EstroBan - Liquid Vitamin (K, A, D, E) Mix

Would you buy custom, liquid suplement with the 4 fat-soluble vitamins (K2, A, D, E)?

  • No

    Votes: 14 3.7%
  • Only if it costs less than $50 for 30 days supply

    Votes: 36 9.5%
  • Only if it costs less than $40 for 30 days supply

    Votes: 31 8.2%
  • Only if it costs less than $30 for 30 days supply

    Votes: 105 27.8%
  • Only if it costs less than $20 for 30 days supply

    Votes: 111 29.4%
  • Only if it costs less than $10 for 30 days supply

    Votes: 81 21.4%

  • Total voters
    378

Amazoniac

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0.01%, the reason to put 'supplementation' before 'diet' in the graph above from the previous post* is for a worst scenario, antecipating the claim that some people are blessed in disguise: incapable of cleaving macabrotenes into poisons. I forgot to point out that the added horizontal line is for the 0.1 umol PA / g liver.

*I'm not falling for it anymore, last post was #780 (20/20), which means that this one should be on a new page.

Regarding the dietary component, the contribution is predictable when preformed:

- Genetic Variations Associated with Vitamin A Status and Vitamin A Bioavailability

"A recent analysis of the results of 11 studies in eight developed countries (representing ≈ 120,000 participants) has shown that preformed VA intake accounted for about 65% of total VA intake, while provitamin A carotenoids represented 35% of total VA intake (βC: 86%; α-carotene: 10%; β-cryptoxanthin: 4% thereof, respectively) [13]."​

You know that hypothyroidism and diabetes are associated with poor cleavage of macabrotenoids and macabrotenemia, it can be tempting to supplement the preformed toxin liberally presuming that the body is too pure, but what can be perplexing is that liver reserves of poison A are particularly elevated in these conditions as well (detected through biopsy; open Grant's thread or any anesthesiology book for more details , part or all there)) Perhaps the excess stores is one factor downregulating cleavage on purpose.

In terms of genetic variations that affect proteins function, we is usually concentrated on the main carotenoid oxygenase (that cleaves centrally), but alterations can occur at other levels of poison A metabolism and are overlooked. It's possible to have more of them occuring together with a counteracting effect on status. Example from the link:

"Kovarova et al. [94] showed that an SNP in PNPLA3, a gene involved in the mobilization of retinyl esters stored in stellate cells [64], was associated with increased RP liver storage in a group of 42 patients undergoing liver surgery. Interestingly, the minor allele of the SNP is highly prevalent in populations from Latin American (about 70%), whereas it is found at a much lower frequency (around 20%) in populations from Europe and Africa [95]. We suggest that the effect of this SNP could be due both to a lower hydrolysis of liver RP, but also to a lower hydrolysis of intracellular triglycerides that solubilize RP. Indeed, it has been demonstrated that a loss-of-function mutation in PNPLA3 impairs triglyceride hydrolysis [65] and promotes intracellular lipid accumulation by reducing the lipidation of VLDL [96]. Furthermore this mutation, as well as mutations in ATGL, which is the other lipase known to hydrolyze both RP and triglycerides [63], are genetic determinants of chronic liver diseases [97,98,99]."

"For the time being, there are only three studies dedicated to identifying genetic variations associated with postprandial blood VA concentration (Table 1)." "These studies were dedicated to βC metabolism and measured either postprandial chylomicron βC [113] or postprandial triglyceride-rich lipoprotein βC and RP concentrations [114,115] after test meals that provided βC."


Just like before, a poor cleaver may be a poor mobilizer too, and there's no need to invoke genes.

Despite being inferior, it remains possible to derive poisonoids from macabrotenes when the main enzyme fails. I'm bringing this up because there are various factors to consider that can be conflicting.
- Knockout of the Bcmo1 gene results in an inflammatory response in female lung, which is suppressed by dietary beta-carotene

- Challenges to Quantify Total Vitamin Activity: How to Combine the Contribution of Diverse Vitamers?

