Opinions - Best nootropics to combat benzo memory loss?

[lulz]

My crazy uncle Joe has recently started taking benzos on a regular basis, not to get high, but to treat a long-term case of anxiety.

He takes his benzos responsibly, and researches everything he puts into his body, but his only concern about benzos is the issue of memory-loss/retrograde amnesia.

He ran out of his supply of nootropics before he started taking benzos, but the new college year is starting fairly soon, and he is concerned about how memory loss will affect his academic performance.

Currently he is awaiting delivery of an order containing piracetam and vinpocetine. He also plans to supplement the piracetam with DMAE and choline, which are readily available in health food stores.

The question here is two part:

a) How effective can nootropics be at combatting memory problems?

b) Which are the most effective nootropics to combat memory problems?

Any input would be greatly appreciated. Joe will report back as soon as his nootropics order arrives, and share his findings in relation to this issue.

[eltimmy]

Beta-carbolines are antagonists at benzodiazepine receptors and these are found in one of my favorite things I consider a nootropic, coffee. I bet there's some use in reducing cognitive impairment (but also to some extent anxiolytic effect) in it.

edit: Well, I also recommend meditation to reduce/replace the use of benzodiazepines, but that's neither here nor there.

[lulz]

Originally Posted by eltimmy

coffee

Unfortunately that's not an option for me. I've had to cut coffee completely out of my diet. It's a long story, but I suspect I may be allergic to caffeine, either naturally or as a result of drinking about a half dozen espressos per day for years.

Since cutting coffee out of my diet I've felt better than I have in years. I tried to quit drinking it a number of times, but I had undiagnosed ADD for most of my life til recently, and caffeine was necessary for me to function. After being diagnosed with ADD I was prescribed Ritalin, which worked better than coffee, but I also experience anxiety issues, which the Ritalin made much worse. I'm now on Straterra, which is probably why I have been able to avoid coffee for the last few months.

Anyway, caffeine allergy seems to be a pathological in certain individuals:

CAFFEINE ALLERGY: Past Disorder or Present Epidemic?
by Ruth Whalen, Medical Laboratory Technician
Cape Cod, MA USA.
Tenpaisleypark@hotmail.com

With the upswing of "chemical imbalance" disorders that surfaced in the latter twentieth century, many researchers frantically attempt to unravel the brain's intricate clockworks. In turn, as the number of persons suffering with mental issues mount, it seems that doctors, pressed for time, are quick to refer patients to psychiatrists. Failing to request a medical physical, many psychiatrists hand out medications, often masking the underlying physical problem.

People have overlooked two simple but deleterious factors: 1,3,7 trimethylxanthine and allergy. Simply put: caffeine allergy. It is medical knowledge that the longer a person is exposed to a drug, the higher the chances are for developing a tolerance, and an allergy to the substance. Once this happens, caffeine allergic persons can't properly metabolize caffeine, which is rapidly absorbed by all organs, and distributed into intracellular compartments, and extracellular water.

Mentioned in a 1936 article by Drs. McManamy and Schube, a young woman, allergic to caffeine, presented with alternating states of delirium and mania, resembling schizophrenia (1). After the recorded case, allergy documentation becomes rare. And not surprisingly.

The drug's stimulating properties masks its allergic symptoms. Circulating adrenaline (epinephrine) increases in caffeine consuming persons (2,3). In its synthetic form, epinephrine is the drug of choice for anaphylactic reactions, halting allergic reactions. But added to a stimulant reaction, excess adrenaline may induce delusions. And the breakdown of some adrenaline byproducts mimics symptoms of schizophrenia (4).

Brain levels increase proportionately with dosage (5). In allergic persons, each cup of coffee, cola, tea, every piece of chocolate, and any ingested caffeine products, intensifies toxic psychosis. Half-life increases. Subsequent doses, including minute amounts, act as a bolus. Cells are poisoned, including neurons.

Symptoms of cerebral allergy can range from minimal reactions, such as lack of comprehension and inability to focus, to severe psychotic states, such as delusions, paranoia, and hallucinations (6). It's known that amphetamine psychosis can't be distinguished from schizophrenia (7,8). With a caffeine allergic person's inability to eliminate, continually ingesting caffeine, neurotransmitter levels, including dopamine and adrenaline, quickly increase. Cells rapidly absorb the drug.

