COMPOSITIONS WITH CANNABINOIDS OF CANNABIS SATIVA FOR TREATING ERECTILE AND SEXUAL DYSFUNCTION 1. ABSTRACT The present invention is related to compositions containing only natural products for the treatment of erectile and sexual dysfunction (ESD). More specifically relates to compositions containing Cannabis extract, and other herbal extracts. In accordance with the present invention, the compositions herein described can be used as medical Cannabis to treat ESD in a subject in need thereof. The present invention has been challenged by the problems of finding natural compositions and methods for prevention, treatment and inhibition of ED in men and sexual dysfunction in women that are practical for short and long term routine administration, while avoiding side effects of existing formulations, enable treatment of and prevention of ESD in patients that cannot utilize prior art ED treatments, and/or provide new practical and cost effective compositions to prevent as well as treat ED. 2. FIELD OF THE INVENTION Current invention relates to herbal over-the-counter formulation for treating, inhibiting the onset, and/or slowing the rate of development of erectile and sexual dysfunction. In some embodiments Cannabis or extract thereof, is administrated in an amount of 1 mg to about 200mg. Current invention does not involve anti-erectile and sexual dysfunction drugs (AED). In some embodiments of the aspect described, other herbal extracts may comprise Baccharis trimera or extract thereof, L-citrulline/L-arginine extract, Mucuna pruriens or extract thereof, Angelica sinensis or extract thereof, Turnera Diffusa or extract thereof, Pfaffia extacts or extract thereof, Achyrocline Satureioides or extract thereof. In some embodiments, the Cannabis extract comprises at least one cannabinoid of Cannabisplant. In some embodiments, the Cannabis extract comprises tetrahydrocannabinol and/or its acidic form (THC, THCA). In some embodiments, the Cannabis extract comprises cannabigerol and/or its acidic form (CBG, CBGA). In some embodiments, the Cannabis extract comprises cannabichromene and/or its acidic form (CBC, CBCA). In some embodiments, the Cannabis extract comprises cannabidiol and/or its acidic form (CBD, CBDA). In some embodiments, the Cannabis extract comprises cannabicyclol and/or its acidic form (CBL, CBLA). In some embodiments, the Cannabis extract comprises cannabielsoin and/or its acidic form (CBE, CBEA). In some embodiments, the Cannabis extract comprises cannabinol and/or its acidic form (CBN, CBNA). In some embodiments, the Cannabis extract comprises cannabinodiol and/or its acidic form (CBND, CBNDA). In some embodiments, the Cannabis extract comprises cannabitriol and/or its acidic form (CBT, CBTA). In some embodiments, the Cannabis extract comprises cannabivarin and/or its acidic form (also known as cannabivarol; CBV, CBVA). Furthermore, erectile dysfunction is not just a physical problem, but it can also be a psychological problem. Mental disorders are a common cause of ED. Several studies show us that anxiety and depression are highly prevalent in those with erectile dysfunction and other sexual disorders. The present invention contains compounds that target different phycological components of the problem. 3. BRIEF DESCRIPTION OF THE DRAWINGS Figure 1 shows sex response cycle, highlighting responsive desire experienced during the sexual experience as well as variable initial (spontaneous) desire. Figure 2 shows Oral administration cannabidiol (CBD) dose-normalized concentration-time profiles. Figure 3 shows Diagnostic plots of oral administration model. Figure 4 shows the comparison of oral l-citrulline (nutraceutical grade l-citrulline or watermelon products) versus oral l-arginine. Figure 5 shows the relationship between the 12 groups of men (Group 1 received Formulation 1, Group 2 received Formulation 2, and so on) and the CA PSV. Figure 6 shows the difference between CA PSV baseline values and CA PSV values after treatment with each formulation. 4. BACKGROUND 4.1. ERECTILE DYSFUNCTION Impotence is a serious clinical problem in adult men. Impotence or erectile dysfunction (ED) is a problem that most men will face at some time in their life. In fact, by the time a man reaches 50 years of age, he has about a 1 in 2 chance of having some problem with his erection. The problem could be either attaining and/or maintaining his erection long enough to complete the sexual act. As men get older, the chance of getting ED increases such that a 60-year-old man has approximately a 60% chance of having ED, a 70-year-old man has about a 70% chance, etc. Even men in their 40’s have about a 40% chance of having some form of ED, while it has been extrapolated that men in their 30’s and 20’s have about a 30% and 20% chance, respectively, of having noticed that something has changed with their erectile function. Erectile dysfunction is not always just a physical problem, it can also be a psychological problem. Mental disorders are a common cause of ED. Several studies show us that anxiety and depression are highly prevalent in those with erectile dysfunction and other sexual disorders. The major reason ED manifests itself, regardless of the age of onset, is due to an alteration in the corpus cavernosum smooth muscle (CSM), which is located within the cavernosum or corporal bodies of the penis. The function of the CSM in the erectile process is to receive and trap blood entering the corporal bodies. This is accomplished when the CSM undergoes relaxation that allows it to open and create spaces or sinusoids into which the entering blood pools. The pooling of this blood in sinusoidal spaces increases the pressure within the corporal bodies and when a certain intracorporeal pressure is reached, the pressure closes off the veins that drain the blood out of the corporal bodies, essentially trapping it within the corporal bodies. Clinically, this is how the CSM tissue can attain (by creating spaces for the blood to pool into) and maintain (by closing off the veins) an erection. It is when this CSM begins to degrade in some way or another and becomes incapable of either relaxing sufficiently enough to create these spaces where the blood is normally trapped or it cannot maintain its relaxation long enough so that it fails to compress the veins that provide egress for blood from the corporal bodies that ED begins to be manifested. There are multiple biochemical pathways involved in penile erection and dysfunction. Without stimulation, flaccidity can be considered as the baseline state. Flaccidity is due to corpus cavernosum smooth-muscle cells ("CSM") being contracted and helicine arterioles being sufficiently contracted to limit blood flow to corpus cavernosum sinuses; the sympathetic nervous system and tonic adrenergic discharge maintain baseline contraction of smooth muscle cells and arteriole blood supply (e.g., adrenergic, cholinergic, and nonadrenergic-noncholinergic pathways). Therefore, a combination of metabolic pathways is involved in inducing the erectile processes involving smooth muscle relaxation, arterial dilation, and venous occlusion. When the CSM cells begin to undergo oxidation and deteriorate either as a result of aging or some other cause, the CSM begin to induce an enzyme called inducible nitric oxide synthase (iNOS) which produces nitric oxide in high quantities within the cells that begins to combat the oxidative stress. This induction of nitric oxide (NO) by iNOS is different from the NO that is found in the nerves of the body including the nerves that innervates the CSM cells. This NO in the nerves is produced by a related enzyme, neuronal nitric oxide synthase ("nNOS"), and in the penis it only releases NO when