Home Forums DISCUSSION FORUMS SIGNALS DHEA- difficulties raisng it

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  • #1063
    JanSz
    Member

    I would like to comply to LEF recomendation and get my DHEAs(500-640)mcg/dL

    I am no able to raise it over 288mcg/dL while taking 4-100mg DHEA pills.
    Any suggestions.

    Also my Pregnenolone and progesterone are nil

    I am on (T & HCG) injections, was able to get my BAT, E2, DHT into desirable range.

    After getting on TRT I do not have erection problems, but still have to use Cialis.

    5’9″, 160#, 69yo



    8/26/05 Without DHEA supplementation
    DHEA sulfate–163

    5/5/06 Supplementing with 300mg/day DHEA from LEF
    DHEA sulfate–328

    10/31/06 Supplementing with 300mg/day DHEA from LEF
    DHEA sulfate–369

    8/30/07 Without DHEA supplementation, blood drawn at QuestDiagnostics
    DHEA sulfate–24(25-95)mcg/dL

    3/19/08 Without DHEA supplementation, blood drawn at QuestDiagnostics
    DHEA sulfate–65(25-95)mcg/dL

    5/27/09 Supplementing with 400mg/day DHEA from LEF
    DHEA sulfate–288

    #2010

    @JanSz 171 wrote:

    I would like to comply to LEF recomendation and get my DHEAs(500-640)mcg/dL

    I am no able to raise it over 288mcg/dL while taking 4-100mg DHEA pills.
    Any suggestions.

    Also my Pregnenolone and progesterone are nil

    I am on (T & HCG) injections, was able to get my BAT, E2, DHT into desirable range.

    After getting on TRT I do not have erection problems, but still have to use Cialis.

    5’9″, 160#, 69yo



    8/26/05 Without DHEA supplementation
    DHEA sulfate–163

    5/5/06 Supplementing with 300mg/day DHEA from LEF
    DHEA sulfate–328

    10/31/06 Supplementing with 300mg/day DHEA from LEF
    DHEA sulfate–369

    8/30/07 Without DHEA supplementation, blood drawn at QuestDiagnostics
    DHEA sulfate–24(25-95)mcg/dL

    3/19/08 Without DHEA supplementation, blood drawn at QuestDiagnostics
    DHEA sulfate–65(25-95)mcg/dL

    5/27/09 Supplementing with 400mg/day DHEA from LEF
    DHEA sulfate–288

    One can increase absorption by adding EVO or EFA with your dhea dosage.

    #2016
    JanSz
    Member

    @hardasnails1973 172 wrote:

    One can increase absorption by adding EVO or EFA with your dhea dosage.

    That is basics, I already take them for years.

    #2015
    chaos
    Member

    @JanSz 173 wrote:

    That is basics, I already take them for years.

    What about a liquid sublingual suspension?

    #2011

    It can spike to hard as capsules tend to be more steady in plasma

    #2008
    DrMariano2
    Participant

    @JanSz 171 wrote:

    I would like to comply to LEF recomendation and get my DHEAs(500-640)mcg/dL

    I am no able to raise it over 288mcg/dL while taking 4-100mg DHEA pills.
    Any suggestions.

    Also my Pregnenolone and progesterone are nil

    I am on (T & HCG) injections, was able to get my BAT, E2, DHT into desirable range.

    After getting on TRT I do not have erection problems, but still have to use Cialis.

    5’9″, 160#, 69yo



    8/26/05 Without DHEA supplementation
    DHEA sulfate–163

    5/27/09 Supplementing with 400mg/day DHEA from LEF
    DHEA sulfate–288

    DHEA (dehydroepiandrosterone) is the most common hormone found in the body, outside of the brain. It is made by the adrenal gland’s outer layer, the adrenal cortex.

    DHEA is a very interesting substance since it has BOTH androgen and estrogen activity. It binds to both androgen and estrogen receptors.

    The brain, itself, makes DHEA, lots of it, as a neurotransmitter/neurohormone. The brain makes more DHEA than any other neurotransmitter except for pregnenolone.

