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The aim of this lecture is to give you an overview about some of the most popular and in-demand Nootropics.

As the title suggests, the discussion is the role of Nootropic drugs and nutrients in the ageing individual, or in other words the healthy or normal individual - this is of course a category that no countrys approval body has accepted to date. As such, we will be viewing this information on the basis of international research and experience. The interest around Nootropics is indicative of the nature of all real anti-aging medicine - to spot the very earliest signs of change and to take measures to slow, avert or even reverse the path of deterioration before it becomes a disease.1

Nootropics are the so-called smart-drugs and were first highlighted in the popular books written by Ward Dean, John Morgenthaler and Steven Fowkes- who later founded the: Cognitive Enhancement Research Institute in California both are an excellent source of information on this subject.

Mental deterioration is a common problem, often the butt of jokes and an almost accepted- dare I say; natural effect associated with aging. Some neurologists have even stated, that; If we all lived long enough, we would all become senile!

The problems normally begin with occasional forgetfulness - of relatively unimportant information, slowness of thought, lack of concentration and shortness of attention span.

But clearly, these are all indicators that our mental facilities are not operating at an optimal level. The goal is to spot the signs - often incidental and perhaps even immaterial at first, that may be associated with mental degeneration. 2

The science of Nootropics blossomed in 1972, after the demonstration of the pharmacological uniqueness of Piracetam. It led Dr. Giurgea to formulate an entirely new category of drugs which he named: Nootropics, which is Greek meaning; towards the mind. He defined Nootropics as follows:

They should enhance learning and memory.They should enhance resistance of learned behaviors/ memories, to conditions which tend to disrupt them.They should protect the brain against various physical or chemical injuries.They should increase the efficacy of the cortical/ subcortical control mechanisms and finallyThey should lack the usual pharmacology of other psychotropic drugs and possess very few side effects, and have extremely low toxicity.

It is probably true to say that today the classification is used in a wider sense, but that was the original definition developed by the founding scientist.3

So let us consider the primary areas of action that any Nootropic can enhance.

To ultimately influence the level of a neurotransmitter. Here there are various possibilities, including inhibition - for example reuptake inhibitors. There are also the inhibition of enzymes that would otherwise breakdown neurotransmitters, for example monoamine oxidase. Although extremely rare, there are now even accelerators - actually increasing neurotransmitter uptake - and although not understood yet, this has also been shown to enhance function! Agonists stimulate the production of a given neurotransmitter, and under this heading I also include the precursors - chemicals that pass through the blood brain barrier and simulate the actions of specific neurotransmitters. Plus Methylation, the conversion of one chemical to another, often utilizing key nutrients such as the B-vitamins and their cofactors.

A number of substances have been shown to improve the electrical activity of the brain.

Vasodilation is the improvement of blood circulation. Essential, given that in the case of the brain, the blood has to travel through some of the smallest arteries in the body to supply nutrients for energy.Although closely associated with blood circulation, there are additional energy factors that can come into force, for example- increasing the uptake of glucose.

Receptor sensitivity falls upon another novel category, whereby particular substances can upgrade receptors to react more aggressively to the given stimulus, without actually increasing chemical levels. A good example of this would be the new drug, Modafinil.

Finally, the category of membrane where we will see that good membrane health is also a function in cerebral fitness.

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Just before we look closely at some of the leading Nootropics, let us consider some facts and figures about the brain. Typically, the human brain weighs about 3 pounds, representing 2 to 3% of total body weight. It is estimated to contain 10 to 100 billion neurons and approximately 10 times more glial cells, the structural and nutritional support cells surrounding neurons.

But whilst the brain weighs 3% of bodyweight, it normally receives about 15% of the body's total blood supply and 15% of the body's total inhaled oxygen.The brain must use this oxygen, along with its chief fuel- glucose- to produce and burn approximately 20% of the body's total Adenosine Triphosphate/ ATP.

Unlike most other cells, which can burn either fat or glucose for their energy production needs, neurons can only burn glucose under normal, non-starvation conditions, and they can consume 50% of the total blood sugar.

Unlike liver and muscle cells, which can store large amounts of sugar as glycogen, neurons can only store at most a minute or two's worth of glucose. Thus, they are extremely dependant upon a continuous and uninterrupted blood supply to maintain normal energy metabolism and avoid injury or death.