the patient is sexually stimulated. This NO from nNOS is the major chemical that is involved in the relaxation of the CSM cells and hence is required for the initiation and maintenance of a normal erection. Therefore, while nNOS is normally present in the nerves innervating the penis, iNOS is normally not present in the CSM cells of the penis and is only induced by the CSM cells themselves when the cells experience oxidative stress. However, when iNOS is induced, human erectile dysfunction can be ameliorated by treatment with nNOS or inducers of nNOS. Thus, there remains a ubiquitous and long-felt need to treat ED before it progresses to the point where pharmacological and/or other medical intervention is required in order to have desired sexual performance. Nevertheless, current ED drugs, such as VIAGRA® and CIALIS®, are generally prescribed only after the patient has presented with symptoms of ED. These drugs belong to a class of drugs called Type 5 phosphodiesterase (PDE5) inhibitors. PDE5 is an enzyme that breaks down cGMP (cyclic guanosine monophosphate) and PDE5 inhibitors like Viagra, Cialis and Levitra prevent the cGMP from breaking down so the effect of the cGMP on the tissues is enhanced. With regards to erectile function, cGMP is formed within the CSM from a reaction that is initiated by the NO that is released from the cavernosal nerve following sexual stimulation. The NO that begins the erectile response comes from the enzyme nNOS located in the nerve endings. The NO enters the CSM cells and causes a reaction to occur. NO activates the enzyme soluble guanylyl cyclase (sGC) in the cytoplasm of the CSM and this enzyme in turn converts guanosine triphosphate (GTP) into cyclic guanosine monophosphate (cGMP). An increase in cGMP stimulates protein kinase G to phosphorylate potassium and calcium channels causing a decrease in cytosolic calcium, dilation of the helicine arterioles, and the relaxation of the trabecular smooth muscle where all the CSM cells are located. As noted above, the relaxation of the smooth muscle leads to an increase in the intracavernosal volume, initiating the erectile process. Normally, endogenous PDE5 enzyme degrades cGMP which reverses the relaxation of the smooth muscle cells and leads to loss of erection whereas the intake of these PDE5 inhibitors prior to sexual stimulation prevent the degradation of the cGMP that is formed thereby prolonging any CSM relaxation and enhancing any erectile response. Currently, one suffering from ED needs to see a doctor and get a prescription for an ED treatment in advance in order to be prepared for a satisfying experience. Onset and duration of the effects of PDE5 inhibitors like Viagra, Cialis and Levitra depend on the specificity of the compound. While PDE5 inhibitors are considered the "first line treatment of ED," there are notable side effects (headache, flushing, dyspepsia, rhinitis, visual disturbances, back pain, etc.) and adverse interactions that can limit or bar their use (e.g., patients taking nitrates with a PDE5i can experience hypotension and syncope. Since most men will at some time in their life get ED mainly as the result of CSM deterioration secondary to the aging process, the present inventor faced the problem of whether or not it is desirable to treat men who are asymptomatic but whose refractory period has begun to increase - a subtle sign that the CSM is beginning to undergo deterioration - in order to slow or prevent the progression of this deterioration and the forthcoming ED. For patients who already have noticeable ED symptoms, it may also be desirable to slow if not stop or reverse the progression of the ED. 4.2. CAUSES OF WOMEN'S SEXUAL DYSFUNCTIONS The model in Figure 1 (Sex response cycle) clarifies the importance of women being able to become subjectively aroused. Many psychological and biological factors may negatively influence this sexual arousability. The above-mentioned figure shows responsive desire experienced during the sexual experience as well as variable initial (spontaneous) desire. At the “initial” stage (left) there is sexual neutrality, but with positive motivation. A woman's reasons for instigating or agreeing to sex include a desire to express love, to receive and share physical pleasure, to feel emotionally closer, to please the partner and to increase her own well-being. This leads to a willingness to find and consciously focus on sexual stimuli. These stimuli are processed in the mind, influenced by biological and psychological factors. The resulting state is one of subjective sexual arousal. Continued stimulation allows sexual excitement and pleasure to become more intense, triggering desire for sex itself: sexual desire, absent initially, is now present. Sexual satisfaction, with or without orgasm, results when the stimulation continues sufficiently long and the woman can stay focused, enjoys the sensation of sexual arousal and is free from any negative outcome such as pain (Modified from Basson, 2001). Interpersonal and contextual factors In a recent probability sample of American women 20–65 years of age (Bancroft J et al. 2003), their emotional relationship with the partner during sexual activity and general emotional well-being were the 2 strongest predictors of absence of distress about sex. Women who defined themselves (using standard psychological instruments) to be in good mental health were much less likely than women with lower self-rated mental health to report distress about their sexual relationship (odds ratio 0.41, 95% confidence interval 0.29– 0.59). The healthier women were therefore 59% less likely to report distress about their sexual relationship. Feeling emotionally close to their partner during sexual activity decreased the odds of “slight distress” by 33% relative to “no distress,” and “marked distress” by 43%; in other words, the stronger the emotional intimacy with the partner, the less distress. Other contextual factors reported to reduce arousability included concerns about safety (risks of unwanted pregnancy and STDs, for example, or emotional or physical safety), appropriateness or privacy, or simply that the situation is insufficiently erotic, too hurried, or too late in the day. Personal psychological factors Frequently a woman's arousal is precluded by the nonsexual distractions of daily life, but also sometimes by sexual distractions (e.g., worry about not becoming sufficiently aroused, reaching orgasm, a male partner's delayed or premature ejaculation or a female partner's lack of orgasm). Empirical studies have shown a high correlation of desire complaints with measures of low self-image, mood instability and tendency toward worry and anxiety (without meeting the clinical definition of a mood disorder). Differences between a group of 46 consecutive women with a diagnosis of desire disorder without clinical depression and a control group of 100 healthy women were significant for 6 out of 8 scales in the Narcissism Inventory (a standardized self-administered instrument). The scales indicated that the women with desire disorder had self-esteem that was weak or even fragile, emotional instability, anxiety and neuroticism. Sexual arousal and orgasm, especially in a partner's presence, necessitates a certain degree of vulnerability, which is impossible for some women who cannot tolerate feelings of loss of control generally, and loss of control specifically of their body's reactions (Hartmann U, et al.2002). Further inhibiting psychological factors include memories of past negative sexual experiences, including those that have been coercive or abusive, and expectations of negative outcomes to the sexual experience (e.g., from dyspareunia or partner sexual