    In the body, DHEA also is a precursor for testosterone and estradiol and 7-keto DHEA and estrone, among other things.

    The problem of taking a hormone orally is that:
    1. The liver destroys a lot of the hormone before it goes into the circulatory system. This is called Hepatic First-Pass Metabolism.
    2. The high concentrations of the hormone in the liver can cause changes in liver function.

    For example, 90% of oral progesterone is changed to pregnanolone. Pregnanolone acts like a benzodiazepine or barbiturate by enhancing GABA receptor affinity for GABA. This is responsible for progesterone’s sedative effects. The 10% of progesterone that is left is what would work as progesterone in the body.

    As another example, oral estrogens causes the liver the release inflammatory signals, increasing C-reactive protein levels. Premarin (horse estrogen) hugely induces liver enzymes compared to regular estradiol. This can cause hyperexcretion syndromes where the other hormones are destroyed at a very fast pace, resulting in hormone deficiencies that require large replacement doses to achieve adequate blood levels or hormone activity.

    DHEA, itself, increases the production of Cytochrome P450 3A4 (CyP3A4). This is called Hepatic Induction of the CyP3A4 enzyme. This is the body’s primary enzyme for inactivating drugs, toxins, and various hormones, allowing the metabolites to be excreted. CyP3A4 is the primary enzyme that destroys DHEA.

    Thus, taking oral DHEA increases the enzyme that gets rid of DHEA. The higher the dose of DHEA, the more it induces the production of CyP3A4, which gets rid of DHEA. Thus you reach a ceiling where it becomes more difficult to raise DHEA levels since it gets rid of itself.

    Only by taking huge doses would one overcome the induction of liver enzymes and the blood levels would once again go up. The problem then becomes: what are the dangers of such high levels of the substance? DHEA at high levels can cause problems. For DHEA in men, one can get higher direct estrogen receptor stimulation, the formation of more estrogens themselves, etc. This could lead to strokes, heart attacks as blood clots would be a potential problem. In women, on the other hand, higher DHEA means higher androgen or testosterone signaling, leading to problems of excess androgen signaling – such as body hair, acne, etc.

    Other medications can also induce liver enzymes. For example, Carbamazepine for years has been well known to induce liver enzymes, thus getting rid of itself and other medications and hormones in the process.

    If a person already has high amounts of CyP3A4, then they will tend to have lower amounts of DHEA.

    Blocking CyP3A4 is very dangerous since it is the most important of the enzymes that get rid of drugs and toxins in the body. Medications which reduce CyP3A4 are famous for causing fatal heart arrhythmias.

    Optimizing thyroid hormone, however, is one safe way of reducing DHEA’s ability to induce CyP3A4 activity.

    When Pregnenolone and progesterone are very low, I would suspect adrenal fatigue or hypothalamic-pituitary-adrenal dysregulation of some sort. Usually cortisol is either maintained – by sacrificing production of the other adrenal hormones, or cortisol is low. A low DHEA is another indication of the presence of low adrenal function. The stage of adrenal exhaustion in response to stress is when cortisol production cannot be maintained, even by sacrificing production of the other adrenal hormones.

    Impaired cortisol production will impair activation of thyroid hormone (T4 to T3 conversion). This, in turn, would make it more likely for oral DHEA to induce liver enzymes that get rid of DHEA.

    Transdermal or sublingual DHEA are ways to avoid high concentrations of DHEA in the liver, to thus minimize liver induction of CyP3A4. They bypass first-pass metabolism of DHEA.

    Low doses DHEA given in multiple intervals may be another way to avoid very high DHEA concentrations in the liver, to avoid liver enzyme induction.

    On another point, another reason high dose oral DHEA doesn’t result in high DHEA levels may be poor absorption of oral DHEA.

    DHEA is lipid soluble. This means it may be more easily absorbed if it is taken with other fats. These would stimulate liver bile production, which would then make it easier to absorb fats and fat soluble substances such as the fat soluble vitamins – and DHEA.