Most other cells, reproduce continually throughout a lifetime- yet after the brain reaches a full complement of neurons- at about 2 years of age, neurons never reproduce, so they are an irreplaceable essential of life.Under normal conditions of adequate oxygen supply, neurons convert glucose into energy- as ATP, through a 3-phase process.

The first phase occurs in the cytoplasm of the cell, and is called "aerobic (oxygen using) glycolysis." Glucose is metabolized into ATP and in addition pyruvic acid is produced. This is then metabolized through the Kreb's cycle- inside the mitochondria, to generate more ATP.

An additional energy-rich substance- NADH- is also produced. NADH is the coenzyme of vitamin B3. It is also transported to the mitochondria, where it serves as a fuel in the 3rd phase of energy metabolism- the electron transport side chain to produce more ATP.

So ultimately, through the successful interaction of aerobic glycolysis, the Kreb's cycle, and the electron transport chain, a single molecule of glucose can yield a maximum of 38 molecules of ATP bio-energy. This is assuming there is adequate oxygen for both the glycolysis and mitochondrial "respiratory" metabolism.

However, when neurons are under-supplied with oxygen, a different form of sugar burning occurs- called anaerobic (without oxygen) glycolysis. Here, for each molecule of glucose burned only 2 molecules of ATP are produced. Also, instead of producing the valuable Kreb's cycle fuel- pyruvic acid, anaerobic glycolysis produces the somewhat toxic waste product - lactic acid.

To summarize, when glucose brain fuel is burned without adequate oxygen, it produces only 5% as much ATP energy as when glucose is burned with adequate oxygen!

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Essentially there are 3 main uses for ATP inside neurons - thats maintenance, electrical and neurotransmitter functions. Since neurons don't reproduce and must last a lifetime, they are continually expending energy to repair or replace various cell components.

Neurons also use ATP to produce, transport, package, secrete and reuptake neurotransmitters, which provide cell to cell communication. Massive amounts of ATP are necessary to facilitate the frequent discharges of electrical energy from the receiving end of the neuron (the dendrites) through the cell body, where signal processing occurs and down to the transmitting end (the axon). For this electrical process to occur there must be a rapid and continuous exchange of sodium and potassium ions, back and forth across the neuronal membranes.This exchange process depends on the sodium-potassium pumps, powered by sodium-potassium ATPase enzyme systems. It has been estimated that as much as 45% of a neuron's ATP may be used to power these pumps.

So it should be evident why unconsciousness rapidly occurs if breathing stops, or if brain blood flow is interrupted, even briefly. As the delivery of oxygen to the brain halts, neurons rapidly shift from aerobic to anaerobic energy metabolism with a consequent drop in energy production of 95%!

There will simply not be enough ATP energy to make neuronal electrical activity and neurotransmitter discharge possible - the electrochemical basis for consciousness. Plus if aerobic metabolism ceases for too long, eventually either irreparable damage or even cell death may occur, as even the maintenance neuronal activities fall behind due to the energy shortage.

Now of course for most of us, falling unconscious or suffering brain death due to cessation of breathing or brain blood flow is not a regular problem to contend with! But, a more subtle, insidious, slow-developing form of brain energy crisis can and does occur - to some degree over a lifetime, in the form of cerebral arteriosclerosis, mini-strokes, or transient ischemic attacks, in other words- brief interruptions of brain blood supply often due to blood vessel spasm.

In its early stages, this brain energy crisis may lead to only the slightest of symptoms- subtle memory impairment, occasional confusion, or lapses in concentration, more difficulty in learning etc. But at a more advanced stage the brain energy crisis may manifest itself as senility and eventually may terminate in coma or death.

Dr. Branconnier noted; quote: "...The severity of the dementia is directly correlated to the loss of functional brain tissue, independent of the primary neuropathology. This view is consistent with evidence from studies of cerebral blood flow, oxygen uptake, and glucose utilization that have shown that brain carbohydrate metabolism is impaired in a variety of dementias and that the degree of reduction in brain carbohydrate metabolism is correlated with the severity of the dementia...

Orthomolecular pioneer Abram Hoffer has suggested that when the brain oxygenation becomes deficient, neurons switch to anaerobic glycolysis as their main energy source. This may provide enough energy for the neurons to survive, but it will not provide enough energy to power their functional roles as electrochemical signal processors and transmitters. Then the affected neurons will be "off-line," in an electrically "idling" state.But if normal aerobic metabolism is restored before irreparable cell damage or death occurs, then the neurons and their functions can be restored.