dysfunction) (Graham CA, et al.2004). Biological factors The biological and pathophysiological underpinnings of normal and abnormal female sexual response is only recently receiving attention. Most of the basic science and animal experiments in this area are beyond the scope of this review. Some promising attempts are noted, however, in part because they relate attempts to ameliorate sexual dysfunction by means of off-label use of available drugs and to avoid the negative sexual side-effects of medications such as antidepressants. Depression is strongly associated with reduced sexual function. Of 79 women with major depression surveyed before treatment with medication (Kennedy SH, et al. 1999), 50% reported decreased sex drive; 50%, more difficulty obtaining vaginal lubrication; and 50%, far less sexual arousal when engaging in sex. Only 50% had been sexually active during the previous month. In addition, sexual dysfunction can constitute an adverse event of antidepressant use, especially among patients who had low levels of sexual enjoyment before the onset of their depression (Clayton AH, et al.2002). When patients are specifically asked about sexual side-effects, they are acknowledged by as many as 70% (Montejo AL, et al.2001). Sexual dysfunction is also a common side-effect of treatment with antidepressants. Among women being treated, it has been found to be more common in those who are older, married, without postsecondary education, without full-time work, or taking concomitant medication (any type); those who have a comorbid illness that might affect sexual functioning, or a history of antidepressant- associated sexual dysfunction; those who deem sexual function unimportant; and those whose previous sexual engagements had afforded little pleasure (Mani SK et al.1994). Currently under scrutiny is the role of dopamine and other neurotransmitters in influencing sex hormone receptors and how the neurotransmitters are, in turn, influenced by sex hormones. Oestrogenised female animals change their sexual behaviour when administered progesterone; studies have shown that the same changes can result from dopamine or the presence of a male animal (Mani SK et al.1994 and Blaustein JD et al.2003). Among 75 non-depressed women with a DSM-IV diagnosis of hypoactive sexual desire disorder who received bupropion (a dopaminergic drug; average dose 389 mg/ d) or placebo, improvements in pleasure, arousal and orgasm were statistically significant for those administered the active drug. Interestingly, these changes were unaccompanied by increased desire (Segraves RT, et al.2004). 4.3. ENDOCANNABINOID SYSTEM The endocannabinoid system (ECS) is a complex, evolutionarily conserved homeostatic signalling network. It comprises endogenous ligands (endocannabinoids [eCB], e.g., anandamide [AEA]), eCB-responsive receptors, and a complex enzyme and transporter apparatus. These molecules are involved in the synthesis, cellular uptake, release, inter- and intracellular transport, and degradation of eCBs. Besides eCBs and related endogenous mediators, the Cannabinaceae-derived “classical” and other plants-derived “non-classical phytocannabinoids (pCBs) represent another important, and ever-growing group of cannabinoids. To date, more than 500 biologically active components were identified in the plants of the Cannabis genus, among which more than 100 were classified as pCBs. Depending on their concentration, eCBs and pCBs are able to activate/antagonize/inhibit a remarkably wide-variety of cellular targets including several metabotropic (e.g., CB1 or CB2), ionotropic (certain transient receptor potential [TRP] ion channels) and nuclear (peroxisome proliferator-activated receptors [PPARs]) receptors, various enzymes, and transporters. Importantly, each ligand can be characterized by a unique, molecular fingerprint, and in some cases, they can even exert opposing biological actions on the same target molecule (Molecules 2019, 24, 918). 4.4. CANNABIS SATIVA The plant Cannabis sativa grows in tropical climate. Its seeds, flowering tops, leaves and stalks contain a cocktail of chemicals termed cannabinoids that causes psychoactive manifestations following ingestion or inhalation of smoke. Though the special significance of this plant was first recorded in allopathic medical literature at the turn of the last century, the oriental physicians have been using it as a medicinal plant for many millennia. Dried leaves and flowering tops (grass, marijuana, joint, weed, ganja, hashish), resinous extracts from flowering tops and Cannabis oil (hash oil) are different formulations with psychoactive chemicals that are used for medicinal and recreational purposes. 4.5. CANNABINOIDS The term cannabinoids is used for a number of chemicals found in the extracts of Cannabissativa. Cannabis sativa produces unique secondary metabolites consisting of alkyl resorcinol and monoterpene groups. The plant Cannabis sativa contains more than 60 terpenophenolic compounds, named phytocannabinoids. Cannabis may contain over 140 cannabinoid (tricyclic dibenzopyran) compounds and some, such as cannabidiol, may modulate the response to THC. Cannabinoids (cannabigerol (CBG), cannabichromene (CBC), cannabidiol (CBD), cannabicyclol (CBL), cannabielsoin (CBE), cannabinol (CBN), cannabinodiol (CBND), cannabitriol (CBT), and more) nitrogenous compounds, amino acids, proteins, enzymes, glycoproteins, sugars, hydrocarbons, simple alcohols, simple aldehydes, simple ketones, simple acids, fatty acids, simple esters, lactones, steroids, terpenes, non-cannabinoid phenols, flavonoids, vitamins, pigments and elements are the chemical classes compounds of Cannabis sativa which has been identified. The two major cannabinoids are THC and CBD. 4.6. Δ9‐TETRAHYDROCANNABINOL (TCH) The Cannabis plant (Cannabis sativa) contains many compounds, but Δ9‐ tetrahydrocannabinol (THC) is the main psychoactive ingredient (Figure 1). THC breaks down to produce cannabinol and was identified along with cannabidiol (the main non-psychoactive component). However, THC was not isolated, synthesised, and stereochemically defined until the 1960s. THC is concentrated in the flowering head of the female plant and selective growing in the past 5– 10 years has substantially increased THC content from 1-3% THC in the “flowerpower” era to 6–13% and above. Figure 1. Tetrahydrocannabinol molecular structure. Pharmacokinetics of Cannabis Δ9‐THC which is highly lipophilic get distributed in adipose tissue, liver, lung and spleen. Hydroxylation of Δ9‐THC generates the psychoactive compound 11‐hydroxy Δ9_Tetrahydrocannabinol (11‐OH‐THC) and further oxidation generates the inactive 11‐ nor‐9‐carboxy‐Δ9‐tetrahydrocannbinol (THCCOOH). THCCOOH is the compound of interest for diagnostic purposes. It is excreted in urine mainly as a glucuronic acid conjugate. Δ9‐THC is rapidly absorbed through lungs after inhalation. It quickly reaches high concentration in blood. Approximately 90% of THC in blood is circulated in plasma and rest in red blood cells. Following inhalation, Δ9‐THC is detectable in plasma within seconds after the first puff and the peak plasma concentration is attained within 3-10 minutes. However, the bioavailability of Δ9‐THC varies according to the depth of inhalation, puff duration and breath-hold. Considering that approximately 30% of THC is assumed to be destroyed by pyrolysis, the systemic bioavailability of THC is ~23-27 % for heavy users and 10-14 % for occasional users (Iranian J Psychiatry 7:4, Fall 2012). 