    #2012
    pmgamer18
    Member

    Hi Jan here is what happened to me when I found out I am Hypopituitary and treating my low Cortisol, Thyroid, Aldosterone, Renin and Iron levels. My DHEA started to come back on labs very high taking 25mgs of DHEA the kind that dose not get killed in the stomach.
    It was when I went on Florinef .125mgs that top off all my low hormones and my DHEA come back to high. So I stopped DHEA and my levels came down to the upper mid range.

    Then after heart bypass sugary I was taken off Florinef and put on a low sodium diet still my DHEA is good above mid range.

    One thing I could never tell the difference between low levels and higher levels always felt about the same.

    Today my problem is low BP they have me on a low sodium diet no more then 2000mgs per day. A blood pressure med. and a strong water pill with a beta-blocker. Once they get you on meds it’s hard to get them to stop them. I am walking around feeling like I am going to pass out I don’t dare walk when I first get up I need to stand there until this feeling passes. This morning it’s bad my BP was 80/45 yet I just seen my family Dr. and told him this and showed him my BP levels in the memory on my BP gage. He feels having levels like this are Ok and just try to live with it.

    When I am walking I don’t dare look to the side or up I will fall down from getting dizzy.

    I have had white coat fever for yrs. every time one would take my BP it would be high yet when I am home and take it my self it’s OK.

    I don’t know how long I am going to put up with this but after all the crap I have been through having to feel like this due to meds is stupid.
    Phil

    #2017
    JanSz
    Member

    @DrMariano 176 wrote:

    DHEA (dehydroepiandrosterone) is the most common hormone found in the body, outside of the brain. It is made by the adrenal gland’s outer layer, the adrenal cortex.

    DHEA is a very interesting substance since it has BOTH androgen and estrogen activity. It binds to both androgen and estrogen receptors.

    The brain, itself, makes DHEA, lots of it, as a neurotransmitter/neurohormone. The brain makes more DHEA than any other neurotransmitter except for pregnenolone.

    In the body, DHEA also is a precursor for testosterone and estradiol and 7-keto DHEA and estrone, among other things.

    The problem of taking a hormone orally is that:
    1. The liver destroys a lot of the hormone before it goes into the circulatory system. This is called Hepatic First-Pass Metabolism.
    2. The high concentrations of the hormone in the liver can cause changes in liver function.

    For example, 90% of oral progesterone is changed to pregnanolone. Pregnanolone acts like a benzodiazepine or barbiturate by enhancing GABA receptor affinity for GABA. This is responsible for progesterone’s sedative effects. The 10% of progesterone that is left is what would work as progesterone in the body.

    As another example, oral estrogens causes the liver the release inflammatory signals, increasing C-reactive protein levels. Premarin (horse estrogen) hugely induces liver enzymes compared to regular estradiol. This can cause hyperexcretion syndromes where the other hormones are destroyed at a very fast pace, resulting in hormone deficiencies that require large replacement doses to achieve adequate blood levels or hormone activity.

    DHEA, itself, increases the production of Cytochrome P450 3A4 (CyP3A4). This is called Hepatic Induction of the CyP3A4 enzyme. This is the body’s primary enzyme for inactivating drugs, toxins, and various hormones, allowing the metabolites to be excreted. CyP3A4 is the primary enzyme that destroys DHEA.

    Thus, taking oral DHEA increases the enzyme that gets rid of DHEA. The higher the dose of DHEA, the more it induces the production of CyP3A4, which gets rid of DHEA. Thus you reach a ceiling where it becomes more difficult to raise DHEA levels since it gets rid of itself.

    Only by taking huge doses would one overcome the induction of liver enzymes and the blood levels would once again go up. The problem then becomes: what are the dangers of such high levels of the substance? DHEA at high levels can cause problems. For DHEA in men, one can get higher direct estrogen receptor stimulation, the formation of more estrogens themselves, etc. This could lead to strokes, heart attacks as blood clots would be a potential problem. In women, on the other hand, higher DHEA means higher androgen or testosterone signaling, leading to problems of excess androgen signaling – such as body hair, acne, etc.