"Vast discrepancy exists between conversion factors reported for different foods and across settings (44, 45). A relatively small number of studies have attempted to assess the conversion factor of β-carotene from an oil-based matrix to retinol, which overall ranged from 2.1 to 3.8. Conversion factors are expressed as the amount (μg) of ingested provitamin A required to form 1 μg of retinol. Until 2001, the average conversion factor of β-carotene from food was considered to be 6, whereas it was 12 for other provitamin A carotenoids. This difference was based on chemical structure, which allows central cleavage of β-carotene to produce 2 retinol molecules, whereas α-carotene and β-cryptoxanthin will only yield 1 retinol molecule. This has resulted in reporting of provitamin A concentrations as retinol equivalents (REs) in food composition tables, taking these conversion factors into account. Based on a range of studies conducted at the end of the previous century [IIIIIIIIIIIIIIIIIII], conversion factors for specific fruits and vegetables were shown to vary from 3 to 12 for tubers and fruits, and from 10 to 77 for cooked and raw vegetables (not including tubers) (44, 45). This prompted the Institute of Medicine in the United States to increase the conversion factors to 12 for β-carotene and 24 for other provitamin A carotenoids (RAEs). This was based on food patterns estimated to deliver ∼20% of provitamin A carotenoids from fruit and ∼80% from vegetables, thereby weighing conversion factors for vegetables more heavily than for fruit. Although many countries have followed suit by using the RAE rather than RE in their national food composition tables and nutrient intake recommendations, the WHO has not yet renewed its intake recommendations published in 2004 and therefore still uses the outdated RE (46). Even so, the revised vitamin A intake recommendations for Europe by the European Food Safety Authority in 2015 retained the old conversion factors (47). This is confusing for anyone trying to assess adequacy of dietary vitamin A intake, and especially relevant for populations with a high dependency on provitamin A intake to fulfill their vitamin A requirements (48)."​

Generalizing, the consumption of animal products here is high and the plant pattern is the opposite, with lots of fruits. If a person counts on nutrition apps' estimations for poisonol activity, the efficiency of conversion may be underestimated.

Stunts are not uncommon (such as 120 mg of b-macabrotene) and can be misleading:

- A review of vitamin A equivalency of b-carotene in various food matrices for human consumption

"The fourteen reported VEB measured with labelled b-carotene in oil, presented in Table 2, have a wide range from 2·0:1(54) (healthy children) to 55:1(65) (in one female adult after a pharmaceutical dose of 126 mg b-carotene). In this latter study, a VEB of 3·8:1 was obtained after a labelled dose of 6 mg b-carotene given to the same female subject over 21 d(65). In another study in one male adult, the VEB was 15·9:1 after a very high dose of 16·2mg b-carotene over 23 d(69). These large variations in VEB stress the importance of carrying out experiments to measure VEB using physiological doses of b-carotene."​

And you'll come across more questionable stuff:

- Variability in conversion of β-carotene to vitamin A in men as measured by using a double-tracer study design

"We found that 11 healthy men having a vitamin A status that was neither deficient nor toxic could be grouped as 6 responders and 5 low responders to D6 β-carotene. We had previously found 5 responders and 6 low responders among 11 healthy women (7). In the present study, the 2 responders (subjects 3 and 8) with the highest prestudy intakes of vitamin A (10797 and 9283 IU/d) and β-carotene (6.4 and 4.05 μmol/d) within their group had the lowest absorption of D6 β-carotene and the smallest bioconversion to D3 retinol. Furthermore, the 3 low responders (subjects 6, 11, and 12) with prestudy intakes of vitamin A (47171, 46363, and 68828 IU/d) and β-carotene (34.30, 19.33, and 46.73 μmol/d) far above the recommended dietary allowance may have down-regulated the activity of their β,β-carotene 15,15′-dioxygenase. It may be that, except for subjects 2 and 9, a prestudy intake of vitamin A of ≈15000 IU/d and of β-carotene of ≈20 μmol/d is sufficient to set the vitamin A activity of β-carotene to approximately zero in men fed a mixed diet."​

Thankfully some were low responders.

We need to use our privilege to protect people as much as we possibly can, how can you not see this? Because if we don't, who will? What we may need is a reformulation and I think that the suggestion to reduce the dose is not unfounded.

In food experiments, they get the average response, which will include the low responders; nonresponders must be rare. Preformed poison A can be assigned to cover the minimum effective dose while the rest is left for macabrotenoids, they is safer in uncertainty of excess. Since most of the requirement will be taken care of by poisonol, a person won't need exorbitant amounts of macabrotenes to make up for an inefficiency.

