bombbudpuffa
Sweet Cheeba Chiefa
- Joined
- Oct 28, 2006
- Messages
- 5,880
- Reaction score
- 4,347
In humans. Who knows what it does to plants? If you want to give them hormones seaweed extract is full of PLANT hormones that are beneficial to PLANT growth
.
Birth Control pills Increased Growth ??
- Thread starter BUDISGUD
- Start date
.
Fadeux
Intelligent Moron
- Joined
- Nov 13, 2007
- Messages
- 469
- Reaction score
- 442
bombbudpuffa said:In humans. Who knows what it does to plants? If you want to give them hormones seaweed extract is full of PLANT hormones that are beneficial to PLANT growth
So if you give a women estrogen supplements, will she suddenly grow a better vagina? or bigger ****s? No, her body will up her testosterone, and shell will just have hairy arms, or broader shoulders.
I would say nobody on this board has any sort of insight as to genetically altering weed through hormone therapy. Just take care of your girls normally, and they will do just fine. If you start screwing with her hormones, I can't imagine anything better will come of it.
raoulduke2.0
Norse God of Herbs
- Joined
- Aug 1, 2008
- Messages
- 193
- Reaction score
- 131
slowmo77 said:
Word.
bombbudpuffa
Sweet Cheeba Chiefa
- Joined
- Oct 28, 2006
- Messages
- 5,880
- Reaction score
- 4,347
No too much estrogen in women doesn't cause hairy pits or broad shoulders.Can't get the link to work so i'll copy and paste
.
bombbudpuffa
Sweet Cheeba Chiefa
- Joined
- Oct 28, 2006
- Messages
- 5,880
- Reaction score
- 4,347
Effects of Estrogen
from Journal of the American Pharmaceutical Association
Estrogen and the Brain
Estrogen directly influences brain function throughestrogen receptors located on neurons in multiple areas of the brain.[1,2 ]The hormone also appears to have direct membrane-mediated effects on neurons. Its effects are both neuroprotective and neurotrophic.[2] Estrogen has been shown to protect isolated neurons in vitro from oxidative stress, ischemic injury, hypoglycemic injury, and damage by amyloid protein, which is implicated in the pathogenesis of Alzheimer's disease.[2] It also stimulates production of nerve growth factors, thereby promoting neuronal growth and viability, repair of damaged neurons, and dendritic branching. Brain aging and Alzheimer's disease are thought to represent an imbalance between neuronal injury and repair.[1-3]At neuronal synapses, estrogen increases the concentration of neurotransmitters such as serotonin, dopamine, and norepinephrine.[4] It affects their release, reuptake, and enzymatic inactivation. It also increases the number of receptors'forthese neurotransmitters.[2]
Another significant effect of estrogen on the brain is its influence on blood supply. Unlike many other organs, which can use reserve fuel sources or alternative metabolic pathways, the brain depends solely on blood flow to function. In fact, roughly one-third of the brain is composed of blood vessels.[5] Estrogen increases cerebral perfusion, presumably by mechanisms similar to those known to occur in the coronary arteries.[3,6,7] By binding to receptors in the endothelium, estrogen stimulates the release of nitric oxide, which causes vasodilation.
Recent studies have documented the vasodilatory effect of estrogen. Using Doppler flow ultrasound, Penotti et al.[6] examined the carotid and cerebral arteries of 120 women aged 20 to 59 years who were not taking any hormones. Compared with the premenopausal women participating in the study, the postmenopausal women exhibited a significant decrease in blood flow, and flow decreased further with time past menopause. No significant decrease was attributable to aging alone. Another Doppler flow study of 63 postmenopausal women before and after starting ERT demonstrated that this hormonal therapy reduced impedance to blood flow in carotid circulation.[7] Improvement in perfusion was significant by the second month of ERT, and a gradual increase in perfusion continued over the entire 52 weeks of the study.
Estrogen also influences cerebral blood supply by acting as an anti-inflammatory agent at the blood vessel wall, protecting it from damage by cytokines and free radicals and impeding plaque formation.[1,2,8] Pretreatment with estrogen has been demonstrated to prevent damage to blood vessel walls when a toxic protein is injected into rats' cerebral arteries.[9] MRI was used to document ischemic brain injury in 210 postmenopausal women followed for 10 years.[10] The 70 women taking ERT in this study had fewer and smaller damaged areas than the 140 controls. In addition, the longer the duration of ERT use, the smaller the total area of ischemia.
