Beating Attention Deficit Disorder
Nutrition and Nootropics
For Focus & Attention
by James South MA
denotes the ability to sustain focused attention on a given object, external
(such as people or rocks or colors), or internal (such as thoughts, feelings or
sensations). The power of
concentration also involves the ability to screen out irrelevant distractions
that might divert or disrupt sustained, focused attention.
Concentration is a very practical, mundane necessity of life.
Psychiatrist Daniel Amen reports that adults who come to his clinic suffering
from ADD (attention deficit disorder), a serious disorder of concentration,
typically are concerned with poor school or work performance caused by such
concentration-related symptoms as difficulty sustaining attention to reading or
paperwork; tendency to being easily bored by tedious material; poor planning and
organization; chronic procrastination; restlessness and non-phobic difficulty
staying in confined spaces; difficulty listening carefully to directions;
frequent lateness for work or appointments; and tendency to misplace things.
They also frequently complain of difficulty thinking clearly; poor
self-discipline, mood problems, anxiety, restlessness, drug abuse, temper
problems, marital problems, insomnia, over impulsiveness, and money problems. And all of these problems in turn relate to their difficulty
with sustaining attention and resisting distractions. (1)
brain formula. Raise
ADD and ADHD
notes that ADD has been present in some form in all four of the editions of the
Diagnostic and Statistical Manual of the American Psychiatric Association,
although the condition's name has changed in each edition. ADD is therefore not
just some recent "fad" diagnosis. It is currently labeled
"Attention Deficit /Hyperactivity Disorder" (ADHD), although many
children and adults lack the hyperactivity component of the attention deficit
is a core group of symptoms common to those who have ADD. These include
difficulty focusing attention; difficulty organizing tasks, space and time;
difficulty following tasks through to completion; easy distractibility; poor
self-supervision; forgetfulness; and poor attention to detail and careless
Amen diagnoses AD(H)D based in part on careful symptom questionnaires, as well
as medical and family history. However,
his clinic specializes in using a neuro-imaging technology called SPECT to more
definitively establish the diagnosis. "SPECT"
is Single Photon Emission Computed Tomography. It involves injecting a mildly
radioactive substance into the patient's bloodstream which is easily taken up by
brain cells. Then, either at rest
or during a concentration session, a special gamma ray camera photographs the
brain from multiple angles over a 15 minute period.
A supercomputer then reconstructs 3-dimensional images of brain blood
flow levels. (5)
Clarke and Sokoloff report that neuro-imaging studies "... establish
that local energy metabolism in the brain is coupled to social functional
activity and confirm the local cerebral blood flow is adjusted to metabolic
demand in local tissue." (6)
Through the SPECT maps, physicians have been able to identify certain
patterns of brain activity that correlate with psychological and neurological
illnesses. (7) Amen
is probably the current leading expert on SPECT imaging, having conducted about
10,000 patient SPECT studies. (8)
ADD: The 6 Types
his extensive clinical research conducted over the past dozen years, involving
10,000 SPECT studies and 15,000 patient evaluations, Amen has been able to
subdivide ADD into 6 subtypes. (8A)
Type 1, or "classic" ADD, involves a normal resting brain, but
during concentration there are decreases in metabolic activity in the underside
(orbito-frontal) and topside (dorsolateral) prefronal cortex. (9)
It should be noted that the "lion's share" of brain metabolic
activity - about 40%-goes to operating the membrane sodium-potassium pumps that
make the brain electrical activity possible. (10)
Thus, reduced brain metabolic activity necessarily equals reduced brain
electrical activity. And since
brain electrical activity drives neurotransmitter release (11),
reduced brain metabolic activity also equals reduced brain neurotransmitter
activity. Amen has defined the
primary symptoms of "classic" ADD (really ADHD) as inattentiveness,
distractibility, disorganization, hyperactivity, restlessness and impulsiveness.
2, or inattentive ADD, involves a normal resting brain, with reduced
metabolic activity in the dorsolateral prefrontal cortex during concentration.
Primary symptoms include inattentiveness, sluggishness, slow-moving,
low-motivation, frequent boredom, with sufferers frequently described as space
cadets, daydreamers, or couch potatoes. (13)
Type 3 is called "overfocused ADD." SPECT findings show
increased metabolic activity at rest and during concentration in the anterior
cingulate gyrus, (a brain region connecting the prefrontal cortex and limbic
system). During concentration there
is also reduced metabolic activity in the orbitofrontal and dorsolateral
prefrontal cortex. Over-focused ADD
people have trouble shifting attention and frequently get stuck in negative
thought or behavior patterns. They
are also obsessive and worry excessively. They
tend to be inflexible and are frequently argumentative and oppositional.
4 is temporal lobe ADD. At rest and during concentration there is decreased
(occasionally increased) temporal lobe activity.