Various of these links were shared elsewhere on the forum.
 

Amazoniac

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From the macabrotenoid thread:

- Spinach or carrots can supply significant amounts of vitamin A as assessed by feeding with intrinsically deuterated vegetables

"Our study, which used intrinsically labeled spinach and carrots, showed that vegetable provitamin A carotenoids can provide vitamin A to humans through the conversion of β-carotene and other provitamin A carotenoids (eg, α-carotene) to retinol. Our results showed that the yield of retinol was 21 ± 11 nmol · d per μmol β-carotene (trans β-carotene equivalents) in 14 subjects who received a spinach dose and 32 ± 16 nmol · d per μmol β-carotene for 7 male subjects who received a carrot dose over a 21-d period. Both the spinach and carrot doses were puréed and given to the subjects with a standard liquid diet containing 13.5 g fat. Because of puréeing, we believe that the physical form of each food would be similar and does not explain the difference in the conversion factors seen between spinach and carrot. Therefore, the difference between spinach and carrots was likely due to the food matrix: the β-carotene in spinach leaves is in the form of pigment proteins (31) located in chloroplasts, whereas the β-carotene in carrot is in the form of carotene crystals in chromoplasts (32). Our results also showed that carrots are generally better than spinach at providing carotenes as well as vitamin A (except in one subject, in whom carrot and spinach yielded equal amounts of β-carotene and vitamin A). Thus, it seems that carrot β-carotene crystals in chromoplasts are more easily released during digestion in the gastrointestinal tract than is spinach β-carotene in chloroplasts. It was reported that the addition of dietary fiber (soluble pectin or guar, not cellulose or wheat bran) at a level of 0.15 g/kg body weight (≈8 g fiber for a person with a body weight of 50 kg) reduced the absorption of carotenoids in women (33). When considering the possible effect of fiber in 300 g puréed spinach containing 2 g soluble fiber, 7 g insoluble fiber, and 3 g pectin and of 100 g puréed carrots containing 1 g soluble fiber, 2 g insoluble fiber, and 1 g pectin (34), it is likely that the amount of soluble fiber in the experimental meal could have accounted for only a small portion of the differences of carotenoid absorption and its conversion to vitamin A between spinach and carrots."

"The quantitative evaluation of this conversion at the vitamin A equivalence level in a healthy, well-nourished adult population has been made possible by using an isotope reference dose, ie,13C8 vitamin A. Our results showed that the average provitamin A carotenoid to vitamin A conversion efficiency is 14.8 to 1 (range: 7.7–24.5 to 1, by wt) from carrot β-carotene (trans β-carotene equivalents) and is 20.9 to 1 from spinach β-carotene (range: 10.0–46.5 to 1, by wt). The provitamin A carotenoids to retinol conversion factors are much different from the 6 to 1 conversion factor used in the 1989 edition of the US recommended dietary allowances (RDAs) (35) and the current 12 to 1 conversion factor set by the US National Academy of Sciences (11). Thus, the efficiency of the production of vitamin A from dietary provitamin A carotenoids is for some foods substantially less than previously thought. It is worth mentioning that we observed 4- to 5-fold differences in the yield of vitamin A between subjects, regardless of whether spinach or carrots was fed, which was likely due to variations in intestinal absorption and, thus, the conversion of provitamin A carotenoids. It is well known that blood responses to an acute dose of β-carotene vary greatly (36). However, whether the current observation was also due to the variability of intestinal enzymatic conversion of provitamin A carotenoids needs further investigation.