Hot Flushes
Hot flushes, the classic symptom of menopause, are experienced by up to 85% of perimenopausal women.[11] (Perimenopause begins several years before menopause, when ovarian function starts to decline, and continues for several years after menopause, until ovarian function has reached its nadir.) A hot flush consists of a sudden sensation of heat in the upper body, often followed by perspiration and a chill. Peripheral vasodilation, tachycardia, decreased skin resistance, and sweating have all been documented to occur during a hot flush. Although poorly understood, the episodes certainly originate in the brain, most likely as a direct response to hypoestrogenism in the thermoregulatory center of the hypothalamus.[12]It now appears that hot flushes are not merely symptoms of low estrogen levels; they may themselves lead to other neurologic problems. In oophorectomized women, hot flushes have been directly correlated with memory impairment.[13] In addition, single proton emission computed tomography (SPECT) of healthy menopausal women revealed decreased cerebral blood flow during hot flushes.[14] The greatest change occurred in the hippocampus, a center for memory and cognition. Regional patterns of cerebral blood flow during hot flushes resembled those characteristic of Alzheimer's disease. ERT resolved the hot flushes and restored normal patterns of cerebral blood flow.
Based on this evidence, reproductive biologists have hypothesized that hot flushes contribute to degenerative or aging changes in the brain.[15] Frequent vasoconstrictive episodes might lead to cerebral ischemia and free radical formation. The resulting damage may be analogous to that seen in the coronary arteries with plaque formation. The population of healthy neurons might be reduced, particularly in the hippocampus, leaving the brain with impaired ability to tolerate the neurodegenerative processes of aging and Alzheimer's disease.
Estrogen and Cognition
Even in healthy older women, brain volume begins to decline as estrogen levels fall in the perimenopausal period.[16] This atrophy occurs particularly in the hippocampus and parietal lobe, areas primarily associated with memory and cognition. A similar loss in brain volume does not begin in men until a decade later (around age 60), most likely because male sex hormone production declines much more gradually with age. In fact, because of aromatization of testosterone to estrogen, men over the age of 60 have approximately three times more circulating estradiol than women of a similar age.[17]In women, these cerebral changes may contribute to the frequent perimenopausal complaints of decreased mental clarity and short-term, verbal memory problems (see Table 1).[18] Studies of the effects of ERT on cognitive symptoms have generated inconsistent results, perhaps because dropouts and nonparticipants are more likely to be cognitively impaired.[19] A recent meta-analysis yielded only weak evidence that ERT improves cognition and prevents dementia.[20] However, many research groups have found a significant association between ERT and cognition, particularly in the area of verbal memory. For example, in one study of 727 postmenopausal women, history of estrogen use was associated with significantly higher scores on verbal memory and abstract reasoning tests.[21]
Shaywitz et al.[22] used positron emission tomography to observe brain activity in 46 postmenopausal women performing cognitive tasks. In a crossover design, participants were given conjugated equine estrogens (CEE; 1.25 mg) or an identical placebo for 21 days, then, after a washout period, given the opposite treatment. During the cognitive tasks, women taking CEE demonstrated increased activation of areas involved in verbal and nonverbal memory.
Loss of cognitive function also can be related to endogenous estrogen deficiency. In the Study of Osteoporotic Fractures,[23] women in the lowest quintile for bone density also exhibited the highest incidence of dementia.[23] In another study, premenopausal women who underwent oophorectomy, which results in abrupt and severe decline in estrogen levels, were more likely than naturally postmenopausal women to exhibit memory impairment 5 years later.[24] Decline in cognitive function has been observed as early as 2 months postoperatively,[25] and has been shown to be reversible with ERT.[26]
Another effect of menopause and loss of estrogen on the brain is a slowdown in the speed of brain processing.[27] This change is particularly significant for postural stability, which depends on recognition of sensory input and initiation of an appropriate physical response. After menopause, the incidence of falls among women is three times that of men.[1 ]The risk of fracture in women with osteoporosis appears to be related not only to bone density, but also to postural stability.[28,29]
Brain processing speed and postural stability are significantly improved with ERT. One study documented a 60% decreased risk of falling in a group of postmenopausal women on ERT compared with a group not taking it.[28] Another study compared sway velocity (an indicator of tendency to fall) in 16 postmenopausal long-term users of 17 b-estradiol and 16 postmenopausal women who had never taken estrogen.[29] The postmenopausal women taking estrogen evidenced postural stability similar to premenopausal women, whereas balance deteriorated significantly in the postmenopausal women not on ERT. The fact that ERT improves both postural stability and bone density likely explains why it has proven superior to raloxifene[30] and alendronate[31] in preventing nonvertebral, fall-related fractures.