What we have attempted to indicate here is the massive and constant energy demands of the brain, and the critical consequences if energy production is interrupted for even a brief period. During the course of aging there is a gradual decline in blood flow, reducing energy production capability and altering neuronal and mitochondrial structure etc., which will be discussed later. Plus we strongly believe that the accumulation of toxins, particularly heavy metals - such as mercury, can rapidly speed up this process.

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Lets look at the Nootropics, starting with the original Racetams. The first one was Piracetam - developed from GABA, it was first synthesized by UCB Laboratories in Belgium in the 1960s. Its original use was to treat motion and altitude sickness, but the published references inform us that it can aid learning, protect against various neurotoxins, treat amnesia induced by hypoxia and electro-shock and even accelerate EEG return to normal in hypoxic conditions.

Interestingly, Piracetam has an LD50 better than salt. The LD50 is literally the lethal dose at which 50% of animals die. The fact that piracetam has to actually be dosed at more than salt to reach its LD50, makes it one of the safest pharmacological developments ever produced.

The 2 most consistently available Racetams are Piracetam and Aniracetam, with occasional sightings of Pramiracetam and Oxiracetam. All the analogues have been shown to be more potent than Piracetam when comparing dosage to bodyweight, with usually to of the equivalent Piracetam dosage required. One clinical trial suggested that the optimal dose of Piracetam was 100 mg. per Kg. bodyweight, but that Pramiracetams optimal dose was 15 mg. per Kg. bodyweight, effectively making it 7 times more potent. However, I can tell you that the majority of the analogues cost 2 to 4 times more gram to gram than Piracetam, so that may influence your decision!

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Piracetam has a number of methods of action to improve learning and memory. It protects brain membranes under low oxygen conditions and also has an action on receptors to enhance acetylcholine. But perhaps the most interesting action of Piracetam is its ability to help information pass across the brains corpus callosum. This is the bundle of nerves that connect the two hemispheres. As we know, the right side of the brain controls the left side of the body and vice-versa. The left side of the brain is considered to be language centre as well as the dominant hemisphere. It tends to be logical, analytical and sequential. The right side of the brain tends to be intuitive, holistic and picture orientated. Research shows that people favor one hemisphere over the other, with the dominant cortex being more electrically active.

Piracetam improves this intra-hemisphere communication and enhances electrical activity. As a result, studies indicate that there are improvements to short term memory, enhanced vigilance, attention and most interestingly - the ability to have ideas and turn them into reality.

One way to determine communication over the corpus callosum is a hearing test called Dichotic listening. The speech centers of the brain are located in the left hemisphere, because the nerves from the ears cross over to the opposite side of the brain, most people will recall more words presented to the right ear than the left ear. Words received by the right ear directly reach the left cortex speech centre, while words presented to the left ear have to reach the left cortex speech centre by crossing the corpus callosum. Dimonds experiments with young healthy volunteers show that Piracetam significantly improves left ear word recall.Dimonds conclusion was The fact is, that Piracetam improves verbal learning and in this it would appear to be a substance which is capable of extending the intellectual functions of man. Our subjects were not senile, suffering from generalized brain disorders, confusional states or any other pathology of the brain. It is therefore possible to extend the power which, individuals already gifted with high intelligence and good memory, to still higher levels, despite the fact that the range of their achievement is already high.

Healthy aging individuals note that Piracetam makes them more creative and improves clarity. Piracetam is also noted as being synergistic with other substances, including caffeine and particularly with those of a choline base, such as DMAE or Centrophenoxine. At normal dosages there are virtually no noted side effects, and no known contraindications with the product except for rare cases of hypersensitivity. Piracetam is used in anti-aging medicine at doses of 800 mg. to 2400 mg. two to four times daily and is perhaps the most widely used and best selling memory agent in preventative medicine today.

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Another of the most popular Nootropics is Deprenyl, otherwise known as Selegiline. Its primary medical use is to treat the symptoms of Parkinsons disease, because Deprenyl helps to improve brain levels of Dopamine, the neurotransmitter that is most affected by that disease.

Deprenyl inhibits Monoamine Oxidase type-B, an enzyme that breaks down Dopamine and PEA (phenylethylamine). However, those of you who read the Aging Matters Magazine, antiaging-systems.com or know of Professor Joseph Knolls research, will also be aware that Dr. Knoll now believes that Deprenyls primary mode of action is to resensitize Dopamine and PEA receptors.