During concentration there is typically reduced activity in the
orbitofrontal and dorsolateral prefrontal cortex. Temporal lobe ADD symptoms
include inattentiveness, impulsiveness, learning difficulties, unstable moods,
irritability, dark thoughts, and aggressiveness. (15)
5 is limbic ADD. SPECT findings
include increased deep limbic activity (thalamus and hypothalamus) both at rest
and during concentration, and decreased activity in orbitofrontal and
dorsolateral prefrontal cortex. Symptoms include inattentiveness, low-grade
depression, low energy, feelings of hopelessness, chronic negativity, and
perceiving situations in the worst possible light. (16)
Type 6 is called "ring of fire" ADD.
SPECT findings include, both at rest and during concentration, patchy
increased activity across the cerebral cortex, with focal areas of increased
activity, especially in the parietal lobes, temporal lobes, and prefrontal
cortex. Symptoms are
inattentiveness with extreme distractibility, anger/irritability, moodiness,
verbosity, and extremely oppositional. (17)
Amen's book contains a 71 question
questionnaire to help the reader decide if he might possibly suffer from one of
the 6 ADD types. He also provides many case histories of each ADD type, with
before and after treatment SPECT photographs, that are very helpful in seeing
the psychological/behavioral and neurological differences among the types.
treatment regimen is extremely broad, involving biological, psychological and
social interventions. (18) His
biological treatments focus on eliminating toxins, including caffeine and
nicotine because they decrease brain blood flow; avoiding activities with high
risk of head injury; dietary changes - a high protein, low sugar diet for all
except over-focused ADD; intense aerobic exercise; avoiding prolonged exposure
to video and computer games; medication - including Ritalin® or amphetamines;
and nutritional supplements, including a complete multivitamin/mineral
supplement, as well as St. John's Wort, 5-HTP, DL-phenylanine, tyrosine, GABA,
and fish oils, with the specific supplements varying depending on the type. The
interested reader is referred to Dr. Amen's book for more detail. (1)
To Ritalin® Or Not To Ritalin®?
the most controversial, (at least to orthomolecular nutritionists, naturopaths,
and "holistic' physicians) part of Dr. Amen's treatment regimen is his
frequent use of Ritalin® (methyl-phenidate-MPH) and amphetamines (AMP). Actually, among "mainstream" practitioners of ADD medicine, MPH and
AMP are not controversial - they are routinely used to treat presumed AD(H)D
cases. Yet a growing movement, led by Dr. Peter Breggin, challenges the need,
safety and efficacy of MPH/AMP use in children or adults. (19)
Breggin points out that the effects of MPH and AMP are almost identical,
and that neither are safe. (20)
Breggin quotes a 1995 DEA report that "The potential adverse effects
of methylphenidate and d-amphetamine are almost identical." (21)
These potential side effects include heart palpitations, increased heart
rate, increased blood pressure, excessive CNS stimulation (including
convulsions), toxic or organic psychosis, depression, dizziness, headache,
insomnia, nervousness, irritability, tic syndromes, appetite loss, nausea,
vomiting, stomach pain, weight loss, growth suppression, blurred vision, low
white blood cell count, anemia and hypersensitivity reactions. (22)
also provides evidence that MPH/AMP may cause gross brain malfunction/brain
damage, especially in children, whose brains and synaptic connections are still
Breggin also cites extensive evidence that MPH/AMP may promote what he
calls "the zombie effect," snuffing out enthusiasm, curiosity,
initiative, spontaneity, and exploration, while making children obsessed with
meaningless, robotic activities, and turning them into compliant, docile
Anyone who is on, or who has a child on MPH/AMP, or who is considering
MPH/AMP for their child or themselves, should definitely read Breggin's book
before making a final decision on MPH/AMP use, especially since there are many
non-toxic nutritional/nootropic treatments that may work well in improving
concentration and focus.
The Neurobiology Of Attention 101
order to understand the rationale for the nutritional/nootropic treatments
offered later in this article, it may be helpful to gain at least a brief
overview of the neurobiology of attention. Over the past 50 years, neuroscience
has identified four distinct components that make up the brain's attention
system: arousal, motor orientation, novelty detection and reward, and executive
command. "At the lowest level, the brainstem maintains our vigilance - our
general degree of arousal. At the next level, the brain's motor centers allow us
to physically reorient our bodies so that we can redirect our senses [as
needed]. Then, the limbic system accomplishes both novelty detection and reward.
Finally, the cortex-especially the frontal lobes - commands action and reaction
and integrates our attention with short - and long-term goals." (25)
is mediated through circuits which connect the brain stem reticular activating
system (especially the noradrenaline-using locus coeruleus [LC] and the
dopamine-using ventral tegmental area [VTA] with the prefrontal cortex,
posterior cortex, limbic system (including thalamus and nucleus accumbens) and
sense organs. (26,27)
The locus coeruleus and VTA are essential in activating the frontal lobes
- the most distinctively human brain structures.