Dopamine increases proportionately to the amount of stress (9). The higher the adrenaline level, the greater the increase in dopamine. Serotonin also increases. Dopamine and serotonin decrease during partial, toxic withdrawal states. But as long as caffeine remains in the toxic body, neurotransmitters never adjust to the victim's natural state.

Toxicity is known to cause excitement, agitation, restlessness, shifting states of consciousness, and toxic psychosis (10), mimicking amphetamine psychosis. Allergic individuals may be erroneously diagnosed, medicated, and lost in a dark disturbed world, until death.

Adenosine receptors are blocked by caffeine (11,16), maintaining neuronal firing. Persons remain excited and often euphoric.

Caffeine toxicity may be mistaken for bipolar disorder (1,12). Symptoms include: chattiness, repetitive thought and action (resembling obsessive compulsive disorder, OCD), restlessness, psychomotor agitation, alternating moods, anger, impulsiveness, aggression, omnipotence, delirium, buying sprees, lack of sexual inhibition, and loss of values.

Allergy can mimic Attention Deficit Disorder (ADD) (13). As far back as 1902, T. D. Crothers noted that many caffeine consuming children "exhibit precocity" and "functional exaltation" (14).

Caffeine poisoning may also resemble schizophrenia. One woman's conversational topics wandered from subject to subject. She screamed, and believed that she was in prison. Natural judgement was impaired (1). In 1931, a truck driver brought to the hospital in a confused and irritable condition, complained of being attacked by flies. Flies were never present. Examination revealed that he'd consumed large amounts of cola (15). One gentleman ended his political speech with predictions and threats, out of the ordinary for his personality, stunning the audience (14). Another case describes a man, who imagined himself very wealthy, and assumed that his mental state was normal (14).

Caffeine toxicity may also masquerade as depression, and anxiety. In 1925, Powers described nervousness, visual problems, and dizziness, in patients he discovered suffered from caffeine toxicity (16). In 1974, caffeine toxic patients, experiencing the same symptoms, were erroneously admitted to a psychiatric hospital, for treatment of anxiety (16,17). In other studies, depression and anxiety are also correlated with caffeine intake (18,19,20,21).

In several reports, patients diagnosed with anxiety disorder experienced panic attacks with ingestion of caffeine (18,19,20). One study reveals that six persons improved with caffeine cessation and remained improved for at least six months (21). Other reports reveal that some persons not afflicted with panic disorder, experienced panic attacks with intravenously administered caffeine (22, 23).

Written materials on panic disorder symptoms and anaphylactic symptoms do not clearly differentiate between the two. Parasthesia (pins and needle sensations), a feeling of choking, hyperactive symptoms, chest pains, and hyperventilation, amongst other symptoms, are common in both conditions. They're also common in many caffeine consuming persons.

This suggests that caffeine allergy may be responsible for many cases of panic disorder. In which case, panic attacks in allergic individuals are suppressed anaphylactic reactions - mimicking ADHD, and panic disorder. They're "have to get up and run" and "I think I'm losing my mind" feelings, brought about by increased neurotransmitter levels, associated with the "fight or flight" syndrome.

Dr. William Walsh connected anxiety and severe allergic reactions. Dr.Walsh maintains that allergic anxiety stems from a choking sense, and loss of air; not a psychological deficit (24).

Caffeine converts into many byproducts, including theophylline. Theophylline keeps the bronchial tubes open. Allergic individuals are less likely to suffer respiratory collapse, during an anaphylactic reaction.

A proficient Boston neurologist mentions that sixty-six percent of elevated CPK MM (creatine phosphokinase of muscle) levels are of an "unknown origin" (25). Innumerable mid to late twentieth century studies reveal that a high number of persons diagnosed with mental disorders, including personality disorder, mania, BPD, depression, catatonia, and schizophrenia, exhibit elevated CPK MM levels (26,27,28-38,39,40-50).

The high majority of these studies, and others, attribute elevated CPK levels to a commonality between patients with mental disorders. Not one focuses on caffeine allergy as a contributing factor of mental disorders.