Whilst dosages in the treatment of Parkinsons disease can often be 20 mg. a day or higher, those utilizing deprenyl for an anti-aging program are more likely to use just a few milligrams daily. So why use deprenyl?

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This graph illustrates the point. The vertical axis represents the amount of Dopamine in the brain as a percentage, the horizontal axis represents chronological age. You can see when the levels of Dopamine have declined by 70-80% of optimal that Parkinsons disease is diagnosed. This is a fundamental issue for anti-aging physicians, because they want to concern themselves with recognizing the much early stages of disease. Perhaps in this case, when only 20% of dopamine levels have fallen - so that a course of treatment can begin much sooner, to help delay and prevent the occurrence of a dementia.

We all know the story, you tell a GP that your memory isnt what it was. You cant remember your neighbors name, you seem to forget your appointments and are always searching for the keys, and they tell you that you have to get used to it, youre just getting older! But an anti-aging physician has to consider such items to be an early sign of age-related memory decline, and to then recommend pro-active options. Lets look again at the graph, heres a typical dopamine decline line for someone with rapid Parkinsons disease. You can see that in their 50s they are diagnosed with Parkinsons and that, as death ensues with dopamine levels of 10%, their expiry age is in their 60s.

This line represents the dopamine decline of the average Parkinsons patient, they reach the senile dementia in their 60s and may live onto into their 70s.Now this line represents what an average healthy person may achieve who wont be diagnosed with Parkinsons, not at least if something else doesnt kill them beforehand. They could see an age of 100 before the development of the disease.

Now heres what we may expect with an individual adopting a life extension program, utilizing something like Deprenyl, to help maintain Dopamine and brain function. You can see that the curve is much improved and that function and death is delayed much longer into the future.

Clearly the protection of brain function is a fundamental part of a preventative program. Deprenyl doses for anti-aging purposes are usually utilized at 1 mg. or 2 mg. daily. As these dosages are so small, the preference tends to be for a liquid deprenyl, because dosages can be titrated at 1 drop 1 mg. Although some people prefer to take the 5 mg. tablets 1, 2 or 3 times a week. The positive effects of a Deprenyl supplement program include greater well being, libido stimulation, improved short term memory and enhanced alertness. These affects are sometimes noted within hours of taking the product.

At these lower dosages many of the side effects and issues that are associated with high dose Deprenyl in Parkinsons patients are not prevalent. However, some contraindications may occur when combining with other potent MAO inhibitors. For whilst Deprenyl strictly only acts upon MAO-B, it is known to also interfere with MAO-A at dosages over 10 mg. So is there any evidence that Deprenyl can extend life span?

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A clue may come from Dr. Knolls experiments with rats. The vertical axis indicates the percentage of the animals alive - as a group, and the horizontal axis indicates their age in weeks.This line shows the control animals, i.e., those who did not receive Deprenyl. The first one dying at 148 weeks and the last one dying at 163 weeks.Now heres the line showing the Deprenyl treated animals, the first one dying at 176 weeks and the last one dying at 224 weeks.

As you can see, even the oldest of the rats who were not given deprenyl all died, before the youngest of the rats who were given deprenyl - did. In fact, Dr. Knolls experiments increased the average lifespan of these animals by 30%.

Whats also important to know is that Dr. Knoll noted that the Deprenyl treated rats displayed much more activity, social and sexual behavior - even into old age. This indicates that their optimal health span, as well as their life span was being improved.

Two further researchers, Milgram and Kitani replicated this experiment, and although there were some differences, including the ages and types of rats used, they achieved 16% and 34% models of life extension respectively.

Having proved it is possible to increase the lifespan and activity of rats, what are the implications for humans?

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Dr. Knoll has repeatedly emphasized that the substantia nigra, the tiny Dopamine producing nerve cluster located in the Basal Ganglia, (or so-called old brain), typically dies off at the rate of 13% per decade starting in our 40s. This would literally set the human technical lifespan to approximately 120 years. Is it a coincidence that the maximum verifiable life-span to date was Jeanne Calment, who died in 1997 at 122?Dr. Knoll has suggested that if Deprenyl was used from the age of 40 something onward, and even if it only modestly lowered the nigro-striatal neuron death rate from 13% to 10% per decade, then the average human lifespan might increase 15 years, and the human technical lifespan could increase to about 145.

Dr. Knolls 50 years of research has convinced him that It is the role of the catecholaminergic neurons to keep the higher brain centres in a continually active state, and that this activity reaches a maximum at sexual maturity and then after begins a gradual downhill slide.

