzymes that breakdown catecholamines and serotonin but I don't know if this affects aspirin effects. Eventually the body becomes better at breaking down serotonin.
I suppose it's oke with normal use of aspirin. It is great at inhibiting prostaglandins and inflammation too, I know. I couldn't live without it when I was heavily affected by PUFA release. Ginger root is also good for that and against serotonin.

I taxe 325mg x 3 daily, so for sure no mega doses.

I'm super sensitive to B's so I'll be starting insanely slow with the niacinamide that's for sure.

Maybe I'll find a good low balance for both of them & see how that goes.

I'm guessing my serotonin levels being jacked up are more from my chronic stress vs the small amount of PUFA I ate before going pro-metabolic.

Before I even knew what PUFAs we're I never trusted cooking oil, grew up on lard/butter kinda deal. Although they were for sure hiding in the processed foods I ate in my 20s.

I'll start adding more ginger to my various adrenal cocktails

 

[PeskyPeater]

That's a nice dosage of aspirin, personally I prefer 100mg daily maintenance dose. Yeah high serotonin and probably also estrogen. Very fortunate that you are not spoon fed too much PUFA. I think I got most of the PUFA too when I started living by myself, yikes, ouch. Took me a couple of years before I found Dr Peat, thankfully. It explained why the salmon and mackerel never worked well for me and my inflammation.

The niacinamide is taken up by the stomach and small intestine fairly quickly. I think it's best to take the first dose with lunch, so you already have fuel etc in the system from breakfast to support more energy going into the mitochondria.

I think in your case this sensitivity to B vitamins could be driven by excessive glutamic activity. Then a simple tea of chamomile (apigenin) could help to reduce this via lowering NMDA activity in overactive HPA. For some chamomile can give side effects, then there is dysfunction in the calming GABA complex, but niacinamide works like GABA, so it could work out as a good combo. And of course magnesium. [edit] Some moderate use of licorice also has glutamate reducing effects.
See below for the connection:

Abstract​

Chronic stress stimulates corticotrophin-releasing hormone (CRH)–expressing neurons in the paraventricular nucleus (PVN) of the hypothalamus and leads to hypothalamic-pituitary-adrenal (HPA) axis hyperactivity, but the mechanisms underlying this action are unknown. Because chronic stress enhances N-methyl-D-aspartate receptor (NMDAR) activity in various brain regions, we hypothesized that augmented NMDAR activity contributes to the hyperactivity of PVN-CRH neurons and the HPA axis in chronic stress. We performed whole-cell patch-clamp recordings on PVN-CRH neurons expressing CRH promoter-driven enhanced green fluorescent protein in brain slices from rats exposed to chronic unpredictable mild stress (CUMS) and unstressed rats. CUMS rats had significantly higher expression levels of the NMDAR subunits GluN1 in the PVN than unstressed rats. Furthermore, puff NMDA-elicited currents, evoked NMDAR currents, and the baseline frequency of the miniature excitatory postsynaptic currents (mEPSCs) in PVN-CRH neurons were significantly larger in CUMS rats than in unstressed rats. The NMDAR-specific antagonist 2-amino-5-phosphonopentanoic acid (AP5) significantly decreased the frequency of mEPSCs of PVN-CRH neurons in CUMS rats but did not change the frequency or amplitude of mEPSCs in unstressed rats. Bath application of AP5 normalized the elevated firing activity of PVN-CRH neurons in CUMS rats but not in unstressed rats. In addition, microinjection of the NMDAR antagonist memantine into the PVN normalized the elevated corticosterone (CORT) levels in CUMS rats to the levels in unstressed rats, but did not alter CORT levels in unstressed rats. Our findings suggest that synaptic NMDAR activity is enhanced in CUMS rats and contributes to the hyperactivity of PVN-CRN neurons and the HPA axis.
Enhanced Hypothalamic NMDA Receptor Activity Contributes to Hyperactivity of HPA Axis in Chronic Stress in Male Rats

Abstract​

Using the patch-clamp technique, we studied the modulation of ionotropic gamma-aminobutyric acid (GABA) and glutamate neurotransmission by apigenin, a flavonoid with sedative and antidepressant activity. Apigenin reversibly reduced GABA-evoked currents mediated by alpha1beta2gamma2 receptors expressed in HEK293 cells. Amplitude and frequency of spontaneous postsynaptic inhibitory currents (sIPSCs) mediated by GABA(A) receptors were also decreased by apigenin in cultured cortical neurons. The flavonoid was almost inactive on alpha-amino-3-hydroxy-5-methylisoxazolepropionic acid (AMPA) mediated currents while it reduced N-methyl-D-aspartate (NMDA) receptor mediated responses with a half maximal inhibiting concentration (IC50) of 10 microM. The flavonoid inhibited also peak amplitude and frequency of spontaneous postsynaptic excitatory currents (sEPSCs). Finally, apigenin is neuroprotective against glutamate-induced neurotoxicity in cerebellar and cortical neurons in culture. Our data reveal the antagonistic effect of apigenin on GABA and NMDA channels. While the inhibition on GABA receptor cannot explain the effects of the drug in vivo our data on NMDA channels reveal a new target of apigenin. A reduction of the network excitability could thus account for the sedative effects. Furthermore, our data suggest a potential neuroprotective activity of apigenin.
Apigenin modulates GABAergic and glutamatergic transmission in cultured cortical neurons - PubMed