Under-activity of the locus coeruleus or VTA may in turn lead to
underactive frontal lobes (28,29) - a routine finding in Amen's SPECT studies.
brain's motor centers help us focus/refocus attention in three steps. First, the
posterior parietal cortex helps us disengage from a stimulus.
Then, the basal garglia and frontal parietal attention circuits shift the
focus of attention to something new. Finally,
neurons in the thalamus engage attention by focusing the brain on the new
stimulus while inhibiting other distracting signals. (30) Once we are aroused
and oriented, the brain's novelty/reward system is activated, governed by VTA
dopamine neurons. The VTA-limbic
system (hippocampus) circuit takes note of novelty, while the nucleus accumbens
in the limbic system is a key part of the reward system.
The nucleus accumbens is well-connected to the VTA dopamine system, as
well as other parts of the limbic system. (27,31)
to or under-activity of the reward system leads to difficulty sustaining
attention to matters that don't provide instant gratification. (32)
with "reward deficiency syndrome" are often impulsive, lack
inhibitions, and are quick to act because they are "hooked" on
immediate positive feedback. Monkeys with lesions in the nucleus accumbens are
unable to sustain attention. (33)
fourth system of attention-executive command - directs our actions and
integrates attention with our goals, and is centered in the frontal lobes,
especially the prefrontal cortex. The frontal lobes also interact with the posterior (sensory)
cortex, inhibiting the posterior cortex from raising irrelevant, distracting
stimuli to focal awareness. (28)
frontal lobes ... are linked to intentionally, purposefulness and complex
decision making .... They co-ordinate and lead other neural structure in
concerted action. The frontal lobes are the brain's command post .... even
subtle damage to the frontal lobes produces apathy, inertia, and indifference
and ADHD are caused by subtle dysfunctions of the frontal lobes and the pathways
connecting them to other parts of the brain .... True to its 'executive'
functions, the prefrontal cortex is probably the best connected part of the
brain. The prefrontal cortex is
directly interconnected with every distinct functional unit of the brain.... Of
all the structures in the brain, only the prefrontal cortex is embedded in such
a richly networked pattern of neural pathways." (34)
From this brief description of the neurobiology of attention, several
things should be obvious.
Concentration (focused attention) is a whole-brain activity. Virtually every
part of the brain is involved in mediating attention.
While almost every brain structure is essential to making concentration
possible, the prefrontal cortex is "first among equals."
Under-activity (or over-activity, in "ring of fire" ADD) of the
prefrontal cortex is the common denominator of all 6 ADD types described by
The Brain Is Easily Wounded
Elkhonen Goldberg emphasizes repeatedly in his book The Executive Brain
that the frontal lobes are easily wounded.
Thus he notes "The frontal lobes are exceptionally fragile ....
When neurological illness affects the frontal lobes, the ability to stay
on track becomes lost, and the patient is completely at the mercy of incidental
environmental stimuli and tangential internal associations.... attention deficit
hyperactivity disorder (ADHD), with its extreme distractibility, is usually
linked to frontal lobe dysfunction.... deficit of attention is among the most
common consequences of brain damage .... In most such [ADHD] cases biochemical
disorder affecting the frontal lobe connections is present, but there is no
structural damage to the frontal lobes .... Damage to the frontal lobes produces
wide ripple effects through the whole brain.
At the same time, damage anywhere in the brain sets off ripple effects
interfering with frontal lobe function." (36)
Optimizing Brain Function To Enhance Concentration
is not an all-or-nothing state. There
are gradations in concentration, from none (in coma) to the extremely high level
of a chess grandmaster focusing on 20 moves ahead of his current move on the
chessboard. ADD represents a significant impairment of attention, but
even in ADD it's not all-or-nothing. Both
Amen and Goldberg note that attention deficit in ADD is often selective. (37,
Things that are novel, stimulating, interesting or frightening provide
enough stimulation (through adrenaline release) to help ADD people pay attention
in these contexts. It is the
routine, mundane, boring, trivial, rote activities that fail to stimulate ADD
brains to concentrate. Similarly,
attention is not at a fixed level in "normal" people, either.
The more healthy overall brain function is (especially frontal lobe
function), the more effective and effortless concentration becomes.
