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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 3 of 3. This is the beginning of the thread.
Posted by jrbecker on February 26, 2003, at 12:52:47
this could make a case for augmenting with a low dose of pregnenolone or maybe even DHEA for anxious-type depressives...
Neurosteroids and Psychiatric Disorders
by Christine E. Marx, M.D., M.A.
Psychiatric Times October 2001 Vol. XVIII Issue 10
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The term neurosteroid refers to steroids formed in the brain. It was created in 1981 by Dr. Etienne-Emile Baulieu and colleagues, following the remarkable discovery that the brain appeared to have the capacity to synthesize its own steroids in situ. In a set of rodent experiments, these researchers determined that the steroid dehydroepiandrosterone sulfate (DHEAS) was present in adult rat brains at concentrations up to 20-fold greater than plasma (Corpechot et al., 1981). Moreover, brain DHEAS concentrations persisted unchanged for over two weeks following adrenalectomy and gonadectomy in these animals, demonstrating that central nervous system DHEAS levels were likely independent of peripheral DHEAS formation in the adrenals or gonads. Hence, the brain itself appeared to be a potential site of steroidogenesis, and subsequent efforts confirmed this possibility. These molecules became known as neurosteroids, since they can be synthesized de novo in the brain from cholesterol or from peripheral steroid precursors that cross the blood-brain barrier readily.
A closely related term, neuroactive steroids, includes steroids formed in the brain and periphery that exhibit rapid actions on neuronal excitability. Unlike classical steroid mechanisms that involve the binding of intracellular receptors and the regulation of gene transcription, neuroactive steroids have nongenomic actions (Paul and Purdy, 1992). Specifically, neuroactive steroids bind to membrane-bound ligand-gated ion channel receptors. As a result, their actions occur very rapidly (over the course of seconds to minutes), in contrast to steroid genomic actions that require hours to days. Interestingly, certain neuroactive steroids with rapid nongenomic effects, such as progesterone, also exhibit traditional genomic steroid actions. Progesterone is considered to be a neurosteroid if it is synthesized in the brain, hence, the terms neurosteroid and neuroactive steroid are often used interchangeably.Neurosteroids can therefore alter neuronal excitability very rapidly by binding to receptors for inhibitory or excitatory neurotransmitters at the cell membrane. Neurosteroid actions at inhibitory -amino-butyric acid type A (GABAA) receptors are the most extensively characterized to date, but neurosteroid activity has also been demonstrated at excitatory glutamatergic (N-methyl-D-aspartate [NMDA], -amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid [AMPA], kainate), 5-HT3, glycine, sigma type 1 and nicotinic acetylcholine receptors (Rupprecht and Holsboer, 1999). Neurosteroid actions at GABAA receptors can occur at low nanomolar physiologic concentrations, while neurosteroid activity at other receptor types frequently requires higher concentrations of 1.0 x 10-7 M or greater. In addition to the characterization of neurosteroid actions at membrane-bound ligand-gated ion channel receptors, in the last decade it has also been established with certainty that enzymes leading to neurosteroid biosynthesis are present in glia and neurons in the brain (Compagnone and Mellon, 2000). In other words, the enzymatic biosynthetic machinery facilitating steroid formation from cholesterol in peripheral endocrine organs (such as the adrenals, ovaries and testes) is also present in the brain.
Currently, there are relatively few neurosteroid clinical studies, however, converging evidence suggests that these molecules may be relevant to the pathophysiology and pharmacological treatment of psychiatric disorders such as depression and schizophrenia. Specifically, neurosteroids are differentially regulated in males and females and may, therefore, modulate the neurobiology of gender differences observed in a variety of psychiatric illnesses. Neurosteroids are important in neurodevelopment and regulate neuronal cytoarchitecture (Compagnone and Mellon, 1998), suggesting a potential role for these molecules in the pathophysiology of psychiatric disorders demonstrating a neurodevelopmental component and neuronal cytoarchitectural alterations such as schizophrenia. Finally, neurosteroids modulate GABAergic neurotransmission, are linked to antidepressant and antipsychotic drug action, act as neuroprotective agents, modulate the hypothalamic-pituitary-adrenal (HPA) axis, and represent potential targets for pharmacological intervention. These latter neurosteroid properties are discussed below.
