Does sexual exhaustion actually exist

Sexual Reboot Forum Does sexual exhaustion actually exist

This topic contains 16 replies, has 1 voice, and was last updated by  Kristofer 3 years ago.

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    [This is meant to be a critical look at the phenomenon of sexual exhaustion, not meant to take sides]

    Among others, forum member chipdouglas suspects there might be such a thing as sexual exhaustion but is very suspicious of it’s existence. Could it be that all our conditions are the result of something else other than sexual exhaustion, say the result of adrenal fatigue resulting in exhausted cortisol and DHEA levels due to exhausted adrenals from excessive stress or from elevated prolactin and weakened liver enyzme production from the use of SSRIs?

    Well, sexual activities releases adrenaline especially during orgasm. This is a stress and is one that is missed in Dr.Wilson’s book “Adrenal Fatigue”. Stresses take it’s toll on the adrenals and when the adrenals are exhausted, DHEA level is affected. This is known as Kidney yin deficiency in Traditional Chinese Medicine and is a etiology of impotence. So perhaps adrenal fatigue and sexual exhaustion are linked?

    Many individuals has reported feeling exhausted after engaging in sexual activities, what can be the explanation for this other than depleted hormones and neurotransmitters thus indicating that sexual exhaustion is a reality. So if there is no such thing as sexual exhaustion, does it mean that a person with no other causes of impotence would be able to masturbate/ejaculate four times a day everyday?

    Chipdoulas said: “I suspect there’s is such a thing as sexual exhaustion, however with the scant amount of scientific literature, it’s hard to believe.” Well if science doesn’t yet know about a phenomenon, does this mean that since it’s not in the scientific literature it must not exist?

    There is another way that you can stop porn addiction, chronic masturbation and recover your sexual health without fighting it with willpower. With the right mindset you won't even relapse. You can learn more about the recovery program here



    The medical industry is a scam, one of the highest amounts of deaths goto people dying from the side effects of medicine, there are better alternatives, its not a conspiracy its a fact, prolong someone on poisonous medicine rather than give them a cure its great for money!



    as long as we have those big drug companies then everything going on around us will be a scam.

    the latest scam was that companies pump CO into beef to make it stay red after it passes its expiry date. Whats worse they paid some doctors to come up and say its good and kills a lot of germs. so next time you buy some beef or meat make sure you smell it first before you eat it.



    Ok, I ended my two weeks cycle yesterday.

    Its so clear, I swear I can tell you what this ejaculation does to my body. The longer I stimulate and masturbate, the more it draws the vital energy from my organs to the semen, finally when I ejaculate the body temporarily goes down and leaves me empty. After that the body starts recharging this lost energy so the organs can begin to work effectively again.

    The goal is to build a healthy reserve of energy and jing, so I gain my strength back immediately after ejaculation so there is no need to be down at all, and this way get a win / win situation. Of course, careful attention to healthy and tasty diet and smooth flow of emotions should be given too.



    Over-masturbation would definitely lead to a depletion of hormones and neurotransmitters. although I think the neurotransmitter issue is not really the underlying problem. in fact most of the neurotransmitter boosting supplements are just drugs, of course there are some really good exceptions that can be used as part of the healing regime.

    secondary adrenal insufficiency does seem to be the core of the issue as there is a lot of people who suffer from it, albeit at various levels. Its something that modern medicine doesn’t know much or properly about, like sub-clinical hypothyoridism and prostatitis. and of course all of the other symtpoms that SE triggers with it.

    overall and like editman said cleansing, fasting and indivdual tailored exercise and nutrition/supplements are the main ingredients.



    I think the general definintion of SE is one leading to sexual dysfunction (SD). I also think SE implies someone “exhausted themselves” while SD may be from any number of sources (including SE)… I agree with I’m not so sure SE is a real diagnoses but certainly SD is.