4.7. CANNABIDIOL (CBD) Cannabidiol (Figure 2) was isolated in 1940 and is the major non-psychoactive component of Cannabis sativa. Over the centuries, several medicinal preparations derived from C. sativa have been employed for a variety of disorders, including gout, rheumatism, malaria, pain, and fever. These preparations were widely employed as analgesics by Western medical practitioners in the 19th century. More recently, there is clinical evidence suggesting efficacy in HIV-associated neuropathic pain, as well as spasms associated with multiple sclerosis Figure 2. Cannabinol molecular structure. Cannabidiol pharmacological effects are mediated through G protein coupled receptors, cannabinoid type I (CB1) and cannabinoid type II (CB2), which are highly expressed in the hippocampus and other parts of the central nervous system. When activated, CB1 receptors inhibit synaptic transmission through action on voltage-gated calcium and potassium channels. CB2 receptors are primarily expressed in the immune system and have limited expression in the central nervous system. The effects of CBD are CB2 receptor independent. Studies have demonstrated that CBD has a low affinity for the CB1 receptors, but even at low concentrations, CBD decreases G-protein activity. Cannabinoids are highly lipophilic, allowing access to intracellular sites of action, resulting in increases in calcium in a variety of cell types including hippocampal neurons. CBD actions on calcium homeostasis may provide a basis for CBD neuroprotective properties. Toxicology CBD is well tolerated in humans with doses up to 600 mg not resulting in psychotic symptoms. In the few small placebo-controlled studies performed, no significant CNS effects were noted. Oral CBD undergoes extensive first-pass metabolism via CYP3A4, with a bioavailability of 6%. Following single doses in humans, the half-life of CBD when taken orally is about 1 to 2 days. In vitro studies have shown that CBD is a potent inhibitor of multiple CYP isozymes, including CYP 2C and CYP3A. Whether these in vitro observations are relevant at plasma concentrations likely to be seen in patients is unclear (Epilepsy Currents, Vol.14, No.5 (September/October) 2014 pp.250–252). Plasma levels of CBD were increased when CBD was administered with food or in a fed state, or when a meal is consumed post-administration. Oral capsules with piperine pro- nanolipospheres also increased AUC and Cmax. This is also demonstrated in animal studies; co-administration of lipids with oral CBD increased systemic availability by almost 3-fold in rats (Zgair et al., 2016) and a pro-nanoliposphere formulation increased oral bioavailability by about 6-fold (Cherniakov et al., 2017). As CBD is a highly lipophilic molecule, it is logical that CBD may dissolve in the fat content of food, increasing its solubility, and absorption and therefore bioavailability as demonstrated by numerous pharmacological drugs (Winter et al., 2013). Thus, it may be advisable to administer CBD orally in a fed state to allow for optimal absorption. Results can be appreciated in Table 1. Table 1. Dose proportionality tests of oral capsule at fasted and fed states. n number of study, Cmax maximum concentration, AUC0-∞ area under the concentration-time curve from time zero to infinity, CI confidence interval aonly fed-state data A study has been performed to establish the CBD dose‐exposure relationship and to evaluate the effects of dosage forms, food, and doses on CBD absorption. Single‐dose (range: 5–6000 mg) CBD plasma concentration‐time profiles administered as oral capsule (OC) to healthy volunteers. A dose‐exposure proportionality assessment was performed, and a population‐based meta‐analysis of CBD pharmacokinetics and systemic bioavailability was conducted with a nonlinear mixed‐effects modelling. A three‐compartment model with a Weibull or zero‐order absorption model was used to describe CBD disposition and absorption kinetics. Dosage form, food, and dose were assessed for covariation. It was observed that the bioavailability of OC (5.6%) and fed‐state OM (6.2%) were similar. The absorption rate observed was 2.1 hrs. The results are shown on Figure 2. The effects of doses, dosage forms, and feeding status on CBD pharmacokinetics were quantified and should be taken into consideration for dose optimization. 1.1. CANNABIS SATIVA AND ERECTILE DYSFUNCTION Minor cannabinoids from Cannabis Sativa plant haven’t been proposed as a mean of treating erectile and sexual dysfunction. Cannabinoids (CBD, THC, CBC, CBN, CBG, and other minor cannabinoids) from Cannabis Sativa plant haven’t been proposed as a mean of treating erectile and sexual dysfunction as only active. Herbal formulations have been proposed as a mean of treating erectile dysfunction. See e.g. EP2637505B1. The disclosed compositions do not include cannabis or cannabis derivatives, for instance, the only ingredient that they mention is L-citrulline. Other administration routes for cannabinoids compositions have been disclosed. See e.g. CA30026274. The proposed compositions do not mention oral administration or any other way of administration other than nasal. Thus, their focus in not natural products. Compositions with cannabis have been proposed as a mean of treating erectile dysfunction and sexual performance. See e.g. US2018/0161284A1. The proposed compositions include cannabis or cannabis derivatives + anti-erectile dysfunction medication as sildenafil (VIAGRA®), tadalafil (CIALIS®) and vardenafil (LEVITRA®), avanafil, alprostadil. The publication mentions also damiana, horny got weed and yohimbine as added extra. Patent application US2020/0009107A1 discloses compositions including cannabis or cannabis derivatives + anti-erectile dysfunction medication as sildenafil (VIAGRA®), tadalafil (CIALIS®) and vardenafil (LEVITRA®) AND/OR herbal supplements as damiana, horny got weed, yohimbe root (yohimbine), garlic with vitamin C, gingko biloba, ginseng, goosefoot, Chenopodium ambrosioides (wormseed), Chlorophytum borivilianum (musli) and L-citrulline/L-arginine ; the only herbal product mentioned in above mentioned patent application and that coincides with current invention is L-citrulline/L-arginine. Patent application WO2009/121687 discloses compositions for the treatment of erectile dysfunction comprising L-citrulline and/or Viscum album and/or NADPH. CBD is a non-psychotropic component of Cannabis sativa that binds to CB1 receptors with only comparably very low affinity (Petitet F et al. 1998 and Thomas A et al. 2007) and is devoid of overt cannabimimetic or propsychotic properties (Petitet F et al. 1998). Biochemical studies indicate that cannabidiol may enhance endogenous anandamide signalling indirectly, by inhibiting the intracellular degradation of anandamide catalysed by the enzyme fatty acid amide hydrolase (FAAH) (Petitet F et al.1998). It has been shown that the endocannabinoid anandamide potentiates the neurogenic relaxation of rat corpus cavernosum, possibly through either CB1 or vanilloid receptors (Hartmann U, et al. 2002). Others observed that both CB1 and CB2 receptors activation potentiated neurogenic relaxation of rabbit corpus cavernosum (I. M. Vural, et al.2009). On the other hand, it was observed that anandamide inhibits neurogenic relaxation of corpus cavernosum of human and primates (Van den Bossche et al.2000). The potent vasodilatory influence of anandamide has been shown in a variety of isolated vascular preparations. Its mechanism of action, however, is complex and the subject of intense investigation. In rabbit pail arterioles and mesenteric arteries, the anandamide- induced dilation was blocked by indomethacin and diclofenac, respectively, suggesting it was mediated by generation of vasodilator eicosanoids. Similarly, in isolated bovine coronary arteries, the vasorelaxant effect of anandamide has been suggested to be due to hydrolysis of this cannabinoid to arachidonic acid