The catecholamines refer to the inter-related neurotransmitters of Dopamine, Noradrenaline and Adrenaline. Dr. Knoll has concluded that The regulation of lifespan must be located in the brain. Certainly Dr. Knolls animal research has shown catecholaminergic activity, learning ability, sexual activity and longevity to be inextricably linked.

But fascinatingly, Dr. Knolls key conclusion is that the catecholaminergic system can be improved at any time during life. So it is feasible to transform a lower performing, potentially shorter living individual- to a better performing, longer living one.

Naturally, it is still too early to tell if taking Deprenyl will increase the lifespan of human beings. But as Dr. Knoll himself helped to developed Deprenyl, and has been taking it regularly since the 1970s, he may be the oldest example we currently have and at the age of 80, he is an active University Professor still involved in the pharmacological development of new drugs.

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Lets look at a Nootropic primarily involved in vasodilatation.

The brain and the eyes are where the smallest, so-called micro-capillaries are located.

Arteriosclerosis is associated with aging and whilst everyone is familiar with its cardiovascular issues, the brain is often not thought about in the same way. Yet platelet aggregation in the brain can quickly prevent or inhibit blood flow to the neurons, with a consequent lack of energy. A key chemical that has proven itself to be beneficial for brain blood flow is Vinpocetine.

Vinpocetine is produced by slightly altering the vincamine molecule, extracted from the Vinca-minor plant, otherwise known as the Periwinkle. Vinpocetine has been shown to be a cerebral metabolic enhancer and a selective cerebral vasodilator, enhancing oxygen and glucose uptake from blood by brain neurons, and thereby increasing neuronal ATP bio-energy production, even under hypoxic conditions.

Both Vincamine and Vinpocetine have been widely researched and used clinically for over 30 years, in disorders ranging from cerebral arteriosclerosis to Mnire's disease, senile dementias, diabetic retinopathy and tinnitus. However, research has gradually shown Vinpocetine to be the superior Vinca alkaloid because it has few if any side effects and all are minor, Plus it has a greater range of clinical and metabolic benefits than Vincamine.

Vinpocetine has been shown to reduce the cell death that normally occurs when a brain region is temporarily, but severely deprived of blood flow. It is proven to be unique, in that it is a selective cerebral vasodilator, with a non-steal effect. In other words, it appears to only improve blood flow where it is necessary.

Solti and co-workers reported their results using Vinpocetine on 10 men, having an average age of 49, all suffering from minor cerebrovascular disorders. They concluded that Vinpocetine belongs to a rare class of drugs which exert a potent, yet favorable effect on the cerebral circulation. In particular, they stated that Vinpocetine:

Strongly reduced cerebral vascular resistance, which is typically seen in cerebral vascular disease and aging.Had no marked effect on systemic circulation. For whilst blood pressure and total vascular resistance is decreased very slightly under high doses of Vinpocetine, far from increasing - it actually REDUCES the effort of the heart. Thus, its effects may be assumed to be favorable in cerebral alterations associated with heart disease and hypertension.

Another study with 100 patients suffering from poor blood circulation to the eye, Kahan and Olah noted Vinpocetines inhibition of platelet aggregation. Some of the micro-vessels that feed neurons in the brain and retina are smaller in diameter than a single red blood cell- so they can be easily "clogged up" by clumps of platelets, impairing local micro-circulation.

So Vinpocetine can inhibit unnecessary platelet aggregation, which may be triggered by a high fat diet, magnesium deficiency and stress hormones - among other factors.

Dosages are typically 5 mg. to 10 mg. 2 or 3 times a day.

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Hydergine has been available since the 1970s, it is an ergoloid mesylate - an extract of a fungi grown on rye.

There are a number of actions of Hydergine, which is officially listed as stimulating dopaminergic and serotoninergic receptors and blocking alpha-adrenoreceptors. But one of its most interesting actions is its ability to stabilize oxygen and improve energy availability, so much so that it is used in electro-shock and drowning emergencies.

However it is its impact on Mitochondria that we will focus on today.

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The mitochondria are the intracellular powerhouses where the universal energy molecule ATP is generated.

It is known that Mitochondria are to be found at their highest numbers in rats of 12 -months of age - equivalent to a 25-year old human, and thereafter they progressively decline. There are literally thousands of them in every cell and where high energy environments exist, up to 40% of the cytoplasmic space is occupied by Mitochondria. (i.e. Heart and liver cells are 20-25%).