    I agree with BlueShark statement about the adrenals playing a large factor for SE/SD issues… Lower back pain, leg pain, poor erections, lack of good sleep are all indicators of medula and other adrenal overuse.

    The adrenals are also significantly affected by improper TH1/TH2 ratios. (ie. There is no doubt that various Interlukin components play a role… Im currently looking to reduce IL4 since this mediates IgE/IgG production.) Trying the Earthrise Spirulina IL-4 product which has been clinically tested.



    TH1/TH2 ratios? are these related to the thyroids by any chance?

    I know now that my symtpoms are due to poor thyroid activity.



    TH1/TH2 ratios? are these related to the thyroids by any chance?

    I know now that my symtpoms are due to poor thyroid activity.

    The TH cells are T helper cells which are part of the lymphocytes. They are managerial cells that help direct other immune cells. Why these are important for SE is because when TH2 is too high more ImmunoGlobic cells are created and attached to the Mast cell… When the Ig release from the Mast cells it creates generalized reactions such as back pain, joint pain, eye floaters, diabetes Type II, arthritis, and of course SD. Of course our bodies will release adrenalin to counter the histamine release and hence panic attacks, lack of sleep and adrenal failure. It is my theory this is one cause of SE.

    Here is a excerp from Wikipeida:

    Th1/Th2 Model for helper T cells

    Proliferating helper T cells that develop into effector T cells differentiate into two major subtypes of cells known as Th1 and Th2 cells (also known as Type 1 and Type 2 helper T cells, respectively). These subtypes are defined on the basis of the specific cytokines they produce. Th1 cells produce interferon-gamma (IFN-γ) and tumor necrosis factor-beta (TNF-β, also known as lymphotoxin), while Th2 cells produce interleukin-4 (IL-4), interleukin-5 (IL-5) and interleukin-13 (IL-13), among numerous other cytokines. The Th1/Th2 model also states that interleukin-12 (IL-12) plays an essential role during Th1 development, however IL-12 is not produced by helper T cells themselves, but by certain professional antigen presenting cells, such as activated macrophages and dendritic cells. Interleukin-2 was classically associated with Th1 cells, but this association may be misleading; IL-2 is produced by all helper T cells early in their activation.

    Both of these cytokine profiles appear to be biased in the type of immune stimulation they promote. For example, cytokines in the Th1 response maximises the killing efficacy of the macrophages and in the proliferation of cytotoxic CD8+ T cells, and it has been suggested that their primary role during an immune response is to activate and/or proliferate the cellular immune system. Th2 cells express a variety of cytokines, many of which stimulate B-cells into proliferation, to induce B-cell antibody class switching, and to increase antibody production. Th2 cells are therefore considered necessary for the full maturation of the humoral immune system.

    The stimulation of the above systems is only one way helper T cells manipulate the immune system. Many of the cytokines also act on helper T cells themselves, or on other immune cells, such as the actions of interleukin-5 on eosinophils. There are cytokines in both Th responses that play an important role in preserving the response itself, or in suppressing other functions of the immune system.

    The Type 2 response promotes its own profile using two different cytokines. Interleukin-4 acts on helper T cells to promote the production of Th2 cytokines (including itself; it is auto-regulatory), while interleukin-10 (IL-10) inhibits a variety of cytokines including interleukin-2 and interferon-gamma in helper T cells and IL-12 in dendritic cells and macrophages. The combined action of these two cytokines suggests that once the T cell has decided to produce these cytokines, that decision is preserved (and also encourages other T cells to do the same).

    A similar phenomenon occurs with the Type 1 response. The Type 1 cytokine interferon-gamma increases the production of interleukin-12 by dendritic cells and macrophages, and via positive feedback, IL-12 stimulates the production of IFN-gamma in helper T cells, thereby promoting the Th1 profile. IFN-gamma also inhibits the production of cytokines such as interleukin-4, an important cytokine associated the Type 2 response, and thus it also acts to preserve its own response.