followed by conversion to vasodilatory eicosanoids. In rat renal arteries and cultured endothelial cells, anandamide stimulated the release of nitric oxide via an activation of CB1 receptors, and vasodilation could be blocked by inhibition of NO-synthase. Also, in human vascular endothelium, anandamide stimulated CB1 receptor-mediated NO release. In several vascular tissues anandamide was reported to directly induce vasorelaxation, unrelated to its metabolism or to NO-release. Indeed, exogenous application of the cannabinoid caused vasodilation of the mesenteric and coronary vascular bed, also after removal of the endothelium, a relaxing influence which was inhibited by SR141716A, a selective CB1 receptor antagonist. Since this antagonist also inhibited the endothelium-dependent, NO- and prostanoid-independent dilation induced by carbachol, generally attributed to an endothelium derived hyperpolarizing factor (EDHF), anandamide was even proposed as EDHF. Moreover, it should be noted that anandamide can have actions unrelated to cannabinoid receptor stimulation, such as decreasing gap junctional permeability in astrocytes, an effect which is not induced by other cannabinoid receptor agonists and which is insensitive to SR141716A. The cellular effects of cannabinoids were mostly investigated in neural cells. These include inhibition of adenylyl cyclase, inhibition of Ca ²⁺ -current through N-type, and P/Q-type Ca ²⁺ channels, activation of inward rectifier K+ current and of voltage-dependent A-type K+current. In vascular smooth muscle cells, modulation of K+ channel activity plays an essential role in regulating membrane potential and, thereby, the open probability of voltage operated Ca ²⁺ channels, contractile tone, and blood flow in general (Van den Bossche et al.2000). 1.2. Surveys of Men Evaluating Effects of Marijuana Use on Sexual Function In one of the earliest studies, the National Commission on Marihuana and Drugs reported findings from an informal survey of about 200 marijuana users who were asked, “Do you think being high on marijuana stimulates your sex interest, or not?” Among these 200 users, 44% reported “definitely increases their sexual desire”, with 50% of those being women. They found that women were more likely than men to report an in-crease in desire. They also looked at rare, frequent, and heavy everyday marijuana use. Frequent but not daily marijuana use when compared to heavy everyday use and rare use (less than 1joint a week) was associated with increased sexual pleasure in around 70% of users. In 1974, Koff Performed a survey of 251 college-aged students, who were asked about the amount of marijuana smoked each time the drug was used (1 joint or less, 2-4 joints, or more than 4 joints) and whether their sexual desire increased, decreased, or remained the same. He also asked whether sexual activity was enjoyable after marijuana use. Of the 251 college students surveyed, 128 were female. The results of the survey indicated that 39.1% of males reported an increase in sexual desire, whereas 57.8% of females reported an increase—a significant difference. Also, 43% of the female participants re-ported heightened sexual pleasure. Additionally, Koff found that the effects of marijuana appeared to be dose dependent, noting that, although 71% of female participants reported increasing sexual motivation after 1 joint, the percentage of women reporting increased desire decreased after a larger consumption of marijuana (greater than 4 joints) (49.5%). This study supports the idea that the effect of marijuana on sexual function is dose dependent, such that low doses of marijuana (1 joint) can be sexually stimulating but high doses of marijuana can have the opposite effect. In 1976, Chopra and Jandu interviewed 275 chronic marijuana users (smoked for 6 months to several years) from India and Nepal about the effects of marijuana and included some questions evaluating its effects on sexual function. This study observed similar dose-dependent effects and speculated that sexual inhibition is caused by an increased sedative effect seen at higher doses of marijuana intoxication. They did not divide their findings by gender. A survey of 84 graduate students of health sciences in the south-eastern United States was conducted by Dawley et al (78% male and 22% female). This survey included 57 multiple-choice and true/false questions that were developed to determine the attitudes of individuals regarding the effects of marijuana use on sexual function. The 84 graduate students were categorized as “experienced” (having had a sexual experience while under the influence of marijuana),“non-experienced”(those who have been under the influence of marijuana but have not concurrently had a sexual experience), and “non-smokers.” The study found that the “experienced participants” reported increased sexual pleasure (88%), sensations (48%), and satisfaction when both partners used marijuana (76%), as well as an increase in the intensity of the orgasm (58%). However, this study did not explore any differences between males and females, specifically. These findings were further replicated in a 1982 survey done by Halikas et al. One hundred regular marijuana users (37female users) with an average smoking experience of 2 years were systematically interviewed to assess the psychosocial effects of marijuana use, including effects on sexual function. This study demonstrated that 76% of females reported an increase in sexual pleasure and satisfaction (14% of women reported variable feelings), and 63% of women reported feelings of emotional closeness and intimacy. Additionally, 32% of women reported an enhanced quality of orgasm, and the other 8% and 60% reported variable or no effects, respectively. Overall, 81% of people (men and women) reported pleasure-enhancing effects associated with marijuana use (Lynn B, at al.2020). CBD can decrease performance anxiety and improve blood flow by inhibiting the intracellular degradation of anandamide catalysed by the enzyme fatty acid amide hydrolase and therefore, increasing anandamide levels. The consumption of this cannabinoid produces an increase in dopamine, a neurotransmitter that stimulates our mood, increases sexual excitement and pleasure. The overwhelming data on male sexual function suggest that THC and CBD extracts may enhance the subjective experience of sexual intercourse as it can improve the quality of people’s sexual experiences and soothe anxieties that inhibit intimacy. 2.10 CANNABIS SATIVA EXTRACTS The compositions or dosage forms of current invention may include one or more of the following types of CBD extract: Full spectrum, broad spectrum or isolate: A. Defining Full-Spectrum CBD as an extract that contains all phytochemicals naturally found in the Cannabis sativa plant (comprising any strain type of Cannabis sativa plant), including CBD, trace cannabinoids (which can include any of the following: THC (tetrahydrocannabinol), THCA (tetrahydrocannabinolic acid), CBD (cannabidiol), CBDA (cannabidiolic acid), CBN (cannabinol), CBG (cannabigerol), CBC (cannabichromene), CBL (cannabicyclol), CBV (cannabivarin), THCV (tetrahydrocannabivarin), CBDV (cannabidivarin), ,CBCV (cannabichromevarin), CBGV (cannabigerovarin), CBGM (cannabigerol monomethyl ether), CBE (cannabielsoin), CBT (cannabicitran) among others), terpenes, and essential oils. Full-spectrum extracts from hemp (Cannabis sativa for industrial purposes strains) also might come with a negligible THC content — below 0.3% (worldwide compliance). The full spectrum of the active compounds extracted from hemp work together to amplify the health benefits of each individual cannabinoid. This phenomenon is referred to as the “entourage effect” (synergy achieved by all the components in Cannabis). B. Defining Broad-spectrum as the type of extract that contains cannabidiol and all the other compounds within the plant, save for THC, which is completely removed after the initial extraction. Because broad-spectrum extracts contain multiple cannabinoids - which can include any of the following: CBD (cannabidiol), CBDA (cannabidiolic acid), CBN (cannabinol), CBG (cannabigerol), CBC (cannabichromene), CBL (cannabicyclol), CBV (cannabivarin), THCV (tetrahydrocannabivarin), CBDV (cannabidivarin), ,CBCV (cannabichromevarin), CBGV (cannabigerovarin), CBGM (cannabigerol monomethyl ether, CBE (cannabielsoin), CBT (cannabicitran) among others-, they also might produce the “entourage effect” but without the THC. C. Defining for instance CBD isolate as the purest form of CBD; made by pulling it from its natural environment and removing it from all other ingredients. Isolates are usually 99% pure, meaning that one gram of isolate powder carries about 990 mg of CBD. Same applies for isolates of any other type of cannabinoid. 