from Journal of the American Pharmaceutical Association
Estrogen and the Brain
Estrogen directly influences brain function throughestrogen receptors located on neurons in multiple areas of the brain.[1,2 ]The hormone also appears to have direct membrane-mediated effects on neurons. Its effects are both neuroprotective and neurotrophic.[2] Estrogen has been shown to protect isolated neurons in vitro from oxidative stress, ischemic injury, hypoglycemic injury, and damage by amyloid protein, which is implicated in the pathogenesis of Alzheimer's disease.[2] It also stimulates production of nerve growth factors, thereby promoting neuronal growth and viability, repair of damaged neurons, and dendritic branching. Brain aging and Alzheimer's disease are thought to represent an imbalance between neuronal injury and repair.[1-3]At neuronal synapses, estrogen increases the concentration of neurotransmitters such as serotonin, dopamine, and norepinephrine.[4] It affects their release, reuptake, and enzymatic inactivation. It also increases the number of receptors'forthese neurotransmitters.[2]
Another significant effect of estrogen on the brain is its influence on blood supply. Unlike many other organs, which can use reserve fuel sources or alternative metabolic pathways, the brain depends solely on blood flow to function. In fact, roughly one-third of the brain is composed of blood vessels.[5] Estrogen increases cerebral perfusion, presumably by mechanisms similar to those known to occur in the coronary arteries.[3,6,7] By binding to receptors in the endothelium, estrogen stimulates the release of nitric oxide, which causes vasodilation.
Recent studies have documented the vasodilatory effect of estrogen. Using Doppler flow ultrasound, Penotti et al.[6] examined the carotid and cerebral arteries of 120 women aged 20 to 59 years who were not taking any hormones. Compared with the premenopausal women participating in the study, the postmenopausal women exhibited a significant decrease in blood flow, and flow decreased further with time past menopause. No significant decrease was attributable to aging alone. Another Doppler flow study of 63 postmenopausal women before and after starting ERT demonstrated that this hormonal therapy reduced impedance to blood flow in carotid circulation.[7] Improvement in perfusion was significant by the second month of ERT, and a gradual increase in perfusion continued over the entire 52 weeks of the study.
Estrogen also influences cerebral blood supply by acting as an anti-inflammatory agent at the blood vessel wall, protecting it from damage by cytokines and free radicals and impeding plaque formation.[1,2,8] Pretreatment with estrogen has been demonstrated to prevent damage to blood vessel walls when a toxic protein is injected into rats' cerebral arteries.[9] MRI was used to document ischemic brain injury in 210 postmenopausal women followed for 10 years.[10] The 70 women taking ERT in this study had fewer and smaller damaged areas than the 140 controls. In addition, the longer the duration of ERT use, the smaller the total area of ischemia.
Hot Flushes
Hot flushes, the classic symptom of menopause, are experienced by up to 85% of perimenopausal women.[11] (Perimenopause begins several years before menopause, when ovarian function starts to decline, and continues for several years after menopause, until ovarian function has reached its nadir.) A hot flush consists of a sudden sensation of heat in the upper body, often followed by perspiration and a chill. Peripheral vasodilation, tachycardia, decreased skin resistance, and sweating have all been documented to occur during a hot flush. Although poorly understood, the episodes certainly originate in the brain, most likely as a direct response to hypoestrogenism in the thermoregulatory center of the hypothalamus.[12]It now appears that hot flushes are not merely symptoms of low estrogen levels; they may themselves lead to other neurologic problems. In oophorectomized women, hot flushes have been directly correlated with memory impairment.[13] In addition, single proton emission computed tomography (SPECT) of healthy menopausal women revealed decreased cerebral blood flow during hot flushes.[14] The greatest change occurred in the hippocampus, a center for memory and cognition. Regional patterns of cerebral blood flow during hot flushes resembled those characteristic of Alzheimer's disease. ERT resolved the hot flushes and restored normal patterns of cerebral blood flow.