    While we know about the types of cytokine patterns helper T cells tend to produce, we understand less about how the patterns themselves are decided. Various evidence suggests that the type of APC presenting the antigen to the T cell has a major influence on its profile. Other evidence suggests that the concentration of antigen presented to the T cell during primary activation influences its choice. The presence of some cytokines (such as the ones mentioned above) will also influence the response that will eventually be generated, but our understanding is nowhere near complete.

    Complexities surpassing the Th model

    The interactions between cytokines from the Th1/Th2 model can be more complicated in some animals. For example, the Th2 cytokine IL-10 inhibits cytokine production of both Th subsets in humans. Human IL-10 (coded hIL-10) suppresses the proliferation and cytokine production of all T cells and the activity of macrophages, but continues to stimulate plasma cells, ensuring that antibody production still occurs. As such, hIL-10 is not believed to truly promote the Th2 response in humans, but acts to prevent over-stimulation of helper T cells while still maximising the production of antibodies.

    There are also other types of T cells that can also influence the expression and activation of helper T cells, such as natural suppressor T cells, along with less common cytokine profiles such as the Th3 subset of helper T cells. Terms such as “regulatory” and “suppression” have become ambiguous after the discovery that helper CD4+ T cells are also capable of regulating (and suppressing) their own responses outside of dedicated suppressor T cells.

    One major difference with “suppressor” (or “natural regulatory”) T cells is that they always suppress the immune system, while effector T cell groups usually begin with immune-promoting cytokines and then switch to inhibitory cytokines later in its repertoire. The latter is a feature of Th3 cells, which transform into a suppressor subset after its initial activation and cytokine production.

    Both suppressor T cells and Th3 cells produce the cytokine transforming growth factor-beta (TGF-β) and IL-10. Both cytokines are inhibitory to helper T cells; TGF-beta suppresses the activity of most of the immune system.

    Many of the cytokines in this article are also expressed by other immune cells (see individual cytokines for details), and it is becoming clear that while the original Th1/Th2 model is enlightening and gives insight into the functions of helper T cells, it is far too simple to define its entire role or actions. Some immunologists question the model completely, as some in vivo studies suggest that individual helper T cells usually do not match the specific cytokine profiles of the Th model, and many cells express cytokines from both profiles. That said, the Th model has still played an important part in developing our understanding of the roles and behaviour of helper T cells and the cytokines they produce during an immune response.

    Role of helper T cells in disease

    Considering the diverse and important role helper T cells play in the immune system, it is not surprising that these cells often influence the immune response against disease. They also appear to make occasional mistakes, or generate responses that would be politely considered non-beneficial. In the worst case scenario, the helper T cell response could lead to a disaster and the fatality of the host. Fortunately this is a very rare occurrence.

    Helper T cells and Hypersensitivity

    The immune system must achieve a balance of sensitivity in order to respond to foreign antigens without responding to the antigens of the host itself. When the immune system responds to very low levels of antigen that it usually shouldn’t respond to, a hypersensitivity response occurs. Hypersensitivity is believed to be the cause of allergy and some auto-immune disease.

    Hypersensitivity reactions can be divided into four types:

    Type 1 hypersensitivity includes common immune disorders such as asthma, allergic rhinitis (hay fever), eczema, urticaria (hives) and anaphylaxis. These reactions all involve IgE antibodies, which require a Th2 response during helper T cell development. Preventative treatments, such as corticosteroids and montelukast, focus on suppressing mast cells or other allergic cells; T cells do not play a primary role during the actual inflammatory response. It’s important to note that the numeral allocation of hypersensitivity “types” does not correlate (and is completely unrelated) to the “response” in the Th model.