GABAA Receptor Actions
Certain neurosteroids bind with very high affinity to GABAA receptors. For example, the neurosteroid 3-hydroxy-5-pregnan-20-one (allopregnanolone) is synthesized by the reduction of progesterone via the enzymes 5-reductase and 3-hydroxysteroid dehydrogenase (3-HSD). Astonishingly, allopregnanolone potentiates GABAergic neurotransmission with 20-fold higher potency than benzodiazepines and 200-fold higher potency than barbiturates (Morrow et al., 1990, 1987). Indeed, the neurosteroid progesterone metabolites allopregnanolone, its stereoisomer 3-hydroxy-5ß-pregnan-20-one (pregnanolone) and the deoxycorticosterone metabolite 3,21-dihydroxy-5-pregnan-20-one (THDOC) are the most potent known modulators of GABAA receptors. Many of the physiologic functions of these endogenous molecules in the human brain remain to be determined, but it is likely that allopregnanolone and other neurosteroids with GABAA receptor activity might play an important role in the regulation of GABA, the major inhibitory neurotransmitter in the mammalian central nervous system.
Neurosteroid interactions with GABAA receptors are not completely understood. The GABAA receptor is a pentameric complex with at least 21 subunit types involved in receptor assembly: 1-6, ß1-4, 1-4, , , , , 1-3 (Bonnert et al., 1999; Bormann, 2000; Penschuck et al., 1999). As a result, more than 500,000 different GABAA receptor subunit combinations are theoretically possible (Lambert et al., 1996). Adding yet another level of molecular complexity, subunit composition appears to determine the pharmacological profile of GABAA receptors. For example, benzodiazepines bind to GABAA receptors but require the presence of a 2 subunit to potentiate GABAergic neurotransmission (Pritchett et al., 1989), suggesting that benzodiazepine activity may be limited to a specific subset of GABAA receptors. In contrast, the neurosteroid allopregnanolone acts at a wide variety of GABAA receptor subtypes with similar potency and efficacy and does not exhibit stringent GABAA subunit specificity, possibly reflecting a broad spectrum of action in the central nervous system (Puia et al., 1990).
SSRIs
Recent efforts have linked neurosteroids to selective serotonin reuptake inhibitors. In a clinical study of 15 patients with major depression, cerebrospinal fluid (CSF) levels of the GABAergic neurosteroid allopregnanolone were decreased at baseline compared to control subject levels (Uzunova et al., 1998). Following treatment with fluoxetine (Prozac) or fluvoxamine (Luvox), CSF allopregnanolone levels increased in subjects with depression and correlated strongly with improvements in depressive symptoms. The authors hypothesized that SSRI-induced increases in allopregnanolone may represent a novel mechanism contributing to SSRI efficacy.
Enzyme kinetic studies subsequently demonstrated that fluoxetine, paroxetine (Paxil) and sertraline (Zoloft) increase the efficiency of the enzyme 3-HSD, which catalyzes allopregnanolone biosynthesis from its immediate precursor 5-dihydroprogesterone (Griffin and Mellon, 1999), resulting in dramatically enhanced allopregnanolone formation. In addition, allopregnanolone is known to exhibit marked anxiolytic effects in rodents (Crawley et al., 1986; Wieland et al., 1991), consistent with its GABAA receptor actions. These studies support the possibility that SSRI-induced allopregnanolone biosynthesis may be relevant to SSRI therapeutic actions in depression and anxiety.