    Other medications can also induce liver enzymes. For example, Carbamazepine for years has been well known to induce liver enzymes, thus getting rid of itself and other medications and hormones in the process.

    If a person already has high amounts of CyP3A4, then they will tend to have lower amounts of DHEA.

    Blocking CyP3A4 is very dangerous since it is the most important of the enzymes that get rid of drugs and toxins in the body. Medications which reduce CyP3A4 are famous for causing fatal heart arrhythmias.

    Optimizing thyroid hormone, however, is one safe way of reducing DHEA’s ability to induce CyP3A4 activity.

    When Pregnenolone and progesterone are very low, I would suspect adrenal fatigue or hypothalamic-pituitary-adrenal dysregulation of some sort. Usually cortisol is either maintained – by sacrificing production of the other adrenal hormones, or cortisol is low. A low DHEA is another indication of the presence of low adrenal function. The stage of adrenal exhaustion in response to stress is when cortisol production cannot be maintained, even by sacrificing production of the other adrenal hormones.

    Impaired cortisol production will impair activation of thyroid hormone (T4 to T3 conversion). This, in turn, would make it more likely for oral DHEA to induce liver enzymes that get rid of DHEA.

    Transdermal or sublingual DHEA are ways to avoid high concentrations of DHEA in the liver, to thus minimize liver induction of CyP3A4. They bypass first-pass metabolism of DHEA.

    Low doses DHEA given in multiple intervals may be another way to avoid very high DHEA concentrations in the liver, to avoid liver enzyme induction.

    On another point, another reason high dose oral DHEA doesn’t result in high DHEA levels may be poor absorption of oral DHEA.

    DHEA is lipid soluble. This means it may be more easily absorbed if it is taken with other fats. These would stimulate liver bile production, which would then make it easier to absorb fats and fat soluble substances such as the fat soluble vitamins – and DHEA.

    “Optimizing thyroid hormone, however, is one safe way of reducing DHEA’s ability to induce CyP3A4 activity.”

    On 3 Grains Armour
    T3, Free=486(230-420)pg/dL
    T4, Free= 1.6(0.8-1-8)ng/dL
    T3 uptake=36.3(22.0-35.0)%
    T3,Total=165(60-181)ng/dL
    T4,Total=10.2(4.5-12.0)ug/dL
    TSH=0.01(0.4-5.5)

    Reduced to 2.75Grains Armour
    T3, Free= 359(230-420)pg/dL
    T4, Free=1.6(0.8-1-8)ng/dL
    RT3=23.1(9-35)ng/dL

    Changed to (0.025mgCytomel + 0.025mgCytomel + 1.5GrainsArmour)
    Got better (higher) body temperature, more often at 36.6C= 97.88F
    blood drawn 5/27/09

    T3, Free=458(230-420)pg/dL
    T4, Free= 0.8(0.8-1-8)ng/dL
    T3,Total=205(97-219)ng/dL
    T4,Total=4.1(4.5-12.5)ug/dL
    TSH=<0.01(0.4-4.5)
    RT3=12(11-32)ng/dL


    At first I was eating only DHEA pills (300mg/day) to support my adrenals, with results like this:

    Cortisol AM=18.7(4.0-22.0)ug/dL
    Cortisol PM=10.6(3.0-17.0)ug/dL
    DHEA sulfate=306(25-95)mcg/dL
    Aldosterone=4( Progesterone, LC/MS/MS=1.4 (<1.4)ng/mL
    Pregnenolone=11(13-208)ng/dL

    Now I have not as good cortisol, preg and prog are on the bottom, I am still eating DHEA pills (400mg/day) but (after seeing results below) I also added 30mg HC (hydrocortisone)

    blood drawn 5/27/09

    Cortisol AM=9.3(4.0-22.0)ug/dL
    Cortisol PM=9.8(3.0-17.0)ug/dL
    DHEA sulfate=306(25-95)mcg/dL
    CBG cortisol binding globulin=28(19-45)mg/L
    ACTH,plasma=18(7-50)pg/mL
    Aldosterone=6( progesterone=<0.1ng/mL
    pregnenolone=<5(13-208)ng/mL
    androstenedione=74(50-220)ng/dL

