Chemist - if you're out there, I'm interested to see what you think about this.
Well first I think it's important to note that just because a chemical compound comes directly from nature does not make it any more safer, effective, or tolerable than man-made drugs. An overwhelming number of them cause serious illness, permanent disability, or death. So I would advise people not to automatically associate "natural" with "good for you" and man-made with "bad for you." Where science has taken naturally occurring chemical compounds and turned them into drugs in the past, they're usually "tweaked" to make them much safer and tolerable for humans.
As far as the potential use of the chemical compounds suggested by ronny, I'll say this:
Conessine from Kutaj (Holarrhena antidysenterica) - This chemical compound is in fact a potent and specific H3 antagonist, and H3 antagonists are being studied for the treatment of Excessive Daytime Sleepiness. However, conessine in particular is considered to have no medicinal value due to its exceptionally long half life in the body and its binding to alpha-2 adrenoreceptors. The reason this makes it thoroughly unusable is because H3 antagonists are expected to act as stimulants, and stimulants must have a half-life short enough to allow the majority of the drug to be gone by bed time to prevent interference with sleep and development of chronic tolerance. The half-life of conessine is so long that it would disrupt sleep for a few days until tolerance was established, and thereafter it would have little to no effect on energy levels whatsoever. I found no mention of whether conessine acts as an agonist/antagonist/inverse agonist at the alpha-2 adrenoreceptor, but presumably it acts as an antagonist there as well. This would cause an increase in adrenaline and noradrenaline neurotransmission which could lead to numerous side effects with the most serious being anxiety, rapid heart rate, hypertension, and palpitations.
Ginkgo biloba - There are at least four different biologically active compounds in ginkgo biloba and there has been a lot of research into gingko biloba. The reason for the research is that it does appear to have some weak but interesting medicinal properties and if we can figure out what is responsible for those effects, we may be able to make a man-made drug that acts in a similar fashion but is many times stronger, safer, and tolerable in humans. At present, the only significant properties we find that ginkgo biloba has when taken for more than a few days is some improvement in blood flow, mainly due to its effect on platelets, and moderate norepinephrine reuptake inhibition. Any effects upon GABA(A) receptors are likely to be very weak and essentially of no significance.
Note that generally drugs acting upon GABA either as agonists or antagonists are not very desirable due to the widespread prevalence of GABA receptors in the brain. This means drugs acting on GABA typically cause global effects on the entire CNS as opposed to affecting a small number of functions or pathways in the brain. With GABA agonists like ethanol or benzodiazepines you get sedation, confusion, impaired memory and with GABA antagonists you get hyperexcitability, seizures, and potentially brain damage. Tolerance also builds rapidly to these types of drugs, and the withdrawal from them can cause life threatening complications.
L-Tyrosine is just an amino acid we all produce in our bodies from the essential amino acid L-Phenylalanine that we get in our diets. It is used in our bodies to generate dopamine, epinephrine, norepinephrine, and the thyroid hormones T3 and T4. Using L-Tyrosine supplements does increase its concentration in the blood and does in fact increase the plasma concentrations of the neurotransmitters it's a precursor to, but it has little if any effect on mood or energy. Typically people take the supplement L-DOPA instead of L-Tyrosine, because the rate-limiting step in the biosynthesis of dopamine from L-Phenylalanine is the conversion of L-Tyrosine into L-DOPA. L-DOPA itself is then rapidly converted into dopamine and immediately available for use. Even so, L-DOPA is not typically considered a stimulant and in fact large doses of L-DOPA or certain drugs in the dopamine agonist class actually cause narcolepsy-like sleep attacks. Most of the studies referenced by ronny are those that were conducted before it was known that orexin and histamine were the major players in regulating arousal and not dopamine.
As far as dopamine and norepinephrine activating orexinergic neurons, that's not true. In fact, it's the opposite. Orexinergic neurons have receptors for several neurotransmitters and neuropeptides, all of which can be excitatory or inhibitory and thus increase or decrease the likelihood that the neuron will fire and release orexin. When orexin is released onto catecholaminergic neurons it is extremely excitatory and promotes dopamine and norepinephrine mediated neurotransmission. However, when those catecholamines flood back onto the orexinergic neurons they produce an inhibitory action and provide negative feedback to the orexinergic neuron. The study that ronny referenced had shown that dopamine and norepinephrine INDIRECTLY activate orexinergic neurons, and ONLY when the animals were not anesthetized. When the animals were anesthetized, dopamine and norepinephrine did not activate the orexinergic neurons.
Another important thing to note is that in classic narcolepsy where there is a loss of orexinergic neurons and cataplexy, trying to activate orexinergic neurons is an exercise in futility, because those neurons have physically been destroyed and their debris mopped up. There's no neuron physically present which can release orexin anymore. In other forms of narcolepsy and hypersomnia exciting the remaining healthy orexin producing neurons may prove useful, but orexin agonists will probably be the most useful tool in treating excessive daytime sleepiness (EDS.)
So essentially, and here comes the much shorter answer, the suggested combination of supplements would not be expected to have any significant impact on excessive daytime sleepiness.