How Focusene Works
Focusene gives the distracted brain a powerful herbal boost and provides the nutrients it needs to focus and remember better. These nutrients are basically the "building blocks" of your focus and memory neurotransmitters (chemical messengers). In the end what you have is a two-part formula giving you a Nootropic Supercharge as well as long–term focus and memory support.†
First some background on what is often going on when you have focus, attention or memory problems.
Arguably, the three most important neurotransmitters involved in focus, concentration, memory and general cognition are: dopamine, norepinephrine and acetylcholine. Let's look at what each go these does in your brain.
Nootropic Brainpower Turbocharge
Wait, what the heck is a "nootropic?" We can't hold it against you if you don't know; it is a very new concept. Nootropics are both natural and chemical "smart drugs" that range from ginkgo biloba (the original nootropic) to the "racetam" family of experimental psychoactive chemicals. Every ingredient in Focusene is natural and regarded as safe by the FDA. This is not true of many other nootropics.
For the first few weeks of taking Focusene, you should notice the effects of the fast–acting ingredients most strongly. First, Forskolin and Luteolin have been shown to boost the brain's cAMP, a form of cellular energy involved in brain signal processing. 12 13 14 cAMP, in basic terms, helps the brain to interpret and react to signals once they are delivered. To round this out, a healthy dose of Ayurvedic bacopa provides an extra herbal kick. In basic terms, it is like turning up your brain's "processor speed,".†
Long-Term Cognitive Support System
The key to why Focusene™ grows even more effective over time are the nutritional ingredients. We have all heard the phrase, "you are what you eat." This is as much true for your mind as it is for your body. There are many nutrients in your brain that are critical to mental performance but are not very abundant in everyday food. The brain needs to constantly build natural chemicals like choline, acetylcholine, GABA, Dopamine, Norepinepherine and many more. To do this, it needs precursors or "building block" ingredients. Focusene™ is loaded with these precursors. Phenylalanine, for example, is a precursor for both acetylcholine and dopamine – both critical for mental responsiveness.
To put it simply, the combination of Vitamin B6, L-Theanine, DMAE, and L-Phenylalanine work to build and balance out those critical neurotransmitters and supporting nutrients in the brain. However, this does not happen overnight. With chemical balance and high mental performance as the main goals, the formula works with your body over time, working toward balance and harmony in your mind's support systems.†
How long should you take Focusene?
While it is common to begin feeling a brainpower boost after the first dose, the formula often requires some time to reach its full effectiveness.† We generally recommend taking Focusene for at least three to four months give your body enough time to come into balance with the formula. The wonderful thing about a natural focus and attentiveness booster is that there are rarely any side effects, unlike most prescription medications. However, natural treatments for attention problems rarely have the same strong, immediate effects of a prescription stimulant. Focusene is more about a balance of mental clarity and energy than forcing a sudden mental change.
-  Nora D. Volkow et al., (2009) evaluated biological bases that might underlie a reward/motivation deficit by imaging key components of the brain dopamine reward pathway (mesoaccumbens). Authors found a reduction in dopamine synaptic markers associated with symptoms of inattention was shown in the dopamine reward pathway of participants with attention deficit. ↩
-  Roshan Cools et al., (2011) reviewed evidence from a series of studies with experimental animals, healthy humans, and patients with Parkinson's disease, which highlight two important factors that contribute to this large variability. First, the existence of an optimum DA level for cognitive function implicates the need to take into account baseline levels of DA when isolating the effects of DA. Second, cognitive control is a multifactorial phenomenon, requiring a dynamic balance between cognitive stability and cognitive flexibility. These distinct components might implicate the prefrontal cortex and the striatum, respectively. Manipulating DA will thus have paradoxical consequences for distinct cognitive control processes, depending on distinct basal or optimal levels of DA in different brain regions. ↩
-  Nora D. Volkow et al., (1998) have assessed the relation between measures of brain dopamine activity and indexes of motor and cognitive function in healthy individuals. Age-related decreases in brain dopamine activity are associated with a decline in motor function and may also contribute to impaired performance on tasks that involve frontal brain regions. Interventions that enhance dopamine activity may improve performance and quality of life for the elderly. The fact that correlations remained significant after age effects were partialed out suggests that dopamine activity may influence motor and cognitive performance irrespective of age. ↩
-  H. C. Lou et al., (2008) examined the effect of phenylalanine restricted diet on vigilance, as judged by the continuous visual reaction times, and neurotransmitter synthesis, as judged by cerebrospinal fluid (CSF) homovanillic acid (HVA) and 5-hydroxyindole acetic acid (5-HIAA) levels in a group of 9 patients with classical phenylketonuria (PKU). In 14 patients on free diet supplemented with tyrosine, an improvement in vigilance (reaction times at the 90 percentile) was seen in all 12 patients with values longer than the normal mean (264 msec) (p<0.001). Tyrosine treatment may be a therapeutical alternative when phenylalanine restriction is impractical. ↩
-  Arnsten AF (2006) has reviewed the fundamentals of attention-deficit/hyperactivity disorder: circuits and pathways. Neuropsychological and imaging studies have shown that attention-deficit/hyperactivity disorder is associated with alterations in prefrontal cortex (PFC) and its connections to striatum and cerebellum. The PFC is very sensitive to its neurochemical environment, and optimal levels of norepinephrine and dopamine are needed for proper PFCcontrol of behavior and attention. Recent electrophysiologic studies in animals suggest that norepinephrineenhances "signals" through postsynaptic alpha2A-adrenoceptors in PFC, while dopamine decreases "noise" through modest levels of D1-receptor stimulation. ↩
-  Una D. McCann et al., (1993) examined the effects of Catecholamine Depletion on Alertness and Mood in Rested and Sleep Deprived Normal Volunteers. The findings are consistent with the view that sleep deprivation is associated with decreased functional catecholamine neurotransmission. Furthermore, mood effects following sleep deprivation plus AMPT suggest that catecholamines may be involved in mood changes during sleep deprivation. ↩
-  Michael T. Heneka et al., (2009) have studied the Locus ceruleus controls cognitive decline pathology. Research dating back to the 1960s implicated LC degeneration in the pathogenesis of cognitive decline. Of particular relevance, several studies show that AD patients present with a prominent loss of LC cells, reaching 70% within the rostral nucleus and causing reduction of cortical and limbic norepinephrine (NE) levels. ↩
-  S. Colette Daubner et al., (2011) studied regulation of dopamine synthesis. The biosynthetic pathway for the catecholamine neurotransmitters is explained. Phenylalanine hydroxylase converts phenylalanine to tyrosine, tyrosine hydroxylase hydroxylates tyrosine to L-DOPA and then to Norepinephrine. ↩
-  Arjan Blokland (1995) reviewed the acetylcholine involvement in learning and memory. The cholinergic hypothesis claims that the decline in cognitive functions in dementia is predominantly related to a decrease in cholinergic neurotransmission. This hypothesis has led to great interest in the putative involvement of the cholinergic neurotransmission in learning and memory processes. On basis of the available data, ACh seems to be more specifically involved in attentional processes than in learning and memory processes.