Based on this evidence, reproductive biologists have hypothesized that hot flushes contribute to degenerative or aging changes in the brain.[15] Frequent vasoconstrictive episodes might lead to cerebral ischemia and free radical formation. The resulting damage may be analogous to that seen in the coronary arteries with plaque formation. The population of healthy neurons might be reduced, particularly in the hippocampus, leaving the brain with impaired ability to tolerate the neurodegenerative processes of aging and Alzheimer's disease.
Estrogen and Cognition
Even in healthy older women, brain volume begins to decline as estrogen levels fall in the perimenopausal period.[16] This atrophy occurs particularly in the hippocampus and parietal lobe, areas primarily associated with memory and cognition. A similar loss in brain volume does not begin in men until a decade later (around age 60), most likely because male sex hormone production declines much more gradually with age. In fact, because of aromatization of testosterone to estrogen, men over the age of 60 have approximately three times more circulating estradiol than women of a similar age.[17]In women, these cerebral changes may contribute to the frequent perimenopausal complaints of decreased mental clarity and short-term, verbal memory problems (see Table 1).[18] Studies of the effects of ERT on cognitive symptoms have generated inconsistent results, perhaps because dropouts and nonparticipants are more likely to be cognitively impaired.[19] A recent meta-analysis yielded only weak evidence that ERT improves cognition and prevents dementia.[20] However, many research groups have found a significant association between ERT and cognition, particularly in the area of verbal memory. For example, in one study of 727 postmenopausal women, history of estrogen use was associated with significantly higher scores on verbal memory and abstract reasoning tests.[21]
Shaywitz et al.[22] used positron emission tomography to observe brain activity in 46 postmenopausal women performing cognitive tasks. In a crossover design, participants were given conjugated equine estrogens (CEE; 1.25 mg) or an identical placebo for 21 days, then, after a washout period, given the opposite treatment. During the cognitive tasks, women taking CEE demonstrated increased activation of areas involved in verbal and nonverbal memory.
Loss of cognitive function also can be related to endogenous estrogen deficiency. In the Study of Osteoporotic Fractures,[23] women in the lowest quintile for bone density also exhibited the highest incidence of dementia.[23] In another study, premenopausal women who underwent oophorectomy, which results in abrupt and severe decline in estrogen levels, were more likely than naturally postmenopausal women to exhibit memory impairment 5 years later.[24] Decline in cognitive function has been observed as early as 2 months postoperatively,[25] and has been shown to be reversible with ERT.[26]
Another effect of menopause and loss of estrogen on the brain is a slowdown in the speed of brain processing.[27] This change is particularly significant for postural stability, which depends on recognition of sensory input and initiation of an appropriate physical response. After menopause, the incidence of falls among women is three times that of men.[1 ]The risk of fracture in women with osteoporosis appears to be related not only to bone density, but also to postural stability.[28,29]
Brain processing speed and postural stability are significantly improved with ERT. One study documented a 60% decreased risk of falling in a group of postmenopausal women on ERT compared with a group not taking it.[28] Another study compared sway velocity (an indicator of tendency to fall) in 16 postmenopausal long-term users of 17 b-estradiol and 16 postmenopausal women who had never taken estrogen.[29] The postmenopausal women taking estrogen evidenced postural stability similar to premenopausal women, whereas balance deteriorated significantly in the postmenopausal women not on ERT. The fact that ERT improves both postural stability and bone density likely explains why it has proven superior to raloxifene[30] and alendronate[31] in preventing nonvertebral, fall-related fractures.