2. OTHER EFFECTIVE HERBAL DRUGS FOR ERECTILE DYSFUNCTION 2.1. BACCHARIS TRIMERA (CARQUEJA) Experiments in vitro demonstrated that BACCHARIS TRIMERA induces vascular smooth muscle relaxation (Table 1). Effect/ Result References Chloroform extracts from the plant have shown to induce vascular O. Hnatyszyn et al.2003 smooth muscle relaxation in strips of rat portal vein. Aqueous extracts have shown to relax the guinea pig corpus cavernosum. R.M. Gene et al.1996 Demonstration of the arterial smooth muscle vasorelaxant properties of the infusion of B. trimera towards rat aortic rings, which are likely to be H. Heinzen et al.2016 due to endothelium dependent and independent mechanisms. The effect might correlate with the fall in blood pressure referred in folk medicine. Table 1. In vivo essays. 2.2. L-CITRULINE l-Citrulline is a neutral, non-essential alpha-amino acid that is an important component of the urea cycle in the liver and kidneys (Curis E. et al.2005). As a non-protein amino acid, l-citrulline is rarely found in food, but is highly concentrated in watermelon. The concentration of l-citrulline in watermelon grown in the United States can range from 1.6 to 3.5 g/kg of fresh watermelon. As such, consumption of approximately 1–1.5 kg/day (2.2– 3.3 lbs/day) of fresh watermelon would be needed to achieve the minimum effective dose of l-citrulline (3 g/day) and 3.3–5.0 kg/day (7.3–16.5 lbs/day) of fresh watermelon would be needed to achieve the maximum effective dose of l-citrulline (10 g/day) (Davis A.R. et al. 2012). Increasing numbers of studies now suggest that watermelon extract supplementation and nutraceutical grade l-citrulline (watermelon purified extract of at least 99% L-citrulline) can increase the bioavailability of l-arginine and subsequently lead to elevations in NO synthesis (Allerton T.D. et al.2018). Figure 4 presents the comparison of oral l-citrulline (nutraceutical grade l-citrulline or watermelon products) versus oral l-arginine (Allerton T.D. et al.2018). The activity of the arginase enzyme located in the enterocytes of intestines and liver (first-pass extraction) substantially reduces the availability of oral l-arginine, instead yielding increased urea and l-ornithine production. l-citrulline is not acted on by arginase enzyme or first-pass extraction but is converted to l-arginine by argininosuccinate lyase in the kidneys. Increased circulating l-arginine serves a substrate for the eNOS to produce nitric oxide (NO) and increase smooth muscle vasodilation. l-citrulline may directly activate inducible nitric oxide synthase (iNOS) in skeletal muscle and increase protein synthesis via mTOR activation. l-citrulline may indirectly activate neuronal nitric oxide synthase (nNOS) in skeletal muscle leading to increases in NO and stimulation of mitochondrial biogenesis. l-citrulline has reported actions on adipose tissue to increase lipolysis, fatty acid oxidation, and uncoupling protein 1 (UCP1) expression. l-citrulline has also been reported to indirectly activate iNOS in activated macrophages and increase NO production. l-citrulline’s systemic effects positively impact hypertension, atherosclerosis, inflammation, insulin resistance, type 2 diabetes, and cardiovascular disease. Emerging evidence also suggests that l -citrulline itself can positively impact skeletal muscle and adipose tissue to improve metabolic syndrome. Figure 4 was partially modified from Irving and Spielmann (2016). Both l-arginine and l-citrulline levels have been shown to get lowered in severe ED/ arteriogenic ED (Barassi A et al. 2017). l-citrulline and l-arginine supplementations have been shown to rapidly and effectively increase NO bioavailability and cyclic guanosine monophosphate (cGMP) concentrations (Morita M, et al. 2014). L-citrulline supplementation has been shown to improve erectile function in rats with acute arteriogenic ED, and one study has shown improved erection in mild ED patients (Cormio L, et al.2011), though there have been no studies in humans with l-citrulline and l-arginine combination. The advantage of l-citrulline over l-arginine is that it does not undergo first-pass metabolism, nor it is metabolized by intestinal bacteria. 2.3. MUCUNA PRURIENS M. pruriens seeds are rich source of L-DOPA and its metabolites, which include epinephrine and norepinephrine. It’s been proven that an increase in dopamine level in the brain following M. pruriens treatment may not only induce the activation of sexual behavior but it may also increase plasma testosterone level. It has been reported that L-DOPA and its metabolite dopamine stimulate the hypothalamus and forebrain to secrete gonadotropin-releasing hormone (GnRH) (Vermes I, et al.1979). This, in turn, upregulates the anterior pituitary gland to secrete follicle stimulating hormone (FSH) and luteinizing hormone (LH) causing increased synthesis of testosterone by Leydig cells of the testis (S.M.L. Mendis-Handagama.et al. 2005 and Kaphale K et al 2003). Furthermore, spermatogenesis is controlled by the hypothalamus and anterior pituitary working together. Based on the above stated facts, it may be proposed that increased dopamine level in the brain may not only optimize the release of hormones, including testosterone, leading to increased sexual drive and improved performance, but it may also accomplish reduction of psychological stress. Moreover, treatment with M. pruriens may also contribute to proper functioning of male genital system and facilitate sperm transport, contraction of seminal vesicles and inhibition of lipid peroxidation of spermatozoa (Fait G, et al.2008). 2.4. ANGELICA SINENSIS Coumarins, and Osthole in particular, have been identified as bioactives of Angelica sinensis, which display activities such as, inhibition of platelet aggregation, inhibition of Smooth muscle contraction, Smooth muscle relaxation (Che-Ming et al.1994), inhibition of calcium flux, cyclic nucleotide (such as cGMP and cAMP) phosphodiesterase inhibition, increase in cAMP and cGMP levels, anti-proliferative, anti-inflammatory, enhancement of the increase of cAMP induced by forskolin, vasorelaxation, neurotransmitter receptor binding, such as GABA, 5HT-1A, D-2, and D-1 receptors. Alpha-angelica-lactone also possesses various activities, including, e.g., calcium antagonism. Ferulic acid, another component of Angelica root also has been shown to scavenge oxygen free radicals and increase intracellular cAMP and cGMP. Preferred activities of Angelica are cyclic nucleotide phosphodiesterase inhibition, calcium antagonism, oxygen free radical Scavenging, Smooth muscle modulation, as either vasorelaxant or vasodilatory (July 2013 EMA/HMPC/614586/2012 Committee on Herbal Medicinal Products (HMPC) Assessment report on Angelica sinensis (Oliv.) Diels, radix). 