Thus, both ADD sufferers and "normal" people can improve their
concentration abilities through optimizing their brain function. Various nutritional strategies and nootropic drugs can
synergistically improve neural function, often dramatically.
is the principal brain fuel. Most other cells and organs of the body are able to
"burn" fat as well as glucose to produce ATP bioenergy, but brain
neurons can only burn glucose under normal, non-starvation conditions. (39) The
brain is only 2% of the body mass, yet typically consumes 15-20% of total body
ATP energy. (40)
The brain is dependent on a second-by-second delivery of glucose from the
bloodstream, as neurons can only store about a 2-minute supply of glucose (as
glycogen) at any given time.
brain must routinely have access to a large portion of the glucose flowing
through the bloodstream.
the modern high sugar, high refined carbohydrate lifestyle creates serious
potential problems for the brain. Unlike
most other body tissues, the brain does not require insulin to absorb glucose
from the blood. (39)
the optimal blood status for the brain to acquire its disproportionately large
share of blood sugar is a normal blood sugar level (70-100 mg %) combined with
low blood insulin. When insulin is low or absent in the bloodstream, the rest of
the body will ignore the blood sugar and burn fat or amino acids for their fuel.
chief stimulant for insulin release is carbohydrate. (41)
A surge in blood sugar (glucose) from rapidly absorbed dietary
sugar/refined starch may increase insulin levels 10-fold within minutes, and
keep on increasing insulin to even higher levels for 2-3 hours. (41)
This will cause a rapid glucose uptake by almost all body tissues,
leaving far less than optimal supplies for the brain.
modern Western diet typically contains 50% or more of its calories as
carbohydrates, mostly as simple sugars and refined (de-fibered) starches.
Many ADD sufferers (and "normal" people, as well) start their
day with a super-carbohydrate breakfast. Cereal
with sugar or fruit, toast or muffin and jam, waffles or pancakes with sugar
syrup, doughnuts, pastries, "pop-tarts," etc. are "normal"
breakfast foods in much of Europe and America.
Many people consume mid-morning snacks of doughnuts, pastries or
croissants with sugar-laced coffee. Many people routinely eat lunches rich in
bread, pasta, potatoes, rice, corn/potato chips, etc. topped with sugary
desserts. Dinners are also often
carbohydrate-rich: pizza. pasta, potatoes, bread, chips, sugary dessert, etc.
And these high-carbohydrate meals are often washed down with sugar-rich
soft drinks. The typical Western
diet is a virtual recipe to promote hyperinsulinism, with consequent reactive
hypoglycemia (low blood sugar following carbohydrate-rich meals).
Hypoglycemia & Attention
Among his hypoglycemia patients, 89% suffered from irritability, 67%
forgetfulness, 57% mental confusion, 50% indecisiveness, 43% in-coordination,
and 42% lack of concentration. (44)
These are all signs of hypoglycemia's negative effects on the brain. Goldberg
notes that indecisiveness is a classic indicator of poor frontal lobe function. (45)
Stephen Gyland was an American physician in the 1950s who studied 1307 cases of
hypoglycemia from his clinical practice.
Spring and colleagues reported an experiment that compared high protein and high
carbohydrate meals. They observed that among older (40 or above) subjects eating
a high carbohydrate lunch, attention was significantly impaired in performance
Gibson and Blass state that "... a high carbohydrate diet (78%) low in fat
(12%) and low in protein (10%) markedly decreases brain glucose utilization....
even marginal protein dietary deficiency when coupled with a carbohydrate-rich
diet suppresses cerebral glucose utilization to a degree often seen in metabolic
encephalopathies [brain diseases]."
reports that he has found a high simple carbohydrate diet makes concentration
problems worse for most people, especially those prone to ADD. He has found that
most ADD children and adults function better on a high protein, low simple
carbohydrate (sugar) diet. (48)
the simplest method of enhancing focus and attention is to adopt a high protein,
low simple carbohydrate diet. Reduce or eliminate sugar-and-flour-rich foods,
and derive carbohydrates mainly from nuts, seeds, beans, and peas (moderate
quantities) and low- carbohydrate vegetables, Avoid sugar-laden soft drinks and
noted earlier, the brain must use 15-20% of the body's total ATP energy supply.
Neurons cannot borrow this ATP from other cells - it must all be produced within
the brain from the metabolism of glucose. The conversion of glucose to ATP
energy occurs in 3 stages inside each neuron. The 3 interlocking phases of
glucose metabolism are glycolysis, the Kreb's or citric acid cycle, and the
electron transport chain. The Kreb's cycle and transport chain both occur inside
the mitochondria, the tiny "power plants" of the cell, and produce
most of the cell's ATP. Various enzymes gradually convert glucose to ATP. These
enzymes require an activating partner, a "coenzyme" to function
properly. The coenzymes are all active forms of various B vitamins. The vitamins
used in the 3 interlocking ATP cycles are vitamins B1 (thiamin), B2
(riboflavin), B3 (niacinamide), B5 (pantothenate), biotin, and the
B-vitamin-like substance alpha-lipoic acid, as well as coenzyme Q10. Other B
vitamins, such as B6 (pyridoxine), B12 (cobalamin) and folic acid are used to
transform various amino acids into forms that allow small quantities of them to
be "burned" in the Kreb's cycle. (49)
These vitamins must be converted to their active, or coenzyme, forms to become
functional. E.g., B1 becomes thiamin pyrophosphate, B3 becomes nictinamide
adenine dinucleotide, etc.