With aging, the numbers of Mitochondria decline, but the size of the remaining Mitochondria increase. It would appear that their maximum efficiency is achieved by a large number of small, highly efficient units, which is the young model, unlike the old model, which is fewer, larger inefficient units.

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Whats significant about Hydergine is that it has been shown to change the total volume of old rats Mitochondria, to those of young rats. Furthermore, Mitochondrial size and efficiency is also altered in a youthful direction, as seen in these charts.

Mitochondria are vital cells, however in the process of creating ATP they expose themselves to free radical damage. As each Mitochondria provides energy for the cell it occupies and cannot borrow energy from other sources, their condition is a critical factor.

The conclusion of Bertoni and Freddaris test - shown here, is that Hydergine can significantly restore youthful morphological characteristics to Mitochondria, which for our purposes is highly significant as they assist in the production of brain energy.

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The last item about Hydergine to focus on is its ability to stimulate the growth of dendrite nerve fibers. Dendrites can normally be expected to decline with aging, and some scientists have associated the number and density of Dendrites with intelligence.

Hydergine is therefore used to improve cognitive function, clarity and mood, at dosages of approximately 1.5 mg. to 5 mg. daily.

Controlled clinical tests have revealed that Hydergine improves symptoms of mental deterioration related to aging, such as instability, dizziness, concentration, disorientation, memory loss, lack of initiative, depression, lack of sociability and difficulties in carrying out everyday activities.

On an anecdotal level many report that Hydergine reduces brain fog or situation where physically you are awake, but mentally you want to switch off. Plus Hydergine seems to expand the periods at which high level mental workload can be undertaken, so it can be very useful when you need to get things done.

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Now we turn to Vasopressin, this pituitary hormone is best known for controlling water balance in the body. Its common name is anti-diuretic hormone. This is because of its property of conserving water and inhibiting urine production. Because of this, many parents of children with bed-wetting problems find it useful, as do men with prostate conditions. Vasopressin doesn't affect the prostate, but it does reduce urine production resulting in fewer sleep interruptions.

Our interest lies in the fact that Vasopressin acts as a neuropeptide in the hypothalamus, imprinting new information into our memories. Vasopressin levels decline with age, consequently, it has been used to treat memory deficits due to aging, senile dementia, Alzheimer's disease, Korsakoff's Syndrome and amnesia.

Vasopressin improves attention, retention and recall, (both short-term and long-term) and it is noted to enhance short-term memory in normal adults as well as in those with age-associated memory impairment. In addition, it has been shown to improve both mood and memory in the elderly, including those with Alzheimer's disease.

Vasopressin can be very useful when learning large amounts of new information, because it can improve the ability to memorize and recall later - known as imprinting. It can be particularly helpful when cramming for exams, trying to memorize a speech or when listening to lectures.

A fairly recent study by Perras demonstrated an additional benefit of Vasopressin. Subjects used a dose of 40 IU/ day, administered as a nasal spray at bedtime, 40 IU is 2 sprays. Over a period of 3 months, the researchers found the time spent in slow wave sleep more than doubled. Slow wave sleep is the most restful kind of sleep - it is during this period that growth hormone is released. Perras and colleagues hypothesized that in addition to its direct effects as a neuropeptide, Vasopressin could have other mechanisms including acting as a corticosteroid receptor agonist.

Drs. Sydney and Constance Friedman at the University of British Columbia studied the effects of Vasopressin on the life spans of already old rats. They administered posterior pituitary powder, (a source of Vasopressin) to 2 year-old rats. The study was terminated at 180 days. Only 44% of the controls were still alive, in contrast, 62% of the treated rats survived. The authors also reported better fur condition, increased muscular tone, absence of age-related pituitary and adrenal enlargement and fewer skin lesions in the treated animals.

So here we have yet another brain chemical that is influencing not only brain function, but perhaps also longevity.

If you wish to find a source of Vasopressin you have to ask for Desmopressin nasal spray, this is its synthetic name.

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There is also a relevant hypothesis of aging, one that is not often discussed, and it regards the condition of membranes. With aging there is a loss of water within the cell and its membranes with a consequent decline in the performance of cell to cell communication resulting in a cascade of events.