-  E.K. Perry et al., (1995) studied Acetylcholine and Hallucinations - Disease-Related Compared to Drug-Induced Alterations in Human Consciousness. Newly proposed criteria for Lewy body dementia include alterations in consciousness. The traditional view that derangements of the basal forebrain cholinergic system in cognitive decline relate specifically to memory impairment is assessed in terms of a more general role for cortical acetylcholine in consciousness. This extends the concept that cortical acetylcholine enhances neuronal signal to noise ratio. It is suggested that muscarinic receptor activation in the cortex is involved in confining the contents of the discrete self-reported conscious ′stream." In the absence of cortical acetylcholine, currently irrelevant intrinsic and sensory information, which is constantly processed in parallel at the subconscious level, enters conscious awareness ↩
-  Mirjana B Čolović et al., (2013) studied the Pharmacology and Toxicology of Acetylcholinesterase Inhibitors. Acetylcholinesterase is involved in the termination of impulse transmission by rapid hydrolysis of the neurotransmitter acetylcholine in numerous cholinergic pathways in the central and peripheral nervous systems. ↩
-  F. Bernardo Pliego Rivero et al., (1999) have investigated forskolin-induced expression of tyrosine hydroxylase in human foetal brain cortex. Brain-derived neurotrophic factor (BDNF) has previously been shown by this and other laboratories to work in concert with dopamine (DA) to induce the dopaminergic phenotype in foetal rat and human cerebral cortex during specified sensitive developmental stages. In the present study this induction by BDNF/DA was found to be greatly amplified by adding forskolin (fsk: 10 μM) to the rat and human cerebral cortex cultures together with DA (10 μM) and BDNF (50 ng/ml). Since fsk boosts intracellular levels of cyclic AMP (cAMP), its amplifying action when added together with BDNF/DA is likely to be due to interactions via the cAMP response element/cAMP response element binding protein (CRE/CREB) systems.
-  Susumu Ando et al., (1987) studied delayed memory dysfunction by transient hypoxia, and its prevention with forskolin. Rats were exposed to 40 min hypoxia 3 h before a one-trial learning passive avoidance task showed impaired memory retention 24 h later. This model was used to assess the ability of forskolin to restore the delayed memory dysfunction. Significant amelioration of memory retention was observed when forskolin (500 μg/kg, i.p.) was injected just after hypoxia. Forskolin is suggested to enhance cerebral blood flow and to facilitate memory function through the action of increased cyclic adenosine monophosphate (cAMP).
-  JIANG Dai-xun et al., (2015) studied the prevention fMLP-induced neutrophils adhesion by luteolin via suppression of LFA-1 and phosphodiesterase 4 activity. Luteolin is an active ingredient found early from Folium perillae and Flos lonicerae, and has a specific inhibition on phosphodiesterase 4 (PDE4) activity in vitro. Researches show luteolin has pharmacological effects of anti-inflammation, anti-anaphylaxis, antitumor, antioxidant, protection of nervous system and so on, and has mainly been used for the treatment of respiratory inflammatory diseases, cancer and cardiovascular disease in clinic. PDE4, specific to hydrolyze cyclic AMP (cAMP), is considered to be a new anti-inflammatory target due to the decisive role on cAMP signal in inflammatory cells such as neutrophils. In order to explore the anti-inflammatory mechanism, we further studied the effects of luteolin on the activity and expression of PDE4, the expression of lymphocyte function-associated antigen-1 (LFA-1) and macrophage-1 (MAC-1) in neutrophils, and the adhesion of neutrophils and endothelial cells. The results showed that luteolin had a dose-dependent inhibition on both bare PDE4 activity and PDE4 in cultured neutrophils, and had an obviously promotive effect on gene expressions of PDE4A, 4B and 4D in later period. Luteolin had a significant inhibitory effect on neutrophils adhesion and LFA-1 expression in early stage, and had no obvious effect on MAC-1 expression.