    My 5/27/09 blood tests are on attachments
    5 pages on this post the next 4 on the next post

    #2018
    JanSz
    Member

    #2013
    pmgamer18
    Member

    Jan if my last Estradiol labs come back on Ultra 10 range <29 and from the same blood sample my Sensitive test came back 36 range 13 to 54 pg/ml for me this is to high and the Ultra test is not working right I hate to see what your 46 pg/ml with range of <29 would look like doing the Sensitive test range 13 to 54.

    I added more Arimidex after this lab test and the Sensitive test was right the Ultra was wrong. You might have very high levels on the Sensitive test #4021. My Dr. tells me he called quest and they told him they are having big problems with the Ultra testing.
    Phil

    #2019
    JanSz
    Member

    @pmgamer18 191 wrote:

    Jan if my last Estradiol labs come back on Ultra 10 range <29 and from the same blood sample my Sensitive test came back 36 range 13 to 54 pg/ml for me this is to high and the Ultra test is not working right I hate to see what your 46 pg/ml with range of <29 would look like doing the Sensitive test range 13 to 54.

    I added more Arimidex after this lab test and the Sensitive test was right the Ultra was wrong. You might have very high levels on the Sensitive test #4021. My Dr. tells me he called quest and they told him they are having big problems with the Ultra testing.
    Phil

    Phil;
    note that I did my E2 testing 3 (three) times.
    On Ultrasensitive I got 41, on the other tests it was 20 and 23.

    http://musclechatroom.com/forum/showpost.php?p=42750&postcount=1

    I also did Estrone two ways. Both are LC/MS/MS type tests.
    Also got diametrically different results.

    Estrone, LC/MS/MS=35(< or =68 pg/mL)


    Estrogens, Fractionated, LC/MS/MS
    Estrone, serum=110(< or =68 pg/mL)
    —-

    Taking lots of DHEA (as I do), DHEA may convert to Estrone.
    So now the question is, is it converting or not, I have two tests from same blood draw, each one says something else.
    .
    .
    .
    I was hoping that DrMariano will have something more to say.
    There must be a way to raise my DHEAs, preg and prog.

    .

    #2014
    pmgamer18
    Member

    I know all them Quest labs are all over the place but I have used this 4021 Estradiol for a dam long time it’s been right on by how I feel.

    I see your Aldosterone at 6 is for what I know about this your low you need labs for this that so a range not just < then a number you need to know what the bottom of the range is.
    http://www.labtestsonline.org/understanding/analytes/aldosterone/test.html
    When I went on Florinef .125mgs morning my DHEA come up very fast here is a good link I think you have read this before. But they talk about low Aldosterone levels.
    http://www.tuberose.com/Adrenal_Glands.html

    #2009
    DrMariano2
    Participant

    DHEA:

    DHEA is important – but in the hierarchy of signals in the body, there are more important signals to consider improving first since otherwise DHEA is a minor player in a person’s overall health. For example, in men, the following hormones are more important to address: thyroid, cortisol. If DHEA is greater than 200, I would address the other issues first.

    DHEA can go to estrone rather than testosterone or estradiol. Thus if DHEA levels are difficult to increase, then aside from elimination issues and absorption issues as previously discussed, the metabolism of DHEA is important to consider. If one has an overly active enzyme pathway that leads to DHEA being converted to Estrone, then one has a significant problem. Estrone is a pro-carcinogenic / pro-cancer estrogen. Taking DIM or iodine may help convert this to less carcinogenic estrogens. Addressing the overall impairment in adrenal function to help improve natural production of DHEA may be a better idea than adding more exogenous DHEA. In an older man, where the DHEA producing layer of the adrenal gland has thinned out due to aging, some DHEA supplementation may be necessary – so long as estrone production is minimized.