Are vegetables useful sources of vitamin A? To answer this question, we provide the following calculations. With the use of the spinach β-carotene to vitamin A conversion factor of 21 to 1, 50 g spinach that contains 2.8 mg β-carotene (USDA Nutrient Data Table) (37) can provide 130 μg retinol; with the use of the carrot β-carotene to vitamin A conversion factor of 15 to 1, 50 g carrots (5 medium-sized baby carrots) that contain 3.2 mg β-carotene (USDA Nutrient Data Table) (37) would provide ≈200 μg retinol. That is, a normal portion for adults—a 100-g mixture of equal amounts of cooked spinach and carrots (≈0.5 cups) can provide 330 μg retinol. This is equal to a mixture of one egg (≈50 g containing 85 μg retinol), 1 cup (237 mL) whole milk, or 1 oz of cheddar cheese (≈200 mL milk or 2 tsp cheese containing 90 μg retinol each), and 1 tbsp butter (15 g containing 130 μg retinol), which together will provide a total of 305 μg retinol (≈33% of the US RDA for men and ≈50% of the US RDA for women). When people eat spinach in a form other than puréed, the relative bioavailability between whole-leaf and minced spinach was reported to be 5.1% compared with 6.4%, respectively (38). Taking this fact into consideration, 50 g spinach would provide ≈100 μg retinol (instead of 130 μg retinol). As another example, for children 1 y of age, a portion size of 15 g each of spinach and carrot would provide ≈100 μg retinol, or ≈25% of the US RDA for this age group. Therefore, spinach and carrots, consumed in various cooked ways with fat, could provide a significant amount of vitamin A to humans."

The 'trans b-carotene equivalence' simplification helps to grasp the toxic potential of a food. For example, since only half of the a-carotene molecule has poisonous function, we can ignore the other part and treat it as b-carotene. The same goes for b-cryptoxanthin and b-echinenone. If a medium carrot contains 5 mg of b-carotene and 2 mg of a-carotene, we can consider that it has 6 mg of b-carotene instead of thinking of propoison A macabrotenoids individually.

Even though in theory 1 molecule of b-carotene could be splitted and yield 2 molecules of poisonal, the claim is that the resulting activity is equivalent to only 1 poisonal when the b-carotene is isolated in oil. So, from 6 mg of carotenes, we would obtain 3 mg of poisonal/poisonol. But prior to being cleaved, they has to be absorbed, only a fraction reaches the cell. They assume the absorption rate to be greater than 15%, but it can be lower, such as 7%. However, for someone to experience carotenemia after the ingestion of toxins, the cleavage should be "compromised" more than the absorption. Nevertheless, conversion factors take everything into consideration.
 

Amazoniac

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Heorhiy, more garbage, some of them have been posted elsewhere..

- Vitamin A: from physiology to disease prevention

"The principal forms of preformed vitamin A (retinol) in supplements are retinyl palmitate and retinyl acetate. Beta-carotene is also a common source of vitamin A in supplements, and many supplements provide a combination of retinol and beta-carotene. Most multivitamin supplements available in the U.S. provide 1,500 mcg (5,000 IU) of vitamin A, which is substantially more than the current RDA for vitamin A. This is due to the fact that the Daily Values (DV) used by the FDA for supplement labeling are based on the RDA established in 1968 rather than the most recent RDA, and multivitamin supplements typically provide 100% of the DV for most nutrients. Because retinol intakes of 5,000 IU/day may be associated with an increased risk of osteoporosis in older adults some companies have reduced the retinol content in their multivitamin supplements to 750 mcg (2,500 IU)."​

However, that's not in line with the following information:

- The Vitamins: Fundamental Aspects in Nutrition and Health (978-0-12-802965-7)

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A source of confusion may be:

- Recommendations For Vitamin A Use During Pregnancy

"The National Research Council's recommended dietary allowance for vitamin A during pregnancy is 1,000 mcg retinol equivalents (RE)/day, which is equivalent to 3,300 IU as retinol or 5,000 IU of vitamin A obtained from the typical American diet as a combination of retinol and carotenoids, e.g., beta-carotene. An average balanced diet contains approximately 7,000-8,000 IU of vitamin A derived from different sources."​

- The Experimental Induction of Vitamin A Deficiency in Humans

"[..]approximate agreement was achieved for the human requirement for vitamin A. Booher et al. (21) reported that between 1900 and 3900 iu/d given over 2–3 wk cured human vitamin A deficiency. Wagner (26) restored normal health to his depleted subjects with 1870 iu/d given over 2.5 mo, and recommended 2500 iu/d of vitamin A and 5000 iu β-carotene for good health maintenance. Hume and Krebs (27) recommended as a daily requirement 2500 iu vitamin A or 7500 iu for β-carotene as consumed in vegetables. These amounts compare well with today's RDA, expressed as vitamin A activity, of 3000 iu/d for men and 2300 iu for women."​

It brings us to another layer of confusion:

"Although many countries have followed suit by using the RAE rather than RE in their national food composition tables and nutrient intake recommendations, the WHO has not yet renewed its intake recommendations published in 2004 and therefore still uses the outdated RE (46). Even so, the revised vitamin A intake recommendations for Europe by the European Food Safety Authority in 2015 retained the old conversion factors (47). This is confusing for anyone trying to assess adequacy of dietary vitamin A intake, and especially relevant for populations with a high dependency on provitamin A intake to fulfill their vitamin A requirements (48)."
↳ [48] Dietary vitamin A intake recommendations revisited: global confusion requires alignment of the units of conversion and expression

"In 1967, the FAO and the WHO proposed a unit of dietary reference values for vitamin A, retinol equivalents (RE), which designated 1 µg of preformed vitamin A in the retinoid form as 1 µg RE, and made considerations for a lower bioconversion efficiency for the provitamin A carotenoids as sources of the vitamin (Table 1)(1,2). Based on compelling evidence that the absorption of provitamin A carotenoids, especially from dark green leafy vegetables, is much lower than previously assumed(3-6), the Institute of Medicine (IOM; now called the Health and Medicine Division) concluded that higher bioconversion factors were more appropriate and formulated RDA values for vitamin A using microgram retinol activity equivalents (µg RAE) as the unit of reference in 2001(7). This was later confirmed in follow-up studies(8-14), which largely corroborate the current IOM policy to estimate the bioconversion factors of β-carotene from an average Western diet as 12:1 and of other provitamin A carotenoids as 24:1 (Table 1). For low- and middle-income countries, West et al. (2002)(15) suggested an even higher conversion factor for β-carotene, namely 21:1, based on studies conducted in Asia(16-18), which was later confirmed by other studies in other settings(19,20). The difference in estimated conversion factors between low- and middle-income countries and Western countries can be explained by diet- and host-related factors such as food matrix, fat intake and health status(21)."

"Although [..] recommendations will be similar when all vitamin A from the diet is derived as the preformed vitamin, [they] will diverge greatly when a substantial part is derived from provitamin A sources." "The lower the dietary intake of preformed vitamin A, the wider the gap between the specific recommendations series becomes (Fig. 1)."

"This mismatch in the units of comparison between ingested and required vitamin A intakes makes the assessment of adequacy of vitamin A intake complex, confusing and difficult to communicate."​
 

Amazoniac

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Macrocephalic god, hypomobilization syndrome is real and possibly more prevalent than realized, can occur due to malnutrition of disease and the associated inflammatory signals. Serum "retinol" level tends to normalize as the person recovers or if the inflammation is kepted at the bay. It's another reason to lower dose because even though dietary intake becomes important if the liver stores aren't accessible, I don't think that most users will distribute the dose enough to avoid a short-lived effect, it won't take long for it to be cleared from circulation and add up to the total reserves. Critical functions must not be compromised since the body is expected to prioritize them before the situation gets serious.


Based on that experiment on women, diet and a serving of the supplement may yield about 2,300 mcg of retinol/day. An infant of 6 months can consume on average 400 mcg/day from milk and weight 7.5 kg, that's ~55 mcg/kg. To extrapolate to an adultess, it would be something like 3,400 mcg/day. However, the foetus is on an extremely anabolic phase and has to accumulate the toxin to secure its continuation after weaning. The intake of infants won't vary like that of adults, a liver meal a week can bump the daily intake close to the extrapolation, which is substantial.
 

xeliex

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The toxicity of grant degenerate is taking over this thread...
:lol:

I think vitamin E is always the stankiest. It smells bad after a while. The other vitamins included don't seem to smell as bad. I get the same smell from tocovit and other good vitamin E supplements.
 
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I just applied 8 drops (1 serving) of estroban to each nipple, then i rubbed in some DHT powder, around 15-20 minutes later there is no residue DHT left on nipple meaning it has all been absorbed! Nipples lose 95% of their puffiness and for a few hours. I will be doing this daily from now, thank you so much for this product @haidut!
 