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One of the most popular supplements to assist in the; Rejuvenation of the cellular machinery is Centrophenoxine. The beneficial effects of Centrophenoxine have been observed in various human disorders, including cerebral atrophy, brain injury, post-stroke status, chronic alcoholism and barbiturate intoxication.

Clinical trials with Centrophenoxine in geriatric patients with such symptoms as confusion, extreme weakness and disturbances of memory and intellectual concentration- reveal marked improvement after several weeks of treatment.

Clinical studies have also reported a significant improvement of such symptoms as fatigue, irritability, confusional states and loss of memory in patients treated with Centrophenoxine.

We find that the most common report with Centrophenoxine use is that it, speeds up the memory recall process. In other words, you can remember things faster and with greater clarity.

One of the most interesting actions of Centrophenoxine is its ability to remove Lipofuscin.

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Lipofuscin is a garbage residue, a conglomerate of membrane fragments- damaged proteins and fatty acids that accumulate over time in cells. They are particularly prevalent in the brains of Alzheimers victims. Sometimes referred to as age pigment and occasionally as liver spots, Lipofuscin is known to accumulate in the brain, heart, lungs and skin. The fact that Centrophenoxine is an effective remover of Lipofuscin deposits is a clue to its effectiveness as a Nootropic agent.

Dosages of Centrophenoxine are usually 250 mg. to 500 mg. once or twice daily. Although Centrophenoxine is generally safe and non-toxic, it can sometimes cause problems because it is also an effective cholinergic enhancer. Excessive brain/peripheral nervous system levels of acetylcholine can lead to headaches, neck/shoulder muscle tension, insomnia and agitation. If any of these symptoms occur, simply discontinue the dose for several days and then resume at a reduced dosage. Those especially sensitive to Centrophenoxine may only need to use it on alternate days to avoid cholinergic excess.

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Briefly here are some other substances that are also clinically proven and worthy of mention, they include:

Phosphatidylserine: Effectively a biological detergent for membranes.

Acetyl-L-Carnitine: An amino acid that improves acetylcholine levels and one which was found to be synergistic with the antioxidant Lipoic acid.

Gingko Biloba: Perhaps one of the most popular herbs from the health food shop - it improves brain blood flow.

Galantamine: An extract from the snow-drop plant family. This chemical has been cited to act as an acetylcholinesterase inhibitor and also stimulate nicotinic receptors.

Modafinil and its younger sister Adrafinil. These unique drugs form a class known as Eugeroics, another Greek term meaning good arousal. They stimulate alpha-1 receptor sites to noradrenaline and in so doing create alertness and wakefulness and have revolutionised the treatments of cataplexy and narcolepsy.

SAMe: Involved in methyl-donor conversion, SAMe has diverse uses, as it is widely used in varied chemical processes throughout the body. Therefore has a major role in the production of ATP.

NADH: The co-enzyme of vitamin B3 with vital roles in the production of ATP, plus the published work of Dr. Birkmayer has shown to be useful in the treatment of Parkinsons disease.

Pyritinol: A vitamin B6 analogue that enhances brain energy/glucose levels.

And finally, Pregnenolone, the so-called grandmother sterone because it is the first step from cholesterol. To date Pregnenolone has shown itself to be the most important hormone for neuronal health, being up-to 100 times more effective than DHEA.

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In conclusion.

Dont overlook the potential of Nootropics.

Many of them represent true anti-aging medicine, as they offer both brain protection and enhancement. Furthermore by acting upon the aging control centres in the brain - their benefits could equate beyond mere mental performance.

Protecting and enhancing brain function is a long term benefit most people want to enjoy. To remain lucid and agile in older life is fundamental, for we are nothing without our minds and our ability to communicate clearly and effectively with those around us. But like nearly all senesce, if one recognises it early and treats it early, the outcomes can always be improved.

Waiting for disease is not the answer, and in this case waiting to hear the prognoses of a senile dementia is bad news indeed. For at present, there are no tools on the immediate horizon that can effectively reverse them. This therefore makes measures that slow and arrest mental deterioration of paramount importance.

It is also worth noting that the positive effects of many Nootropics are often felt by the patient within days and sometimes even within hours. This offers effective measurable benefits. This is not often the case with anti-aging medicine, because when dealing with healthy individuals, changes are small and therefore the prescription is often undertaken on faith.

Nootropic products achieve the ultimate goal of any true preventative or anti aging medicine, they extend the healthspan of the individual. We believe this can have a positive effect on the lives of millions and society as a whole.

Thank you very much for your attention. 23