    ESTRADIOL:

    Different tests for estrogen will give you different levels of estradiol. The different protocols involved simply give different numbers. Given this scenario, one has to CHOOSE ONE of the tests and base their clinical decisions on the observations and experience with that one test. It is one’s experience and observations, then, that would help determine the interpretation.

    For myself, I have found that the ultrasensitive estradiol is the most clinically useful test for estrogen signaling activity. This means whether or not estrogen is too high or too low in relationship to the other hormones, neurotransmitters, and other signals. This is particularly important for signals which are directly affected by estrogen: testosterone, thyroid hormone, serotonin, dopamine, norepinephrine.

    The fractionated estrogens test is useful for determining possibly what is happening to estrogens or in the case of DHEA, where it is going. But a 24-hour urine hormone test – where many hormones and their metabolites are measured (such as done by Meridian Labs or Rhein labs) would tell you more about the pathways involved.

    GROWTH HORMONE:

    Growth hormone is generally the last hormone to optimize. This is because it potentially affects many of the other hormones negatively (such as thyroid and the adrenal hormones), causing more problems and complicating the clinical picture if it is added first. Additionally, and possibly more importantly, if one addresses the other hormones and neurotransmitters first, then the dose of growth hormone needed to improve function is LOWER and less costly.

    IGF-1 is one indirect way of measuring growth hormone. IGF-1 is increased by growth hormone, testosterone, DHEA, dopamine, thyroid hormone, among other signals. It is not purely determined by growth hormone. However, IGF-1 does the bulk of the work for growth hormone and is thus a valid measure of its activity.

    At what level of IGF-1 indicates growth hormone deficiency (the only legal indication for growth hormone treatment) is actually subjective. Anti-aging doctors, who want to optimize growth hormone levels, tend to use 250 as the lower end of the reference range for IGF-1. Some doctors use a lower level. For myself, 250 is a bit on the high end for a lower reference range. If it is closer to 150, I would consider growth hormone treatment.

    Growth hormone can improve a person’s sense of well-being when used well. Improved mood, libido, energy can occur – once the other hormone and neurotransmitters are optimized. However, it may not prolong life. It may actually limit one’s lifespan to about the 90s rather than letting one live past 100. Thus one has to assess whether one chooses to live well or live longer.

    THYROID HORMONE:

    A useful target if considering primarily lab tests for optimizing thyroid hormone is the following:

    TSH <= 1.0
    Free T3 between 3.3 to 3.9
    Total T4 between 8-12

    If at least one lab test is below these ranges, then a person may exhibit signs of hypothyroidism.

    T4 levels are important since the brain does its own conversion of T4 to T3. The brain compartment can have different T4 and T3 levels than the rest of the body. The brain and body are in two different compartments, separated by the blood brain barrier. In Alzheimer’s disease, brain thyroid levels are lower than the rest of the body.

    TSH is not as important a measurement compared to measuring Free T3 and Total T4. If a person has some metabolic problem – including having heart disease, diabetes, low iron, etc. then the nervous system cannot function well and TSH will be abnormally low since the brain will have difficulty monitoring thyroid hormone and making TSH.

    FERRITIN:

    Ferritin is the most important measure of iron. Iron in the body is mostly in hemoglobin and myoglobin. However, iron is also used by every single cell in the body as part of many enzymes. Many of the enzymes which participate in the citric acid cycle to generate ATP – the basic energy storage unit in the body – in mitochondria have iron in their structure. Ferritin gives one an idea of how much iron is available to the rest of the body’s cells for metabolic purposes.

    Without iron, cells are significantly impaired in metabolic activity. They can’t make enough ATP to do their activities. Thus, optimizing hormone, neurotransmitters and other signals doesn’t work very well since they are only signals. They are signals to trigger cellular activities. But these activities cannot be done without ATP.

    An optimum iron level as measured by Ferritin in men is about 150. In women, it is about 100-120. These are mid-range values. A ferritin of 75, in one study, was found to be the lower end of normal for senior citizens. They can be even develop iron-deficiency anemia at that level of iron.