Nnik

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Is it safe to take this along with the liver/oyster supplements from Saturee? Just don’t want to overdo it on the vitamin A but have also been struggling with breakouts as a female and wondering if i still need more vitamin A. Any insight is appreciated :)
 

Nnik

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Re: Custom, liquid dietary supplement with vitamins K2, A, D

I was thinking of preparing a batch of maybe 30-50 dropper bottles with labels. Then I would mail them to the people in the forum that would want to try. I am willing to eat the cost of initial trial b/c without it I would not know how much interest there is and if people would like the product. If the reviews are good, then I can invest in more bulk product and hiring a lab to do a certificate of analysis (COA).
As far as the source - for all vitamins I would use a known vendor like Sigma-Aldrich, which can provide products with 99%+ purity. I have several suppliers, and they are all competitors so hopefully I can get them to bid with each other so I can get the lowest price:):
Like I said - I am not trying to become a millionaire doing this. If it can cover its cost of production it would be a nice project for me and my wife, who is a Yale-educated biochemist btw and is looking for something interesting to do while staying at home and looking after our 3-month old:): I have been bombarding her constantly with Ray's ideas and I think she has been "converted" enough that now she wants to try it. She is using my supplement for pregnancy-related cosmetic issues like stretch marks and facial skin health.
Also, her buddy from Yale (who is also a biochemist) is fascinated by Ray's ideas and what I have been flooding her with over the last 2 years. So, you can count her in as well. Her husband would be very grateful that his wife is doing something with her degree instead of sitting bored at home:): At least you'll all know that there are "qualified" people working on the product you are using.
Ah, enough babbling on my end. I will see how the poll does in the next week or so and give it a try.
Thanks for the great responses so far!
What supplement of yours was your wife using for pregnancy stretch marks and facial skin health?
 

bookshelf

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I used cortinon (dhea/progesterone) vaginally instead of vaginal estrogen and used progesterone on my gums for the systemic benefits. I don’t know for certain that vaginal estrogen stays local only that I didn’t have the same negative experience from it as oral or topical HRT. I’m pretty sure Peat isn’t a fan of any estrogen but if you need to use it I think vaginal inserts are safer than the oral pills. Please keep in mind I’m not a scientist just a woman sharing my experience!
Hi Blossom,

Thank you for sharing your experience on this and other similar posts. I know this is an older conversation but am hoping to ask a few questions:

Do you happen to know about how many mgs of progesterone vaginally would be a good daily dose?

Did you (or has anyone reading this) found that using vaginal treatments (e.g. dhea/progesterone/vitamin a) can be done on a maintenance schedule, say like 1-2 times a week vs every night? If so, does it make sense to up the dosage (so instead of say 3.25mg of DHEA a day, maybe 6.5mg one time a week)?

Is there a point where women who need to do this find that it isn't necessary anymore or is this like a forever thing? I think it was @ecstatichamster that said on one of the threads that his wife just puts some combination of this in her naval with good effect. I'm wondering if, at least in a maintenance mode, that would be sufficient for long term use.

Thank you
 

Blossom

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Hi Blossom,

Thank you for sharing your experience on this and other similar posts. I know this is an older conversation but am hoping to ask a few questions:

Do you happen to know about how many mgs of progesterone vaginally would be a good daily dose?

Did you (or has anyone reading this) found that using vaginal treatments (e.g. dhea/progesterone/vitamin a) can be done on a maintenance schedule, say like 1-2 times a week vs every night? If so, does it make sense to up the dosage (so instead of say 3.25mg of DHEA a day, maybe 6.5mg one time a week)?

Is there a point where women who need to do this find that it isn't necessary anymore or is this like a forever thing? I think it was @ecstatichamster that said on one of the threads that his wife just puts some combination of this in her naval with good effect. I'm wondering if, at least in a maintenance mode, that would be sufficient for long term use.

Thank you
This thread has a discussion about mixing progesterone and dhea for vaginal use. It’s been a long time since I needed to do this but I remember I ended up making a mixture with cortinon and cocoa butter and let it harden in a small candy mold in the refrigerator for easy insertion.
EDIT: I used it every night for many months and just gradually decreased it with time as things improved for me.
 

bookshelf

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This thread has a discussion about mixing progesterone and dhea for vaginal use. It’s been a long time since I needed to do this but I remember I ended up making a mixture with cortinon and cocoa butter and let it harden in a small candy mold in the refrigerator for easy insertion.
EDIT: I used it every night for many months and just gradually decreased it with time as things improved for me.
Thank you!
 

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