bombbudpuffa
Sweet Cheeba Chiefa
- Joined
- Oct 28, 2006
- Messages
- 5,880
- Reaction score
- 4,347
Estrogen and Mood
In general, perimenopausal women do not appear to be more susceptible to clinical depression than women at other life stages.[32] However, in certain groups of women, including those with a history of postpartum or premenstrual depression, those who undergo the abrupt hormonal changes of surgical menopause, and those in whom perimenopause is prolonged, risk for depression may be increased during this time.[33] In addition, up to 80% of perimenopausal women develop mild depressive symptoms beyond the malaise that might be attributed to hot flushes, night sweats, and insomnia.[34] These symptoms may occur because areas of the brain involved in emotion are rich in estrogen receptors and estrogen directly influences synaptic concentrations of neurotransmitters.The neurotransmitter serotonin plays a key role at brain synapses involved in mood regulation. In oophorectomized rats, administration of estradiol induced a significant increase in serotonin uptake in the frontal cortex and hypothalamus.[35] Also in rats, the antidepressant imipramine did not exert its therapeutic effect on synaptic concentrations of serotonin unless estrogen was present.[36]
In women of reproductive age, serum estradiol levels have been shown to correlate positively with blood levels of serotonin.[37] Researchers have also demonstrated that blood serotonin is decreased in postmenopausal women and that ERT raises it to premenopausal levels.[37 ]Estrogen also competes with tryptophan, the precursor of serotonin, for binding sites on plasma albumin, thus making tryptophan more available to the CNS.[38]
Estrogen affects concentrations of other neurotransmitters and neuromodulators as well. It competitively inhibits the enzyme that inactivates norepinephrine, thus providing a stimulatory effect similar to that of many antidepressant medications.[39] Like pharmaceutical monoamine oxidase (MAO) inhibitors, estrogen reduces MAO activity, resulting in higher levels of both catecholamines and serotonin in the brain.[40] Estrogen also increases opioid and endorphin production by the hypothalamus.[41]
Clinically, women taking the selective estrogen receptor modulator tamoxifen[42] and women on gonadotropin-releasing hormone therapy,[43] which induces hypoestrogenism, have been shown to exhibit increased depressive symptomatology. In randomized controlled trials oophorectomized and perimenopausal women undergoing ERT have experienced a heightened sense of well-being and improved mood.[44] A recent meta-analysis of 26 studies in postmenopausal women found that ERT had a moderate-to-large beneficial effect on depressed mood.[45] This positive effect often was not apparent until after 3 months of treatment, was dampened by the addition of a progestin, and was enhanced by supplementation with an androgen.
In general, perimenopausal women do not appear to be more susceptible to clinical depression than women at other life stages.[32] However, in certain groups of women, including those with a history of postpartum or premenstrual depression, those who undergo the abrupt hormonal changes of surgical menopause, and those in whom perimenopause is prolonged, risk for depression may be increased during this time.[33] In addition, up to 80% of perimenopausal women develop mild depressive symptoms beyond the malaise that might be attributed to hot flushes, night sweats, and insomnia.[34] These symptoms may occur because areas of the brain involved in emotion are rich in estrogen receptors and estrogen directly influences synaptic concentrations of neurotransmitters.The neurotransmitter serotonin plays a key role at brain synapses involved in mood regulation. In oophorectomized rats, administration of estradiol induced a significant increase in serotonin uptake in the frontal cortex and hypothalamus.[35] Also in rats, the antidepressant imipramine did not exert its therapeutic effect on synaptic concentrations of serotonin unless estrogen was present.[36]
In women of reproductive age, serum estradiol levels have been shown to correlate positively with blood levels of serotonin.[37] Researchers have also demonstrated that blood serotonin is decreased in postmenopausal women and that ERT raises it to premenopausal levels.[37 ]Estrogen also competes with tryptophan, the precursor of serotonin, for binding sites on plasma albumin, thus making tryptophan more available to the CNS.[38]
Estrogen affects concentrations of other neurotransmitters and neuromodulators as well. It competitively inhibits the enzyme that inactivates norepinephrine, thus providing a stimulatory effect similar to that of many antidepressant medications.[39] Like pharmaceutical monoamine oxidase (MAO) inhibitors, estrogen reduces MAO activity, resulting in higher levels of both catecholamines and serotonin in the brain.[40] Estrogen also increases opioid and endorphin production by the hypothalamus.[41]
Clinically, women taking the selective estrogen receptor modulator tamoxifen[42] and women on gonadotropin-releasing hormone therapy,[43] which induces hypoestrogenism, have been shown to exhibit increased depressive symptomatology. In randomized controlled trials oophorectomized and perimenopausal women undergoing ERT have experienced a heightened sense of well-being and improved mood.[44] A recent meta-analysis of 26 studies in postmenopausal women found that ERT had a moderate-to-large beneficial effect on depressed mood.[45] This positive effect often was not apparent until after 3 months of treatment, was dampened by the addition of a progestin, and was enhanced by supplementation with an androgen.