 

[I'm.No.One]

That's a nice dosage of aspirin, personally I prefer 100mg daily maintenance dose. Yeah high serotonin and probably also estrogen. Very fortunate that you are not spoon fed too much PUFA. I think I got most of the PUFA too when I started living by myself, yikes, ouch. Took me a couple of years before I found Dr Peat, thankfully. It explained why the salmon and mackerel never worked well for me and my inflammation.

The niacinamide is taken up by the stomach and small intestine fairly quickly. I think it's best to take the first dose with lunch, so you already have fuel etc in the system from breakfast to support more energy going into the mitochondria.

I think in your case this sensitivity to B vitamins could be driven by excessive glutamic activity. Then a simple tea of chamomile (apigenin) could help to reduce this via lowering NMDA activity in overactive HPA. For some chamomile can give side effects, then there is dysfunction in the calming GABA complex, but niacinamide works like GABA, so it could work out as a good combo. And of course magnesium. [edit] Some moderate use of licorice also has glutamate reducing effects.
See below for the connection:

Abstract​

Chronic stress stimulates corticotrophin-releasing hormone (CRH)–expressing neurons in the paraventricular nucleus (PVN) of the hypothalamus and leads to hypothalamic-pituitary-adrenal (HPA) axis hyperactivity, but the mechanisms underlying this action are unknown. Because chronic stress enhances N-methyl-D-aspartate receptor (NMDAR) activity in various brain regions, we hypothesized that augmented NMDAR activity contributes to the hyperactivity of PVN-CRH neurons and the HPA axis in chronic stress. We performed whole-cell patch-clamp recordings on PVN-CRH neurons expressing CRH promoter-driven enhanced green fluorescent protein in brain slices from rats exposed to chronic unpredictable mild stress (CUMS) and unstressed rats. CUMS rats had significantly higher expression levels of the NMDAR subunits GluN1 in the PVN than unstressed rats. Furthermore, puff NMDA-elicited currents, evoked NMDAR currents, and the baseline frequency of the miniature excitatory postsynaptic currents (mEPSCs) in PVN-CRH neurons were significantly larger in CUMS rats than in unstressed rats. The NMDAR-specific antagonist 2-amino-5-phosphonopentanoic acid (AP5) significantly decreased the frequency of mEPSCs of PVN-CRH neurons in CUMS rats but did not change the frequency or amplitude of mEPSCs in unstressed rats. Bath application of AP5 normalized the elevated firing activity of PVN-CRH neurons in CUMS rats but not in unstressed rats. In addition, microinjection of the NMDAR antagonist memantine into the PVN normalized the elevated corticosterone (CORT) levels in CUMS rats to the levels in unstressed rats, but did not alter CORT levels in unstressed rats. Our findings suggest that synaptic NMDAR activity is enhanced in CUMS rats and contributes to the hyperactivity of PVN-CRN neurons and the HPA axis.
Enhanced Hypothalamic NMDA Receptor Activity Contributes to Hyperactivity of HPA Axis in Chronic Stress in Male Rats

Abstract​

Using the patch-clamp technique, we studied the modulation of ionotropic gamma-aminobutyric acid (GABA) and glutamate neurotransmission by apigenin, a flavonoid with sedative and antidepressant activity. Apigenin reversibly reduced GABA-evoked currents mediated by alpha1beta2gamma2 receptors expressed in HEK293 cells. Amplitude and frequency of spontaneous postsynaptic inhibitory currents (sIPSCs) mediated by GABA(A) receptors were also decreased by apigenin in cultured cortical neurons. The flavonoid was almost inactive on alpha-amino-3-hydroxy-5-methylisoxazolepropionic acid (AMPA) mediated currents while it reduced N-methyl-D-aspartate (NMDA) receptor mediated responses with a half maximal inhibiting concentration (IC50) of 10 microM. The flavonoid inhibited also peak amplitude and frequency of spontaneous postsynaptic excitatory currents (sEPSCs). Finally, apigenin is neuroprotective against glutamate-induced neurotoxicity in cerebellar and cortical neurons in culture. Our data reveal the antagonistic effect of apigenin on GABA and NMDA channels. While the inhibition on GABA receptor cannot explain the effects of the drug in vivo our data on NMDA channels reveal a new target of apigenin. A reduction of the network excitability could thus account for the sedative effects. Furthermore, our data suggest a potential neuroprotective activity of apigenin.
Apigenin modulates GABAergic and glutamatergic transmission in cultured cortical neurons - PubMed

Funny, I drink chamomile daily & have since I was a teen.