    Type 2 and Type 3 hypersensitivity both involve complications from auto-immune or low affinity antibodies. In both of these reactions, T cells may play an accomplice role in generating these auto-specific antibodies, although some of these reactions under Type 2 hypersensitivity would be considered normal in a healthy immune system (for example, Rhesus factor reactions during child-birth is a normal immune response against child antigens). The understanding of the role of helper T cells in these responses is limited but it is generally thought that Th2 cytokines would promote such disorders. For example, studies have suggested that lupus (SLE) and other auto-immune diseases of similar nature can be linked to the production of Th2 cytokines.

    Type 4 hypersensitivity, also known as delayed type hypersensitivity, are caused via the over-stimulation of immune cells, commonly lymphocytes and macrophages, resulting in chronic inflammation and cytokine release. Antibodies do not play a direct role in this allergy type. T cells play an important role in this hypersensitivity, as they activate against the stimulus itself and promote the activation of other cells; particularly macrophages via Th1 cytokines.

    Other cellular hypersensitivities include cytotoxic T cell mediated auto-immune disease, and a similar phenomenon; transplant rejection. Helper T cells are required to fuel the development of these diseases. In order to create sufficient auto-reactive killer T cells, interleukin-2 must be produced, and this is supplied by CD4+ T cells. CD4+ T cells can also stimulate cells such as natural killer cells and macrophages via cytokines such as interferon-gamma, encouraging these cytotoxic cells to kill host cells in certain circumstances.

    The mechanism that killer T cells use during auto-immunity is almost identical to their response against viruses, and some viruses have been accused of causing auto-immune diseases such as Type 1 Diabetes mellitus. Cellular auto-immune disease occurs because the host antigen recognition systems fail, and the immune system believes, by mistake, that a host antigen is foreign. As a result, the CD8+ T cells treat the host cell presenting that antigen as infected, and go on to destroy all host cells (or in the case of transplant rejection, transplant organ) that express that antigen.

    It should be noted that some of this section is a simplification, and that many auto-immune diseases are more complex; a well known example is rheumatoid arthritis, where both antibodies and immune cells are known to play a role in the pathology. Generally the immunology of most auto-immune diseases is not well understood.



    If this was the case, they should stop doing research today since they apparently know about everything that exists.

    They are doing studies all around the world trying to learn about the human body.

    You are giving science & human understanding WAY too much credit.

    Every other branch of medicine other than Western knows about sexual exhaustion. (TCM, Ayurvedic, Homeopathic, etc.)

    Western medicine has now been reduced to “If you can’t detect it with lab work….it doesn’t exist”.



    So after you ejaculate your body feels exhausted? like you just ran a marathon? Just trying to understand, because I definantly dont feel like that. I mean for about a minute I just wanna lay back, but after that, I’m back to normal. Hey man, do you masturbate to porn or to your imagination?



    your not exhausted mate-what are you doing here?



    Time …and why do you say I’m not exhausted?



    …and why do you say I’m not exhausted?

    So after you ejaculate your body feels exhausted? like you just ran a marathon? Just trying to understand, Because I definantly dont feel like that. I mean for about a minute I just wanna lay back, but after that, I’m back to normal.



    your suppose to be tired after ejaculation, but i think it has something todo with serotonin not being fired, i cant remember, machine told me one time why he thinks you dont get tired after ejaculation, you dont feel it but actually your very tired.



    Max I do get tired after ejaculation and I’ll just sit/lay there. After about a minute or so, I wont be tired anymore and I’ll get up and get on with my day. I was making a point that I dont feel like all my energy has just been sucked out of my body aftewards.




    can you get an erection?

    how long can you have sex for before ejaculating?

    can you feel sex and do you have an orgasim?



    Time To porn after some manual stimulation. Sometimes to things I find sexually apealing that isnt porn, and sometimes to my thoughts(only if I havent looked at porn and masturbated in a few weeks.

    Quote:Have never had sex because whenever I tried I could never get an erection when with the girl, and if I did, it would be extremely soft or would just go completely limp.

    Quote:Again, dunno, because I never had sex because of my lack of erection.

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