2.5. ACHYROCLINE SATUREIOIDES (MARCELA) Ethanol extract of the aerial parts of Achyrocline satureioides (Lam.) DC. (Asteraceae) showed a significant, dose dependent, relaxant effect on the smooth muscle of corpus cavernosum strips, obtained from Guinea pig (65.5 +/- 4.1% of relaxation at the dose of 25.0 mg/ml). Bioassay guided fractionation of this extract furnished two flavonoids, quercetin and quercetin 3-methyl ether, with important vasorelaxing effects on the corpus cavernosum strips (79.8 +/- 8.4 and 66.0 +/- 4.8% of relaxation respectively at the dose of 0.075 mg/ml). Two methyl derivatives of quercetin obtained by synthesis, quercetin 3,7,3',4'-tetramethylether and quercetin 3,5,7,3',4'-pentamethylether, showed similar relaxant effects at the dose of 0.075 mg/ml (86.4 +/- 8.5 and 67.31 +/- 1.4% of relaxation respectively). The results show that the ethanol extract of A. satureioides and the assayed compounds exhibit significant vasorelaxing properties. 2.6. TURNERA DIFFUSA and PFAFFIA PANICULATA Sexually potent and sexually sluggish/impotent male rats were treated orally with different amounts of Turnera diffusa and Pfaffia paniculata fluid extracts (0.25, 0.50, 1.0 ml/kg). While having no effect on the copulatory behavior of sexually potent rats, both plant extracts--singly or in combination--improved the copulatory performance of sexually sluggish/impotent rats. The highest dose of either extract (1 ml/kg) (as well as the combination of 0.5 ml/kg of each extract) increased the percentage of rats achieving ejaculation and significantly reduced mount, intromission and ejaculation latencies, post-ejaculatory interval and intercopulatory interval. Neither extract affected locomotor activity. These results seem to support the folk reputation of Turnera diffusa and Pfaffia paniculata as sexual stimulants. 5. DETAILED DISCLOSURE The present invention surprisingly discovered that ED is arrested, inhibited, and even reversed in some instances by use of a composition of the present inventions and methods of treatment utilizing same. The present invention surprisingly discovered that the most effective treatment is the one that treats every aspect and angle of the problem from a holistic point of view, targeting different physiological and phycological components of the problem. In vitro experiments have established that the tested formulations induce vascular smooth muscle relaxation of the corpus cavernosum which can treat and/or prevent ED and SD effectively. The precise dosage will vary according to a variety of factors such as subject-dependent variables (e.g. age, gender, medical history, etc.), the disorder or condition and the type of treatment. The aspects herein described are not limited by the illustrated ordering of acts or events, as some acts may occur in different order and/or concurrently with other acts or events. Preferred compositions of the present inventions do not contain compounds that require a prescription and avoid side effects of current "first line" treatments for ED (AED). In particular aspects of the present disclosure, the combination therapy of cannabis extract with other herbal extracts elicits the desired biological and medical, when administrated in therapeutically effective amounts. Aspects of the present disclosure provide compositions comprising the following herbal drugs: Cannabis, cannabis extracts or one or more cannabinoid, and three other herbal drugs or herbal extracts listed herein. According to an aspect of the present invention, there is provided oral dosage composition for use in the treatment of male erectile dysfunction (ED) and/or related erectile dysfunction (RED), wherein the composition comprises 1-200 mg of a chosen cannabinoid or combination of cannabinoids, provided in the form of a Full spectrum extract, broad spectrum extract or isolate extract - said extract could be in liquid, semi-liquid or solid form, plus, 400 mg of a composition consisting of at least one member of the group consisting of L-citrulline and L-arginine; the amount of arginine or a compound that can produce arginine in vivo in a daily formulation is preferably from about 100 mg to about 3 g for treatment of erectile dysfunction. Preferably, the arginine is L-arginine and the compound that can produce arginine in vivo is citrulline, preferably L-citrulline. Some or all the L-arginine can be replaced with L-citrulline. The composition comprises also at least 200 mg of Baccharis trimera or derivative of Baccharis trimera; the derivative may comprise or is derived from dried extract of aerial parts and leaves of Baccharis trimera; the extract may be used fresh or may be partially or completely dehydrated. The formulation for the treatment of erectile dysfunction also comprises at least 400 mg of Mucuna pruriens or derivative of Mucuna pruriens; the derivative may comprise or is derived from dried extract of seeds of Mucuna pruriens; the extract may be used fresh or may be partially or completely dehydrated. An embodiment of the present formulation may also comprise at least 200 mg of Angelica Sinensis or derivative; the derivative may comprise the dried root of Angelica sinensis; the extract may be used fresh or may be partially or completely dehydrated. The present formulation may also comprise at least 200 mg of Turnera diffusa and/or Pfaffia paniculataor derivative; the derivative may comprise the leaves and stems of Turnera diffusa and/or Pfaffia paniculate; the extract may be used fresh or may be partially or completely dehydrated. The composition may comprise also at least of 200 mg Achyrocline Satureioidesor derivative, the derivative may comprise inflorescences of Achyrocline Satureioides; the extract may be used fresh or may be partially or completely dehydrated. A dosage form of the composition contains an amount of each ingredient sufficient when administered for a sufficient period of time to produce a beneficial effect in treating ED or SD, wherein the beneficial effect includes at least one of slowing, stopping or reversing worsening symptoms of ED or SD, slowing, stopping or reversing the appearance of symptoms of ED or SD, shortening refractory period between erections, and/or reducing, slowing or stopping increases in refractory period between erections. In an embodiment, indicia of ED or SD are treated and/or indicia of satisfactory sexual experience are improved. When determining the efficacy of a composition of the present invention in treating ED or RED by IIEF score, the presence of all ingredients CBD extract, THC extract, CBN extract, CBG extract, CBC extact, L-Citrulline, Baccharis trimera extract, Mucuna pruriens extract, Angelica Sinensis extract, Turnera Diffusa and Pfaffia extacts, Achyrocline Satureioides extract, were tested. The active ingredients of compositions of the present invention can be combined using well known and standard processes and agents. Preferably, a gelatine capsule contains the combined ingredients in powder form. Exemplary compositions for base formulations are presented below. The ingredients, in powder form, are inspected, weighed, blended and encapsulated in gelatine capsules. The blending process includes standard screening, blending and metal detection at standard temperatures and in a sterile environment at least sufficient for food supplements. The compositions or dosage forms may include optional pharmaceutically acceptable excipients as fillers, binders, and colorants, and can be packaged in standard gelatine capsules (hard or soft gelatine) or formed into solid tablets, taken in