was Linus Pauling, in 1968, who first observed that dietary and blood levels of
various B vitamins that are adequate to feed all the other cells of the body,
may not be adequate to nourish the brain. This
is due to the blood-brain barrier. (50)
blood-brain barrier serves to protect the vulnerable brain from many toxins, but
it is primarily water-soluble substances that the blood-brain barrier excludes.
the B vitamins are water-soluble, and are only poorly transported across the
blood-brain barrier. Thus, Pauling
noted that many people (especially those with any form of brain malfunction),
may require much higher than RDA (recommended dietary allowance) levels of
vitamins to achieve high enough blood levels to "push" adequate
amounts of B vitamins through the blood-brain barrier. (50)
one clinical example of this phenomenon, Lonsdale and Shamberger reported in
1980 that 20 patients consuming a "junk food" diet showed biochemical
evidence of a serious thiamin deficiency, and presented with symptoms similar to
ADHD. When supplemented with
150-300 mg thiamin/day, their behavioral problems improved - yet the 1980 RDA
for thiamin was only 1.7mg. (51)
In his classic book Nutrition and Vitamin Therapy, psychiatrist M.
Lesser reported inability to concentrate, poor memory, apathy and slowing of
intellectual processes as consequences of deficiency in vitamins B1, B3, B6, B12
and folic acid. (52)
also routinely recommends B vitamin supplementation at higher-than-RDA levels
for optimal mental health and functioning. (52)
simple nutritional method to improve mental energy and concentration is the
routine supplementation of B vitamins, alpha-lipoic acid, and CoQ10 (or its
improved analogue, idebenone). Lipoic acid and idebenone also provide
important antioxidant benefits to the brain, as well. Lipoic acid, and its
inter-convertible reduced form, dihydrolipoic acid (DHLA), scavenge a broad
range of free radicals and oxidants, including hydroxyl/radicals, peroxynitrite,
hydrogen peroxide, singlet oxygen, superoxide radical, and peroxyl radical. (65)
also recycles the major cell antioxidants vitamin E, vitamin C, glutathione and
Idebenone reduces oxygen radical formation, and is a far more effective
antioxidant than CoQ10. (66,67)
These benefits are especially important to the brain, as it has
relatively poor antioxidant defenses, and increasing brain mitochondrial energy
production will also increase free radical formation. (65)
Magnesium: Mineral For The Mind
is the activator mineral for over 300 different enzymes - more than any other
Magnesium serves as the mineral activator for most of the enzymes of the
glycolytic and Krebs' cycles. (54)
ATP is produced, it is normally complexed with magnesium
stable storage. (55)
Magnesium activates sodium potassium ATPase, the membrane pump which
transfers sodium and potassium across neural membranes to allow repeated bursts
of electrical nerve activity (56),
and which consumes up to 40% of neural ATP. (10)
the activity of NMDA glutamate receptors, and thus glutamate nerve activity. (57)
Glutamate nerves are the chief excitatory nerves, and are the primary
neurons, along with the GABA nerves, in the brain areas connected with
attention: the frontal cortex, hippocampus, striatum, thalamus, hypothalamus,
and posterior cortex. (58)
roles in human physiology, it is perhaps not surprising that cellular magnesium
deficiency leads to
a wide variety of symptoms: anxiety, fear, restlessness, poor attention,
confusion, memory loss, mood changes including depression, lack of
co-ordination, appetite loss, weakness, insomnia, muscle tremors,
disorientation, learning disability, apathy, fatigue, heart disturbances,
problems in nerve conduction and muscle contraction, muscle cramps, and
predisposition to stress, to name just a few! (59-62)
Note that many of these symptoms are common to ADHD.
common enough to think that it might play a role in difficulties with attention,
memory, learning abilities, restlessness, etc.?
Actually, most people in the Western world are probably at least
Dietary surveys show women on typical Western diets to average 175-225mg
men 225-275mg magnesium /day.
A typical modern "junk food" diet, consisting primarily of soft
drinks, hot dogs, hamburgers, white bread, French fries, cheese, pastries,
candy, pizza, snack chips, etc. might fail to provide even 200mg Mg/day. The RDA
for magnesium has
been set at 300-400mg/day. Yet
Mildred Seelig, M.D., has done extensive research which indicates that 8mg/kg
bodyweight is probably a more optimal intake level. (63)
This would be a 560mg/day requirement for a 70kg (154 pound) person.
In addition, there are many factors
that impair intestinal absorption of magnesium.