Antipsychotic Drug Action
Neurosteroids have also been linked to antipsychotic drug action in recent rodent investigations. For example, the antipsychotic olanzapine (Zyprexa) dose-dependently increases the potent GABAergic neurosteroid allopregnanolone in rat cerebral cortex (Marx et al., 2000a), and preliminary evidence indicates that clozapine (Clozaril) has similar effects (Marx et al., 2001). Since GABAergic neurotransmission appears to be altered in schizophrenia (Lewis, 2000), antipsychotic-induced elevations in allopregnanolone may be relevant to this component of schizophrenia pathophysiology. If olanzapine also induces elevation in allopregnanolone in humans, it is possible that allopregnanolone may contribute to the efficacy of this antipsychotic. Olanzapine also has anxiolytic-like effects in animals (Arnt and Skarsfeldt, 1998), and, therefore, olanzapine-induced elevations in the anxiolytic neurosteroid allopregnanolone may represent a mechanism contributing to these actions. Finally, olanzapine has marked effects on rodent serum progesterone levels, a steroid that appears to have non-reproductive functions in addition to its well-established reproductive actions. For example, recent evidence suggests that progesterone plays an important role in myelination (Baulieu and Schumacher, 2000), a finding that may be relevant to schizophrenia, since recent evidence suggests a dysregulation in myelin-related genes in the disorder (Hakak et al., 2001). Future investigations will be required to determine the potential clinical significance of antipsychotic-induced neurosteroid alterations for schizophrenia pathophysiology and treatment.
Neuroprotection
Many lines of investigation demonstrate that neurosteroids have neuroprotective properties. For example, the GABAergic neurosteroid allopregnanolone demonstrates anticonvulsant effects in a variety of animal seizure models (Belelli et al., 1989; Devaud et al., 1995). A synthetic homologue of the inhibitory neurosteroid pregnanolone sulfate inhibits NMDA-induced current and cell death in rat hippocampal neuronal cultures and significantly reduces cortical and subcortical infarct size in rats (Weaver et al., 1997). The neurosteroid DHEA and its sulfated derivative DHEAS protect rodent embryonic cerebral cortical neurons from anoxia (Marx et al., 2000b), a neurodevelopmental stressor associated with increased schizophrenia risk. DHEA also protects neurons against glutamate and amyloid ß-protein toxicity (Cardounel et al., 1999), glucocorticoid toxicity (Kimonides et al., 1999), and numerous other insults resulting in oxidative stress.
Interestingly, DHEA and DHEAS levels decrease markedly with age in humans, and levels in elderly populations are reduced to 20% to 30% of peak levels in young adulthood (Labrie et al., 1997; Orentreich et al., 1992), but the clinical relevance of this finding has not yet been established. Since DHEA has memory-enhancing effects in animals (Flood et al., 1992; Roberts et al., 1987), it has been hypothesized that DHEA has neuroprotective effects on cognition and that its age-related decline may be related to declining cognitive function with age in the elderly. Since a number of neurosteroids demonstrate prominent neuroprotective effects in a variety of rodent experimental systems, these molecules may function to modulate neuronal insults leading to psychiatric morbidity and merit further exploration in the clinical realm.
The Role of Stress
Several neurosteroids, including allopregnanolone and THDOC, have pronounced effects on the HPA axis. Allopregnanolone decreases corticotropin-releasing factor release from the hypothalamus (Patchev et al., 1994) and also dampens adrenocorticotropin hormone (Patchev et al., 1996) and corticosterone release (Guo et al., 1995; Patchev et al., 1996) in rats. Allopregnanolone is known to increase with stress (Purdy et al., 1991), and, therefore, stress-induced elevations in this neurosteroid would ultimately suppress the HPA axis. It has been hypothesized that stress-induced allopregnanolone induction may therefore represent an endogenous autoregulatory mechanism to restore homeostasis following a stressful event (Morrow et al., 1995).
The GABAergic neurosteroid THDOC also appears to demonstrate HPA axis modulation. Specifically, THDOC appears to be protective against early adverse events in neonatal rats subjected to intermittent maternal deprivation (Patchev et al., 1997). Rats treated with THDOC and exposed to this stressor were protected against HPA axis dysregulation. Since many psychiatric disorders are stress-sensitive and illnesses such as depression demonstrate a dysregulation in stress hormones (including cortisol), neurosteroid modulation of the HPA axis may have important clinical ramifications.
Pharmacological Intervention
Given accumulating evidence suggesting that neurosteroids may be important in psychiatric disorders and treatment strategies, the possibility that neurosteroids (or the enzymes leading to neurosteroid biosynthesis) may serve as targets for pharmacological intervention has received increasing attention. Limiting factors in drug development have included the rapid metabolism and poor water-solubility of neurosteroids, but efforts are currently underway to address these difficulties. For example, the synthetic neurosteroid ganaxolone is a 3ß-methylated analogue of allopregnanolone with more favorable pharmacokinetic properties (Gasior et al., 1999). Similar to allopregnanolone, it demonstrates anticonvulsant efficacy. At this time, it appears likely that neurosteroid drug development initiatives will yield a number of promising compounds to be utilized in the treatment of neuropsychiatric disorders in future years.