    Excessive iron is dangerous. It is highly oxidizing. It is destructive to tissues – causing cell death in the testes, ovaries, thyroid gland, liver, brain, etc. In testing Ferritin, I have surprisingly found a large number of patients, who have been treatment resistant, to have hemochromocytosis – a disease of excessive iron storage.

    CORTISOL:

    Outside of Addison’s disease, where there is actual destruction of the adrenal glands, low cortisol and adrenal cortex output may occur from stress-related conditions. This has been called “Adrenal Fatigue”. However, in retrospect, I don’t think this is a good term in that it implies something is wrong structurally with the adrenals – a bone of contention and misunderstanding. A better term is hypothalamic-pituitary-adrenal axis dysregulation (HPA dysregulation, for short). Then the problem may lie anywhere from the nervous system, endocrine system, immune system, metabolism and nutrition, etc. Posttraumatic stress disorder is an example where there is hypothalamic-pituitary-adrenal axis dysregulation, resulting in low cortisol. Frequently, in PTSD, I find cortisol levels around 6 and below. When I see such levels, I would inquire about a person’s traumatic experiences.

    Cortisol treatment may help. The problem is that Cortisol treatment also slows down the output of the adrenal cortex – including DHEA, Pregnenolone, Progesterone, Testosterone, Estradiol, etc. These other signals also are important. They also can regulate mood. Thus in some people, it is not enough to add cortisol. It is also important to optimize the other adrenal hormones/signals to avoid causing mood dysregulation and other problems with a cortisol-alone treatment.

    Improving sleep is a huge help in improving adrenal cortex function.

    PREGNENOLONE:

    Pregnenolone is the most produced neurotransmitter in the brain. It is important for memory and attention. DHEA is the second most produced neurotransmitter in the brain. Pregnenolone is also produced by the adrenal glands. Pregnenolone treatment is a drop in the ocean when addressing low pregnenolone levels. Thus I don’t expect levels to improve. But enough exogenous pregnenolone can improve memory and mood when at least some gets into the brain. It can also be metabolized to the other steroid hormones. Thus these may have to be monitored if problems occur.

    GLUCOSE:

    From a behavioral point of view, the optimal range for Glucose is between 93-100. They would have problems with gluconeogenesis or glycogenolysis usually secondary to impaired cortisol or thyroid hormone production, though metabolic issues such as low iron problems may cause this as well.

    CHOLESTEROL:

    The liver also does signal processing.

    The liver is the major signal ender for the long-distance fluid-transmitted signals in the body – e.g. the hormones. A signal needs to be ended as well as transmitted.

    The liver produces the major hormone binding proteins which then influence hormone signaling. These binding proteins also prolong the signals – causing them to be slow-release signals.

    The liver also monitors hormone status, such as the level of steroid hormones. When steroid hormone levels are low, the liver produces cholesterol from glucose. Cholesterol is the building block for the steroid hormones. Thus, a high cholesterol indicates one may have a hormone deficiency.

    Vitamin D is a steroid hormone.

    #2020
    keithdolby
    Member

    @DrMariano 176 wrote:

    DHEA (dehydroepiandrosterone) is the most common hormone found in the body, outside of the brain. It is made by the adrenal gland’s outer layer, the adrenal cortex.

    DHEA is a very interesting substance since it has BOTH androgen and estrogen activity. It binds to both androgen and estrogen receptors.

    The brain, itself, makes DHEA, lots of it, as a neurotransmitter/neurohormone. The brain makes more DHEA than any other neurotransmitter except for pregnenolone.

    In the body, DHEA also is a precursor for testosterone and estradiol and 7-keto DHEA and estrone, among other things.

    The problem of taking a hormone orally is that:
    1. The liver destroys a lot of the hormone before it goes into the circulatory system. This is called Hepatic First-Pass Metabolism.
    2. The high concentrations of the hormone in the liver can cause changes in liver function.

    For example, 90% of oral progesterone is changed to pregnanolone. Pregnanolone acts like a benzodiazepine or barbiturate by enhancing GABA receptor affinity for GABA. This is responsible for progesterone’s sedative effects. The 10% of progesterone that is left is what would work as progesterone in the body.