High intake of phosphate (common in meat, soft drinks and baked goods)
calcium, fat, phytate (found in unleavened bread and wheat bran), lactose (milk
sugar), oxalate (found in spinach, rhubarb, chocolate), and alcohol, as well as
laxative abuse, all inhibit intestinal magnesium absorption. (53,
59, 60) Healthy kidneys may reabsorb up to 95% of magnesium before it
is lost in the urine, yet many factors promote magnesium urinary loss: the
stress hormones adrenaline and cortisol, diuretics (including caffeine), some
antibiotics, digoxin, alcohol, high sodium/calcium/sugar intake (i.e. the
typical western diet) and birth control pills, among others. (53, 59, 64)
Thus anyone who lives the typical modern high stress/ high fat and sugar/
high soft drink/ high coffee and alcohol lifestyle may be an appropriate
candidate for magnesium supplementation, with increased focus, attention, stress
resistance, memory and learning powers as possible benefits.
However, magnesium repletion at the cellular level is a slow process, and
may take weeks to months to achieve maximum benefit.
Most people can safely and beneficially take 100 - 200mg magnesium 2 - 3 times
daily (with some at bedtime for insomniacs).
If diarrhea develops, reduce dosage and /or frequency. Anyone with
serious kidney disease should check with a nutritionally knowledgeable physician
before adding magnesium. Best
supplement forms are magnesium malate, orotate, succinate, taurinate, glycinate,
aspartate, and chloride.
Nootropics For Alertness & Attention
drugs are one of the premier classes of proven anti-aging drugs. They are
especially effective at enhancing memory, alertness and attention. The concept
and definition of a nootropic drug was first proposed by Giurgea in 1973. The
characteristics of a nootropic drug include:
enhancement of learning and memory (and concentration is the gateway to learning
enhancing the resistance of learning and memory to conditions which tend to
disrupt them (e.g. electroconvulsive shock, poor brain blood flow);
3) protection of the brain against
various physical and chemical injuries (e.g. barbiturates, scopalamine);
lack of the usual pharmacology of other psychotropic drugs (e.g. sedation,
stimulation, restlessness, etc.) and possessing very few and only minimal side
effects and very low toxicity. (68)
that concentration is a whole-brain activity, that decreased brain blood flow
and energy metabolism (especially in the frontal lobes) is a key element in
decreased attention, and that "deficit of attention is among the most
common consequences of brain damage" (36)
the following nootropics are excellent aids to enhanced focus and
is a slightly altered form of vincamine, an alkaloid extracted from the
Periwinkle plant, vinca minor. In
use for almost 30 years, research has gradually shown vinpocetine to be the
superior vinca alkaloid, having few and minor if any side effects, with a
greater range of metabolic and clinical benefits than vincamine.
Vinpocetine has been shown to be a cerebral metabolic enhancer and a
selective cerebral vasodilator (i.e. one which increases blood flow only to
brain regions where it is compromised). (69,
has been shown to enhance oxygen and glucose uptake from blood by brain neurons,
and to increase neuronal ATP energy production, even under hypoxic (low oxygen)
Both animal and human research has shown vinpocetine to restore impaired
brain carbohydrate/energy metabolism. (69,
An important objective measurement of
impaired concentration and alertness is the EEG (electroencephalogram) record.
In 1991 J. Lubar published his results of 15 years of EEG research on ADD
subjects. Comparing ADD children to
normal controls, he discovered that ADD children "...produce excessive
theta activity in the 4-8 Hz [cycles/second] range and were particularly
deficient in beta [14 Hz and above] production .... Specifically, increased
theta activity was obtained in many [brain regions] particularly frontal and
centrally .... Decreased beta activity was found in many frontal and temporal
EEG is a measure of brain electrical activity.
Theta (slow wave activity) is typical of deeply sedated mental states,
while beta is associated with concentration and focused mental activity.
Saletu and Grunberger report that "Human brain function as measured
by ... [EEG] shows significant alterations in normal and pathological aging
characterized by an increase of [slow wave] delta and theta activity and a
decrease of alpha and … beta [fast wave] activity…. These changes are indicative of deficits in the vigilance
regulatory systems. By the term vigilance we [mean] the …dynamic state of
total neural activity [remember - concentration is a whole brain activity] ….
Elderly subjects with bad memory exhibit slower [EEG] activity and less … beta
activity than those with good memory …. nootropic drugs such as … vincamine
alkaloids [vinpocetine & vincamine] induce interestingly just oppositional changes [to the
age-related slowing of EEG waves] in human brain function, thereby improving
vigilance [and attention]." (75) Two things follow from this:
both the normal and pathological aging brain become more and more like an
ADD child's brain; and
Vinpocetine can reverse these ADD-like brain states to more normal alert and
attentive brain states!
has very few side effects and is extremely non-toxic (76), although some experts
caution against its use in pregnant women. (76) Gastric upset, increased heart
rate, and skin rash are the main (rarely occurring) reported side effects.
A dose of 2.5 - 5mg 2 to 3 times daily is generally safe and effective.