Concluding Remarks
Neurosteroids are fascinating molecules with potential relevance to the pathophysiology and treatment of psychiatric disorders. Although future research will be required to characterize the precise roles of neurosteroids in psychiatric illness, current evidence is compelling and justifies further investigations into the actions of these unique compounds in the central nervous system.
Dr. Marx is assistant professor in the department of psychiatry and behavioral sciences at Duke University Medical Center and the Durham VA Medical Center. Her research interest is the relevance of neurosteroids to schizophrenia pathophysiology and antipsychotic drug action.
Posted by Ron Hill on February 26, 2003, at 20:55:50
In reply to interesting article on neurosteroids, posted by jrbecker on February 26, 2003, at 12:52:47
Posted by jrbecker on February 28, 2003, at 15:26:07
In reply to interesting article on neurosteroids, posted by jrbecker on February 26, 2003, at 12:52:47
Whoops, I need to clairfy an important point from my original post on this thread. I stated that pregnenolone, and to a lesser degree, DHEA, would be beneficial for 'anxious-type' depressives. That's pretty much 180 degrees off!! I meant to say that it is beneficial for 'atypical/anhedonic' types, like myself. This is because Pregnenolone has a trickle down effect to helping boost corticosterone production as well as the adrogen steroids. It is known as the "happy hormone" and is also great for boosting memory and energy...thus, it's obvious benefits for atypical types. HOWEVER, pregnenolone also antagonizes the production of GABA in the brain, so it can also increase anxiety in those already prone to it, or even in the normal individual who takes a high dose. Although many brands offer it in anywhere from 10 - 50 mg tablets, many recommend starting low. I had the unfortunate mistake of starting out at 50mg. For the first week I felt both physically and mentally terrific but as the levels built up, I also began to have insomnia as well. Right now, I am at 25 mg daily, but still trying to see if this is the ideal dosage level. Your ideal dose will depend on a lot of factors, including age, gender, and baseline hormone levels.
So if you're going to try it, start low, even 5 to 10 mg at first (some recommend starting even lower, but I don't believe doses lower than this will come close to helping depressive individuals vs. the normal population). Go slow while you increase it, since its effects are quite subtle at first...nothing like the on-off switch of psychotropic meds. It takes a full 1-2 weeks to notice the effects of a dosage increase. And it is recommeded that you take drug holidays from it often so your body doesn't become dependent on it.
So, all in all, it's been great for me as an adjunct to my atypical depression tx. I definitely have more energy and cognitive enhancement, as well a slight but noticeable mood boost from it. But be very cautious if you have anxiety symptoms! [On a very ironic note though, people known to have social anxiety have been measured to have LOW pregnenolone. The theory on why this is the case is because pregnenolone helps modulate dopamine, which is also known to be a factor in social anxiety]. Visit "socialfear.com" for more on this.
For more interesting info on this, I've pasted a link from Dr. Ray Sahelian's (author of Mind Boosters) website:
PREGNENOLONE
"http://www.raysahelian.com/pregn.html";Benefits of pregnenolone
Some people find pregnenolone improves energy levels, vision, memory, clarity of thinking, and wellbeing, perhaps also sexual enjoyment. Some women report lessening of hot flashes or premenstrual symptoms. Studies in rodents show pregnenolone to be one of the most effective and powerful memory boosters. Pregnenolone may increase levels of acetylcholine in the hippocampus and other memory regions in the brain.Side effects of pregnenolone:
Overstimulation and insomnia
Irritability, anger or anxiety
Acne
Headaches
Possible scalp hair loss
Irregularities of heart rhythm, palpitations
Unknown effects on the thyroid gland or other organsby Ray Sahelian, M.D.
Cautions
We're still in the early stages of learning about pregnenolone and its full effects on the human body.