CPK MM, a muscle enzyme, increases with severe muscle trauma, burns, inflammatory states, and poisoning. This may stem from drugs (36,37,38,39), including cocaine, alcohol, amphetamines, heroin, and stimulants (37,40). Antihistamines, salicylates, cyclic antidepressants, theophylline, and others also cause this disorder (37).

This condition, called rhabdomyolysis, stresses and inflames tissues, including brain cells, breaking down muscle fibers, and discharging potentially toxic cellular matter into the bloodstream (37). Caffeine poisoning can cause rhabdomyolysis (10,37,41).

Myoglobinuria is a symptom of rhabdomyolysis, but often urine myoglobin disappears early in the course of the disorder, or is absent altogether (37). Generalized muscle cramping (associated with rhabdomyolysis) (14,37) may also be absent, or subside early on. Accumulation of caffeine acts as morphine, alleviating pain and discomfort, often inducing muscle rigidity.

With toxins leaking into the bloodstream, the CPK increases. The higher the CPK, the higher the neurotransmitters, and the deeper into psychosis a person spirals.

In the late 1960's, Bengzon et al proposed that the leakage of CPK and aldolase might explain schizophrenia (26). Studies on patients with non-restrictive diets, concentrated on various factors, including medication, but failed to include caffeine as a possible factor (26). More recent studies have also overlooked caffeine allergy as a factor in any mental disorders, including schizophrenia.

A study theorized caffeine as a possible, psychosis inducing agent. Researchers eliminated patients' caffeine for a short duration. It was decided that caffeine aggravates symptoms of thought disorder and psychosis (42). Caffeine was reintroduced-never allowing for sufficient withdrawal times-and significant improvements.

Proportionate to toxicity, physical withdrawal may take up to 12 months, or longer. Recovery symptoms include memory loss, confusion, tremors, agitated states, insomnia or somnolence, and nightmares associated with amphetamine withdrawal. Following physical recovery, residual mental symptoms, primarily confusion and mood alterations, may exist for several months.

Evidence suggests that caffeine, and synthetic neurotransmitter altering medications, merely balance one another, and that upon cessation of caffeine, medication is no longer needed. Several reports indicate that upon caffeine cessation, tremors increased in lithium consuming individuals (43). In some patients, caffeine withdrawal increased lithium levels (44). After experiencing a 10-year course of seasonal BPD, a woman eliminated caffeine from her diet. She no longer needed BPD medication (45).

Caffeine may compete for benzodiazepine receptors (5). In which case, benzodiazepines reduce caffeine's effects and vice versa; balancing each other.

Chronic toxicity may affect functional aspects of every organ (14). Allergic persons may become sensitive to bright light, and resort to sunglasses. It's not uncommon to find dilated but reactive pupils on examination (14). Toxic persons usually present with a whitish, or grayish coated tongue (14, 46). Other findings imply that caffeine inhibits anaphylaxis, by suppressing histamine release (47,48). Due to caffeine's antihistamine properties, a skin test for caffeine allergy may be negative.

Several laboratory tests may be used as markers for allergic toxicity. A detectable Theophylline level in a patient not receiving Theophylline therapy, and an elevated CPK level are indicative of caffeine toxicity. Along with these, an increased glucose level (10,49) and an elevated white blood count (1,49) may also be significant of toxicity, as many patients assumed afflicted with mental disorders present with elevation of these (1,50). An elevated sedimentation rate, indicative of inflammatory processes, might signify rhabdomyolysis.

It's highly probable, that millions of consumers developed an allergy to caffeine, especially since availability and production increased rapidly mid- twentieth century. In which case, natural insights, and physical and mental health, have been sacrificed to chronic toxicity, resulting in organic brain, silently posing as ADD, ADHD, anxiety, BPD, depression, OCD, panic, and schizophrenia. Physical ailments resemble amphetamine poisoning, and include drug eruptions, masquerading as "rosacea."

Back in 1936, McManamy and Schube maintained that in all probability, many people of that era might have already been erroneously diagnosed with some form of mental illness. The doctors further predicted, that in the future, with lack of time, and proper medical insight, many doctors would not be able to diagnose simple disorders such as caffeine allergy, and would label many patients as psychotic (1).