particulate form, or mixed into and/or suspended in solution. The composition might comprise other optional ingredients, such as a binding agent, an agent that increases dissolution and digestion in vivo, preservatives and/or colorants. Standard ingredients in powder formulations are used for preparing and compounding preferred exemplary formulations of the present inventions. For example, carrier silica can be used to convert liquids into free-flowing powders and/or can be used to enhance flowability and shelf life of powdered products. Desintegrants are an excipient used to enhance the disintegration process of tablet formulation when they make contact with gastrointestinal fluid, for example: starch, croscarmellose sodium, crospovidone, and sodium starch glycolate. Magnesium stearate can be used as a diluent with lubricating properties helpful to prevent the composition and its ingredients from sticking to manufacturing equipment and can also serve as a binding agent. According to an aspect of the present invention, an oral dosage form comprises a composition in accordance with the first, second and third aspects of the inventions, wherein the dosage form is selected from the group consisting of a tablet, capsule, lozenge, powder or suspension comprising the foregoing ingredients. Preferred suspensions are aqueous and/or alcohol (ethanol) based. Flavourings or taste masking agents may be employed. Tablets or other dosage forms may include diluents (for example lactose), desintegrants, for example cross-carmelose sodium or binders, for example, polyvinylpyrrolidone. Lubricants for example magnesium stearate, or other conventional excipients may be employed (e.g., silicas, carbohydrates, etc.). Film coated tablets may be provided. The extracts may be used fresh or may be partially or completely dehydrated. Fresh natural products used for ingredients of the present invention may be chopped, pulped or otherwise comminute before incorporation into a dosage form. For example, an ingredient may be concentrated to facilitate transportation, storage, and administration. The raw materials and ingredient extracts may be dried, for example by freeze-drying or vacuum drying, before compounding into oral dosage forms. Individual dosage forms may comprise compressed tablets, capsules, lozenges or may be provided in sachets. Suspension formulations may be provided. CBD extract, THC extract, CBN extract, CBG extract, CBC extact, L-Citrulline, Baccharis trimera extract, Mucuna pruriens extract, Angelica Sinensisextract, Turnera Diffusa and Pfaffia extacts, Achyrocline Satureioides extract are all commercially available, with preferred sources and analyses provided. Preferably, the ingredients are combined and encapsulated in hard gelatine capsules, but other dosage forms are anticipated that will produce equivalent results. EXAMPLES Examples of various embodiments of the present invention will now be further illustrated with reference to the following examples. Thus, the following examples are provided to illustrate the invention, but are not intended to be limiting thereof. Example 1 One hundred and sixty men over the age of 40 (40 years<x) with sexual dysfunction based on history were entered in this open-label, nonrandomized study. Different patients received randomly capsules containing one of the 12 FORMULATIONS presented above or placebo enough for 12 weeks treatment, 2 capsules/day. Efficacy was assessed at weeks 4, 8, and 12 using the International Index of Erectile Function Questionnaire. By use of this standard questionnaire, many patient histories, with identities redacted, can be combined with questionnaire results to generate statistically significant data when compared with questionnaire results following administration of different compositions (or placebo). Echo-doppler studies have been performed before and after treatment with each formulation; an increase in blood flow can be appreciated through CA PSV values on Figure 5 and Figure 6. Cavernosal artery peak systolic velocity (CA PSV) ≥25 cm/s were considered normal and that formed the basis of normalcy in our study. Figure 5 shows the relationship between the 12 groups of men (Group 1 received Formulation 1, Group 2 received Formulation 2, and so on) and the CA PSV. No significant discrepancy was noted between PSV of the right and left cavernosal arteries (P = 0.436), hence, the PSV of the right and left cavernosal arteries was analysed together. Figure 6 shows the difference between CA PSV baseline values and CA PSV values after treatment with each formulation. The data suggested that all 12 formulations were well tolerated in men over 160 with sexual dysfunction. Overall sexual function improved significantly; resulted in a high percentage of increased libido, decreased performance anxiety, improved blood flow and sexual satisfaction mostly while administration of FORMULATIONS 1, 2, 4, 5, 7, 8 and 11. Greater penile stiffness was observed in those in whom FORMULATION 1, 2, 4, 5, 7, 8 and 11 was administered. Results: FORMULATIONS 1, 2, 4, 5, 7, 8 and 11 have been proven to be an effective treatment of erectile dysfunction showing no side effects during the terms of the studies. Example 2 A clinical trial was performed to evaluate the efficacy and safety of the composition of current application (FORMULATION 2) for sexual dysfunction in men. Single blind-study was carried out for 12 weeks, in a group of 120 patients also over 20 years of age (20 years<x), who were administered a placebo or FORMULATION 2, obtaining a statistically significant high percentage of vasodilation. The participants who received placebo did not perceive improvements in their sexual performance while those who received FORMULATION 2 were shown to effectively and safely improve erectile function regardless of the pathology´s cause. Results: FORMULATION 2 has been proven to be an effective treatment of erectile dysfunction showing no side effects during the terms of the studies. Example 3 Two double-blind parallel studies (placebo – FORMULATION 2 and placebo - Sildenafil) in men with organic and psychogenic erectile dysfunction or mixed causes was performed for 24 weeks to evaluate the efficacy and of FORMULATION 2 for sexual dysfunction in men when compared with sildenafil.250 men over the age of 20 (20 years<x) received treatment with FORMULATION 1, one hour or more before sexual activity, which allowed them to have satisfactory activity in 86% of cases. In this group, we performed echo-doppler studies before and after FORMULATION 2 treatment, highlighting an increase in blood flow that varied from 30% to 40%. Greater penile stiffness was observed in those in whom FORMULATION 2 was administered. Results: A total of 250 patients signed consent to participate in the study. The mean age of the patients was 56 years. Seventy-five patients were assigned to receive FORMULATION 2 and 50 were assigned to receive placebo, with 70 patients who received FORMULATION 2 completed the treatment and 57 who were assigned to receive placebo completed the treatment. Seventy-five patients were assigned to receive sildenafil and 50 were assigned to receive placebo, with 68 patients who received sildenafil completed the treatment and 59 who were assigned to receive placebo completed the treatment. Preferably dosage form comprises at least about 25mg CBD or CBD derivative and at least about 400 mg of L-citrulline or L-arginine or a mixture thereof, at least about 200mg of Baccharis trimera and at least about 400mg of Mucuna pruriens; said dosage form can be administered at least once a day, preferably twice a day, for a sufficient period of time to treat erectile dysfunction or age related erectile dysfunction.