Taking vinpocetine right after a meal reduces chance of gastric upset.
is the original nootropic drug, for which the category was first defined. (68)
Piracetam is one of the least toxic drugs ever discovered: "Piracetam
is apparently virtually non-toxic …. Rats treated chronically with 100 to
1,000 mg/kg orally for 6 months and dogs treated with as much as 10 gm/kg orally
for one year did not show any toxic effect." (77)
For a human equivalent, 10 gm/kg would be 700 gm (11/2 pounds!) for a 70
kg (154 pound) person. Piracetam has been shown to improve memory, EEG, alertness
and mental performance in a wide variety of human clinical studies.
Piracetam restored normal EEG and state of consciousness in people
suffering acute and chronic cerebral ischemia (decreased brain blood flow).
Piracetam has improved alertness and IQ in elderly psychiatric patients
suffering from "mild diffuse cerebral impairment." (80)
Piracetam increased memory and verbal learning in dyslexic children, as
well as speed and accuracy of reading, writing and spelling. (81,82)
Piracetam has improved mental performance in "aging,
non-deteriorated individuals" suffering only from "middle-aged
Elderly outpatients suffering from "age-associated memory
impairment" given Piracetam showed significant improvement in memory
consolidation and recall (84),
and as Smith and Lowrey note in a study on concentration in elderly subjects,
"Concentration is intimately involved in the process of reception, storage,
and recall [of memories]." (85)
Like vinpocetine, Piracetam reversed typical EEG slowing (which mimics
the EEG of the ADD brain state) associated with normal and pathological human
aging, increasing beta (fast) EEG activity, while simultaneously increasing
vigilance, attention and memory. (86) In a 1987 study, Grau and co-workers fed
rats i.v. radioactive deoxyglucose to help measure brain metabolism.
Compared to saline controls, piracetam rats had a 22% increase in whole
brain glucose metabolism, while the increase in 12 specific brain regions ranged
from 16 to 28%. The increase in
brain energy metabolism occurred under normal oxygen conditions. (87)
And remember - decreased brain energy metabolism equals reduced focus and
attention, while increased brain energy metabolism equals enhanced focus and
piracetam dosages range from 800 - 1600 mg 2 to 4 times daily.
Piracetam may (very rarely) cause headache, insomnia, over-stimulation or
irritability. This is most likely to occur in heavy caffeine-users, or those
taking high doses of other nootropics. I
have personally used piracetam continually for 12 years and have never noticed
any side effects from it. Along
with Vinpocetine, it is one of my favorite concentration-enhancing drugs.
also called selegiline, is a popular anti-aging drug.
is a potent neuroprotector. (88) It
is also a selective MAO-B inhibitor. (88) MAO-B is the
neuro-enzyme that breaks
down the neurotransmitter dopamine and the neuromodulator phenylethylamine
(PEA). Deprenyl and its
"cousin" PEA are catecholamine activity enhancers (CAE). (88)
Catecholamines include dopamine, noradrenaline and adrenaline.
Dopamine and noradrenaline are the neurotransmitters for the key
activating brain circuits: the mesolimbic-cortical (MLC) circuit and the locus
coeruleus. The MLC and locus coeruleus both activate the frontal lobes, and are
critical for maintaining focus, alertness, concentration, and effortful
pioneering research of Dr. Joseph Knoll has shown Deprenyl and PEA serve to more
effectively couple the release of dopamine and noradrenaline to the electrical
impulse that triggers their release, thus enhancing the activity of the MLC and
locus coeruleus attention circuits. (88)
Deprenyl also increases brain levels of PEA dramatically. (88)
Baker and colleagues presented evidence in 1991 that a deficiency of
brain PEA may play a role in ADD, and that this may result in part from a
deficiency of the amino acid phenylalanine, the precursor of PEA. (90)
A 1984 study showed a unique synergy between deprenyl and phenylalanine
in treating anti-depressant drug-resistant depression patients.
a combination of 1.5 - 5mg deprenyl daily plus 250 mg phenylalanine may prove
helpful to those who suffer impaired concentration and attention connected with
a "spacey," "foggy," under-aroused state of consciousness.
Deprenyl has been shown to increase attention, alertness and memory in
various Alzheimer disease studies. (89,
In some cases, deprenyl, with or without phenylalanine, may lead to
over-stimulation, irritability, or insomnia. Reduce dosage or discontinue if
DMAE & Centrophenoxine
also known as Lucidril and meclofenoxate, is one of the oldest nootropic drugs -
it was developed in 1959. (
Zs-Nagy, M.D. the world's most prolific centrophenoxine researcher, has called
centrophenoxine a "brain metabolic stimulant" and a "neuroenergeticum" -
i.e. a neuroenergizer. (
"stimulates glucose uptake, oxygen consumption, and carbon dioxide
production in vivo [in the living organism] …." (94)
"…centrophenoxine can stimulate cerebral electrical activity in
the aging brain." (
brain metabolic and electrical activity are the basis for improved attention and
alertness. "Clinical studies
with [centrophenoxine] in geriatric patients with such symptoms as confusion …
and disturbances of memory and intellectual concentration revealed marked
improvement after several weeks of treatment …. Clinical studies in European literature have reported a
significant improvement of such symptoms as fatigue, irritability, confusional
states [the opposite of alert, focused attention] and improvement of memory in
the geriatric patients treated with centrophenoxine." (95)
is a combination of two other biochemicals - DMAE (dimethylaminoethanol) and
PCPA (paarachlorophenoxyacetic acid). DMAE
is a natural brain constituent, closely related to choline. (
Centrophenoxine is, in effect, a super-DMAE: "Pharmacokinetic
studies of centrophenoxine revealed that … much higher levels of DMAE were
found in the brain after centrophenoxine treatment, as compared to DMAE, alone,
since apparently the esterified form of DMAE with PCPA penetrates much easier
the blood-brain barrier." (94)
This is significant, because DMAE was used successfully to treat children
suffering form "minimal brain dysfunction" (the earlier name for ADHD)
during the 1958 - 75 period, with increased attention span as the result.