    As another example, oral estrogens causes the liver the release inflammatory signals, increasing C-reactive protein levels. Premarin (horse estrogen) hugely induces liver enzymes compared to regular estradiol. This can cause hyperexcretion syndromes where the other hormones are destroyed at a very fast pace, resulting in hormone deficiencies that require large replacement doses to achieve adequate blood levels or hormone activity.

    DHEA, itself, increases the production of Cytochrome P450 3A4 (CyP3A4). This is called Hepatic Induction of the CyP3A4 enzyme. This is the body’s primary enzyme for inactivating drugs, toxins, and various hormones, allowing the metabolites to be excreted. CyP3A4 is the primary enzyme that destroys DHEA.

    Thus, taking oral DHEA increases the enzyme that gets rid of DHEA. The higher the dose of DHEA, the more it induces the production of CyP3A4, which gets rid of DHEA. Thus you reach a ceiling where it becomes more difficult to raise DHEA levels since it gets rid of itself.

    Only by taking huge doses would one overcome the induction of liver enzymes and the blood levels would once again go up. The problem then becomes: what are the dangers of such high levels of the substance? DHEA at high levels can cause problems. For DHEA in men, one can get higher direct estrogen receptor stimulation, the formation of more estrogens themselves, etc. This could lead to strokes, heart attacks as blood clots would be a potential problem. In women, on the other hand, higher DHEA means higher androgen or testosterone signaling, leading to problems of excess androgen signaling – such as body hair, acne, etc.

    Other medications can also induce liver enzymes. For example, Carbamazepine for years has been well known to induce liver enzymes, thus getting rid of itself and other medications and hormones in the process.

    If a person already has high amounts of CyP3A4, then they will tend to have lower amounts of DHEA.

    Blocking CyP3A4 is very dangerous since it is the most important of the enzymes that get rid of drugs and toxins in the body. Medications which reduce CyP3A4 are famous for causing fatal heart arrhythmias.

    Optimizing thyroid hormone, however, is one safe way of reducing DHEA’s ability to induce CyP3A4 activity.

    When Pregnenolone and progesterone are very low, I would suspect adrenal fatigue or hypothalamic-pituitary-adrenal dysregulation of some sort. Usually cortisol is either maintained – by sacrificing production of the other adrenal hormones, or cortisol is low. A low DHEA is another indication of the presence of low adrenal function. The stage of adrenal exhaustion in response to stress is when cortisol production cannot be maintained, even by sacrificing production of the other adrenal hormones.

    Impaired cortisol production will impair activation of thyroid hormone (T4 to T3 conversion). This, in turn, would make it more likely for oral DHEA to induce liver enzymes that get rid of DHEA.

    Transdermal or sublingual DHEA are ways to avoid high concentrations of DHEA in the liver, to thus minimize liver induction of CyP3A4. They bypass first-pass metabolism of DHEA.

    Low doses DHEA given in multiple intervals may be another way to avoid very high DHEA concentrations in the liver, to avoid liver enzyme induction.

    On another point, another reason high dose oral DHEA doesn’t result in high DHEA levels may be poor absorption of oral DHEA.

    DHEA is lipid soluble. This means it may be more easily absorbed if it is taken with other fats. These would stimulate liver bile production, which would then make it easier to absorb fats and fat soluble substances such as the fat soluble vitamins – and DHEA.

    Can you take all of the fat soluble supplements ( dhea, pregnenolone, omega 3’s, vitamin d3, COQ10, etc) with a straight shot of extra virgin olive oil, avocado oil? If so, which oil is recommened and how much should be used ( teaspoon, tablespoon?) Can you even drink extra virgin olive oil or avocado oil by itself because I have never heard of anyone doing this. I dont want to be the only one drinking extra virgin olive oil straight ( meaning not cooking with it or dipping it in bread, but just taking a tablespoon or two by itself) if no one has ever done this before. Thanks

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