It is best to proceed with caution until more information is available. This means using the lowest effective dose and seeking supervision by a knowledgeable health care provider. There are some medical or psychiatric conditions where pregnenolone can be used temporarily and then stopped. With this conservative approach, it is unlikely that any problems would arise. Our major uncertainty at this time involves the long-term use of pregnenolone as hormone replacement therapy, especially if high doses are used. Pregnenolone can also cause heart palpitations in high doses.With time, as more and more people use this hormone, we'll have a fuller understanding of its benefits and side effects. Those who have already found pregnenolone to be helpful in terms of mood elevation, stress reduction, arthritis help, visual and auditory enhancement, and so forth, but are concerned about unknown long-term effects, may feel more comfortable using pregnenolone only as needed and frequently taking time off from it. Taking these "hormone holidays" will mitigate any potential unknown risks.
Daily use of pregnenolone over prolonged periods should be no more than 1 to 3 mg unless you are closely followed by a health care practitioner familiar with the clinical uses of this hormone. Current dosage available over the counter, such as 10, 25, 50, or 100 mg are too high.
Suppliers of natural supplements
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Index of Vitamins, Herbs, Supplements, and Natural TherapiesPregnenolone is a hormone that may be useful in medicine but its potential has yet to be fully explored. Why is this?
Pregnenolone is a natural hormone which cannot be patented. Back in the 1940's, when researchers started experimenting with the use of Pregnenolone, they realized that it could be helpful for people under stress and it could increase energy in those who were fatigued. However, about the same time, cortisol, another closely related hormone, was discovered. Cortisol stole the limelight. When cortisol was given to individuals with rheumatoid arthritis, there were outstanding short-term improvements. Photographs of these remarkable recoveries were circulated and the medical community was impressed. Scientists basically put Pregnenolone aside to focus on cortisol. The structure of cortisol was altered to make similar molecules such as dexamethasone and prednisone, much more powerful steroids. Dexamethasone and other similar corticosteroids could be patented, and thus a pharmaceutical company could make a lot of money by owning patents.Pregnenolone has stayed in relative obscurity since the 1940's, with only rare mentions in the medical literature. A review of Medline, the computer system that records all articles published in scientific journals, shows only a few studies published on Pregnenolone in 1995 and 1999, and only a couple involve human subjects.
Q. What is a Steroid?
A. A steroid is chemical substance with four carbon ring structures attached to each other in a very specific way. Cortisol, DHEA, testosterone, pregnenolone, progesterone, and estrogen are all steroid hormones that chemically look very similar to each other in terms of their backbone. However, they differ from each other in only small ways, and even tiny changes in the chemical make up of a substance can make enormous differences in how it functions and what role it plays in the chemical factories of our bodies. For instance, testosterone, the male hormone, is only slightly different chemically from estrogen, the female hormone. Yet that slight difference causes men to grow facial hair and women to develop breasts.
Q. Is pregnenolone different that progesterone?
A. Pregnenolone is converted in the body to progesterone and these two hormones have some overlapping similarities, but we still don't know exactly how their effects overlap. Pregnenolone is also converted into DHEA, which, in turn may convert into androstenedione, testosterone, and estrogens.
Q. How is pregnenolone made?
A. There is a type of plant called a wild yam that is grown in certain parts of the southern U.S. and in Mexico. This wild yam contains a compound called diosgenin that is the precursor to steroid hormones. In a laboratory, diosgenin is converted into pregnenolone. Further laboratory processing can convert pregnenolone into DHEA. The human body does not have the ability (the required enzymes) to convert diosgenin (a six ring structure) into pregnenolone (a four ring structure). Therefore, if you swallow pills that are extracts of wild yams (diosgenin), you will not get pregnenolone or DHEA. The conversion of diosgenin to pregnenolone has to be done in a laboratory. If you want Pregnenolone or DHEA, the bottles you buy must say that they contain actual pregnenolone or DHEA, not extracts of wild yams or diosgenin.
Q. What form of pregnenolone is best?
A. Oral pills work well. Sublingual or micronized are also good options.
Q. Can I take pregnenolone if I'm already on DHEA, estrogens, or other hormones?
A. Since both DHEA and pregnenolone have some similar effects (however, they have differences, too), you should lower your dose of DHEA when you go on pregnenolone. The lowering of the dose should by the same amount as the pregnenolone dose. Before you add pregnenolone, though, make sure you try it separately to see what kind of effects it has on you, Once you know how you react to DHEA and pregnenolone separately, you can then combine them. The amount of conversion of pregnenolone to estrogens is not fully known.