I had planned to use it in the afternoon & to eat it with lot's of carbs for sure.

 

[Baleia]

@Blossom, do you mind sharing how much is your microdose, also, what type of T?

 

[Blossom]

@Blossom, do you mind sharing how much is your microdose, also, what type of T?

I was using about 300 mcg of testosterone base in dmso applied topically to my lower abdomen. I haven’t needed it much recently. I actually can’t remember when I used it last but I did benefit from it for several years through my transition into menopause.

 

[CMPnutrition]

I was using about 300 mcg of testosterone base in dmso applied topically to my lower abdomen. I haven’t needed it much recently. I actually can’t remember when I used it last but I did benefit from it for several years through my transition into menopause.

@Blossom Hi!. Thanks for sharing your experience. I just found this thread. I am a 52 yo woman about 5 yrs post menopausal as well and just in the last year I have lost a drastic amount of muscle especially in my arms which used to be very muscular. All this since going Peat I used to be paleo and PUFA and had great muscle tone, so not sure how or why this is happening perhaps estrogen getting liberated from my tissues? Anyway would you possible mind sharing where you got the T base? I went on purple panda labs that was suggested on this thread and there are several options. I used to take 1mg T troches and really did pretty well on that but that was years ago and I am in a different place metabolically now. If topical is better I would go that route.
Did you notice any benefit from muscle mass for you ? I am a small woman and used to looked somewhat toned on my upper body never in my legs tho and now I just look more like skinny fat regardless of my training. Would love to know if you had good experience with T that way too.

 

[Blossom]

@Blossom Hi!. Thanks for sharing your experience. I just found this thread. I am a 52 yo woman about 5 yrs post menopausal as well and just in the last year I have lost a drastic amount of muscle especially in my arms which used to be very muscular. All this since going Peat I used to be paleo and PUFA and had great muscle tone, so not sure how or why this is happening perhaps estrogen getting liberated from my tissues? Anyway would you possible mind sharing where you got the T base? I went on purple panda labs that was suggested on this thread and there are several options. I used to take 1mg T troches and really did pretty well on that but that was years ago and I am in a different place metabolically now. If topical is better I would go that route.
Did you notice any benefit from muscle mass for you ? I am a small woman and used to looked somewhat toned on my upper body never in my legs tho and now I just look more like skinny fat regardless of my training. Would love to know if you had good experience with T that way too.

Unfortunately a male friend from this forum mailed me the testosterone base but I can ask him where he got it and let you know.
It sounds like we have a similar history. Testosterone did really seem to be one of a couple key things that helped me restore muscle mass. I also added a weighted vest to my walks at @10% of my body weight which I’m sure helped as well. I haven’t been using it recently and seem to be maintaining pretty decently although I wouldn’t hesitate to use it again if I felt I needed it. Right now I’m in the process of awaiting labs to see how I’d like to proceed. My goal is just to maintain my strength and functioning as I age and not necessarily mimic the sex hormone profile of a premenopausal woman if that makes sense? With that said I’m still interested in what if anything my body is producing.

 

[frannybananny]

I do not know. I have taken boron for years without any kidney issues. Walter Last writes about borax. As I recall, he indicated that it was very safe. You might find something in his writing to help with your question.

https://mmsinfo.org/misc/The_Borax_Conspiracy-by_Walter_Last.pdf

That is such interesting information! Thanks for the link, I have saved it and plan on taking my boron/borax again. I have been a believer for a long time but have been lax.

 

[frannybananny]

@Blossom Hi!. Thanks for sharing your experience. I just found this thread. I am a 52 yo woman about 5 yrs post menopausal as well and just in the last year I have lost a drastic amount of muscle especially in my arms which used to be very muscular. All this since going Peat I used to be paleo and PUFA and had great muscle tone, so not sure how or why this is happening perhaps estrogen getting liberated from my tissues? Anyway would you possible mind sharing where you got the T base? I went on purple panda labs that was suggested on this thread and there are several options. I used to take 1mg T troches and really did pretty well on that but that was years ago and I am in a different place metabolically now. If topical is better I would go that route.
Did you notice any benefit from muscle mass for you ? I am a small woman and used to looked somewhat toned on my upper body never in my legs tho and now I just look more like skinny fat regardless of my training. Would love to know if you had good experience with T that way too.

You can take HMB to prevent losing any more muscle. Please research first.

 

[frannybananny]

I think if you make sure you are getting 2000 mg or more of calcium each day and eat something starchy every 3 hours or so that would really help lower your stress.

I knew several young women who regularly took aspirin recommended by their physician. They could not lose weight and were not less stressed than their peers. I think aspirin is helpful on occasion but not daily.

Please don't recommend that people take that much calcium... it could just go into their soft tissue and cause different cancers like breast cancer depending on other deficiencies in their bodies. Be careful of what you recommend. Please do your own research folks.