(96 - 98)
Thus centrophenoxine can be expected to provide even better results in
is considered an extremely non-toxic drug. (
Doses used in human clinical studies are typically 250 - 1,000 mg twice
daily (breakfast and lunch). (
For use in enhancing focus and attention span, where no major brain
pathology is present (that would increase dosage), 250 mg once or twice daily is
a generally safe and useful dose. Although
centrophenoxine is generally safe and non-toxic, there are a few precautions to
its use. Centrophenoxine is a
powerful enhancer of brain acetylcholine levels.
Excessive brain/peripheral nervous system levels of acetylcholine can
lead to headaches, neck/jaw/shoulder muscle tension, insomnia, irritability,
agitation and depression. This is NOT a toxicity reaction - it is simply too
much of a good thing, acetylcholine. If
any of these symptoms occur, simply discontinue centrophenoxine for several
days, then try a reduced dosage. Those
especially sensitive to centrophenoxine may need to take it only on alternate
days to avoid acetylcholine excess. Any
persons suffering from major depression, mania, seizure disorders or Parkinson's
disease should avoid centrophenoxine, as too much acetylcholine may worsen these
conditions. Also, pregnant women
should avoid centrophenoxine.
is a nootropic that had been in use over 40 years. Pyritinol is a compound of 2 pyridoxine molecules which are joined
together by 2 sulphur atoms. (
"[Pyritinol] has been shown to increase glucose uptake and
utilization, tending to normalize or increase transport across the blood-brain
barrier. Oxygen consumption … and
cortical acetylcholine release are … improved by the drug. Nerve cells may be
protected in cerebral deficiencies, with cell membrane structures and functions
undergoing improvement after damage, and regional blood flow increases [after
damage]. Pyritinol has also been
shown to produce a vigilance [alertness] response, both behaviourally and
electrophysiologically (EEG recordings) in animals and healthy human volunteers.
research has shown that pyritinol 600 - 800 mg per day is effective in improving
… activity, alertness, mental power, interest and emotional stability in
individuals suffering from mental insufficiency and clinical dementia. (
In a South African study on Pyritinol with hyperkinetic and
learning-disabled children, it was noticed during the placebo-controlled trial
that "… 8 children in one of the [test] groups were making great strides
in many ways: drive, alertness and concentration were improving …. These 8
pupils were all in the [Pyritinol} group." (100)
In a study of Pyritinol in senile dementia (Alzheimer and stroke
dementia), "… EEG mapping demonstrated significant differences between
placebo and pyritinol, with the latter decreasing slow [theta/delta] and
increasing fast alpha and beta activity, which reflects improvement of vigilance
Pyritinol is generally a very safe nootropic, with few and mild
side-effects. (101, 103)
However, in a study of those suffering severe rheumatoid arthritis
and taking high dose (600 mg/day) long term (1 year) Pyritinol, there was
a 2% incidence of serious side-effects. (102)
For those wishing to use Pyritinol to enhance general brain function and
improve concentration, 100 mg once or twice daily (breakfast and lunch) is a
reasonable dosage regimen.
this article has indicated, concentration is a function of whole-brain activity
and health, and impaired attention is a natural consequence of any brain damage
- structural or functional. For
most people not suffering any major brain damage or pathology, simply adopting a
high protein/ low sugar and refined carbohydrate diet, combined with a good B
complex vitamin, Magnesium, CoQ10 or idebenone, and lipoic acid, will promote
improved focus, alertness and attention span.
those wishing to "go the extra mile," adding one or more of the
nootropics discussed above will usually provide even further benefit. I have
personally interviewed many (more or less) healthy people who use one or more of
these nootropics in their health regimens, who have found noticeably enhanced
alertness, concentration and memory.
have used nootropics for many years to aid in the intense concentration and
focus I need to get through the dense, technical, tedious and often boring books
and papers I have to read to write my many anti-aging/ nootropic / nutritional
articles. They do work!
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