Q. Is it true that some people notice improvement in vision while taking pregnenolone?
A. A good number of individuals have reported enhancement of visual perception. Colors are brighter and clearer. Patterns are more noticeable. Looking becomes more enjoyable. However, not everyone seems to be attuned to this perceptual enhancement.Jan 2003, emails
Q. I'm 53 and have been using preg for about 4 to 5 years, slowly increasing the dosage from 10 mg per day to the 100 mg (2 x 50 mg) that I now take with no time off from the supplement. I've had no bad side effects. As I increased the dosage, I noticed an increase in strength. Not massive, but noticeable. I feel good, memory is sharp. Only need 6 to 7 hours of sleep a night. I feel like I'm 25 in a 53 year old body. I've had blood work during this period with no bad results.
A. Well, I hope your positive results continue, however, I'm quite uncomfortable with the high dosages you are taking.Q. You may be interested in additional data backing up your cautions on your web page. I had been taking 50 mgs of DHEA and pregnenolone each for about 9 months when I went in for a routine physical exam. The exam turned up hyperthyroidism and atrial flutter - neither of which had existed in any prior physicals.
So, another profound 'thanks;' this time for your internet article. With the information it contained, I was able to alert my physician as to the probable cause of both conditions which was most helpful in reaching an accurate diagnosis. Fortunately, with medication (methimazole & propafenone) and 2 cardioversions, both conditions have now been eliminated.
As you might guess, I've learned a lesson about charging off on my own.
A. Yes, Playing with hormones can be dangerous.Q. I am trying Pregnenolone to help with PMS/PMDD & depression. I just purchased some and the label says "Do not take if under 40 yrs old". Can you explain this?
A. Pregnenolone is a powerful over the counter hormone. There is no specific age cutoff for its use, but the body's production does decrease with age. There have not been studies to evaluate whether this hormone is appropriate for hormone replacement therapy. Most of the dosages available in stores are too high for regular daily consumption and can lead to side effects. It’s best this hormone be used under medical guidance, and only in low dosages. I consider any dosage over 5 mg to be high for long term use.
Q. I am a doctor writing from Germany. Do you hold the use of Pregnenolone in the treatment of the concentration-weakness of children? It seems to work namely, but isn't it contraindicated ? Or is it effective as normal basis-component of the hormone-synthesis without creating negative feedback problems?
A. Pregnenolone is a powerful hormone and I would not recommend its use in children unless they have adrenal insufficiency.
Q. My son is 9 yrs old and suffers from a very rare condition called congenital adrenal hypoplasia. This basically means he has no adrenal cortex at all and receives replacement therapy of hydrocortisone and fludrocortisone. The complexity of the other 40 odd hormones produced in the cortex and their pathways are such that these other hormones are not added to this replacement regime. If DHEA is the most abundant of hormones in the body and given the increased understanding of it and its interaction in the body, is not logical that some sort of replacement therapy would be offered to people suffering from adrenal insufficiency. It would seem that a hormone related to moods, coping, blood sugar level management,, stress, testosterone synthesis.......... would be needed by people who do not produce a drop. Any thoughts would be greatly appreciated.
A. The medical profession has not focused replacement of natural hormones for adrenal malfunction. Pregnenolone is the "grandmother adrenal hormone" from which all other adrenal hormones are made, while DHEA is the son of pregnenolone. It does seem reasonable to assume that perhaps replacing pregnenolone or DHEA might offer advantages that cortisones alone may not provide. The research on this is very limited but replacing or combining one or both of these hormones is theoretically a reasonable approach while under the care of an endocrinologist.Q. I was wondering since Pregnenolone is a "steroid", does it increase strength or mass?
A. Pregnenolone is a steroid, and converts into progesterone and DHEA. Although I am not aware of studies that have tested it in terms of increasing muscle mass, it probably has some effect, although not as direct as androgens.
Q. I have 26-day cycles, heavy periods with much pain, mild diagnosed endometriosis, and obvious estrogen dominance and sensitivity. What might pregnenolone do for me in terms of possibly minimizing my menstrual discomfort (w/pms, much water retention, etc.) or even stretching out the length between cycles, etc.???
I've heard that pregnenolone is beneficial for overall well-being and I'd like to know how it may help me. I've also been told I have a very short luteal phase and very low progesterone.
A. Pregnenolone's actions, are, in many ways, similar to progesterone. It is difficult to predict how pregnenolone will influence your cycle. As with progesterone, I prefer medical supervision if you plan to take pregnenolone. Even though pregnenolone is available over the counter, it is a powerful hormone and should be treated with respect.
Q. Do you think a man with prostate cancer can take pregnenolone? If so would you suggest long term or short term use? Please specify how long short or long term would be.
A. Although the effects of pregnenolone on the prostate gland are not as direct as testosterone, I don't recommend any kind of steroid hormone in a person who has prostate cancer.
For more information about the cognitive effects of pregnenolone and its role in hormone replacement, and how to safely combine it with DHEA, progesterone, and estrogen, see
MIND BOOSTERS: A Guide to Natural Supplements That Enhance Your Mind, Memory, and Mood
Suppliers of Pregnenolone
iherb
Index of Vitamins, Herbs, Supplements, and Medical ConditionsA Personal Story (submitted by email July 2000)
Pregnenolone is nothing short of a small miracle to me!
I am a 37 yr. old female who since birth has had allergies and many sensitivities. I also got sick a lot.
You get the picture. After giving birth to 3 kids in 13 months ( I had Premie twins with health issues) I was left with no mental or physical reserves. At that point I started having horrible mood swings, awful PMS, fatigue, and at really bad times would self injure. Of course I got help, counseling, different meds, relaxation techniques etc. I faithfully tired all with little help.The worst times however were my periods so one concerned Dr. tired different things but finally decided on doing a Hysterectomy.Then the problems slowly began even though I took Estratest. Problems as they appeared.Fatigue- off and on
Horrible ( and I mean really bad) carb. cravings
Really low sex drive. No feelings in nipples etc.
Stomach problems: IBS, heartburn
Joint and muscle aches
Unexplained hives- This led to use of anti-histamines.
Weird nerve like pains in left wrist.
Extra hair growth then loss, weight gain then loss (sometimes weekly!)
Really high moods then low, this could switch within hours.
And last but not least the migraines which besides the pain it would cause me really weird things
like having to urinate tons right before the onset of one, and a feeling like my heart rate was changing.All through this I was also sometimes depressed, anxious, and crabby a lot.
I went to many Doctors and was told my blood tests were normal (although they never did one to check hormonal levels) they just said all my symptoms were stress related which I sometimes wondered if that was all. I was put on Luvox for four years and while that helped for some things like the emotional elements I still had lots of the other things. I finally went off the luvox, when I gained 40 pounds and felt really tired all the time.. After that I started over again in my quest to feel better.Now we're up to date and I started seeing my regular M.D., my migraine specialist, and a psychiatrist. All agreed that Depakote would help for some of my problems. I was able to take it for about 2 weeks.
It triggered my IBS really badly! So they told me to stop. My psychiatrist said I probably had some kind of auto-immune disorder, but at the current time they didn't know what it was. This got me thinking and spending days on the internet researching.I finally decided to try to buck-up my body naturally. I had only tried the usual vitamins so I went further, I started looking into mood enhancers etc. That's when I came across Pregnenolone!
When I read what it was and what it did a light went on. I have never to this point been one to jump up and rush off to try something. I have had too many bad reactions to do that! But for some reason I had to try Preg. OH MY GOD! I took 10 mg. and that very day (thats another thing the Docs. could never fathom is how tiny amounts of meds could instantly cause a change) I felt different, better! My grandmother was always the same she could take 1/4 of the normal dose and have a good or bad reaction instantly. Anyway I have been taking 10 mg. a day for 3 weeks. It is the longest period of time that I have had energy, no headaches, or awful food cravings in ten years. The jury is still out on my other complaints but feeling less stressed has got to be a helpful thing. Please if you ever have a frustrating, hyper-sensitive patient that needs a little balance in their bodies try the pregnenolone!
This is the end of the thread.
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