Well, here we are. Welcome to the future.

http://www.doctoryourself.com/caffeine_allergy.html

This report on erowid is somewhat similar to how caffeine affected me:
http://www.erowid.org/experiences/exp.php?ID=816

[eltimmy]

Howdy sir. This was written on another forum by a all around good guy named Chairman_MAO:

----

According to my research, the best drug for this is the nootropic galantamine (Reminyl, Nivalin). It has been shown in animal studies to counteract the benzodiazepine-induced decrease of ACh release (I forget the specific region of the brain, but it was relevant to memory). They have used it for decades in Eastern Europe to treat benzodiazepine-induced memory imapairment. To treat schizophrenia/psychosis there, at times they would place the patient on up to 20mg/day of clonazepam. The galantamine would help the cognitive symptoms of the schizophrenia while counteracting the clonazepam-induced sedation, memory impairment, and myorelaxation. IMHO, this is far more humane than using e.g. haloperidol!

Try it, it works.


----

Tobacco also contains beta-carbolines, btw, not that I would recommend one take up smoking ... if they don't already.

Reputation Comments on this post:

Invaluable information. Good post.

[lulz]

Originally Posted by eltimmy

According to my research, the best drug for this is the nootropic galantamine (Reminyl, Nivalin). It has been shown in animal studies to counteract the benzodiazepine-induced decrease of ACh release (I forget the specific region of the brain, but it was relevant to memory).

Very interesting, thank you! I was unfamiliar with this nootropic. It seems to inhibit the enzyme that breaks down acetylcholine. My crazy uncle Joe will definitely look into this nootropic.

To treat schizophrenia/psychosis there, at times they would place the patient on up to 20mg/day of clonazepam. The galantamine would help the cognitive symptoms of the schizophrenia while counteracting the clonazepam-induced sedation, memory impairment, and myorelaxation.

20mg/day?! Good god, that should put down a small elephant. Joe will try to get his hands on this galantamine, and see how it works in various combinations with DMAE+choline. He's also planning to try out clonazepam, but at about a tenth of the dosage mentioned above.

[kareena]

I've used ginkgo biloba with definate success in the past to aid with memory (it's good for circulation too) but from what I've read vinpocetine is like "super" ginkgo biloba so your uncle's probably in there. Omega-3 and Omega-6 oils from supplements or preferably a load of oily fish is excellent for cognitive function.

Galantamine sounds interesting...

[fnord]

caffeine works well for my grandmother when shes abusing benzos.she just pops a caffeine pill of two and is all set.

[sterling77]

"A muscarinic receptor agonist is an agent that enhances the activity of the muscarinic acetylcholine
receptor...M1-type muscarinic acetylcholine receptors play a role in cognitive processing."

---Wikipedia

"Some components of the phosphokinase pathways that could conceivably be modulated by muscarinic
receptors in vivo have the potential to enhance cell survival by upregulation of certain protection
systems and/or blockade of apoptosis, or modulation of learning and memory."

---http://www.cas.md/Content/PDF/Presentation/September
Talk/Associated%20Pdf/muscuranic%20receptors.pdf


I though this was a very relevant study:
Note: Meclofenoxate is also known as centrophenoxine.


Effect of the combination of the benzodiazepine tranquilizer medazepam and the nootropic agent meclofenoxate on the activity of rat brain muscarinic receptors.
Popova JS, Petkov VD.
Institute of Physiology, Bulgarian Academy of Sciences, Sofia.

1. The effect of 7-day treatment with the benzodiazepine tranquilizer medazepam (5 mg/kg), the nootropic agent meclofenoxate (100 mg/kg) and their combination in the same doses on the binding activity of muscarinic receptors in four rat brain structures (cerebral cortex, striatum, hippocampus and hypothalamus) were studied using the antagonist [3H]-1-quinuclidinyl benzylate [( 3H]-QNB) as radio-ligand. 2. Medazepam treatment caused significant decrease of muscarinic receptor binding affinity (Kd) and of the receptor binding capacity (Bmax) in the brain structures studied. The number of muscarinic binding sites was unsignificantly decreased only in the hippocampus. 3. Meclofenoxate treatment caused an increase of muscarinic receptor affinity and a decrease of the binding capacity in the cerebral cortex and hypothalamus and an increase of the binding affinity in the striatum and hippocampus. 4. The combination of medazepam and meclofenoxate caused no significant changes of both muscarinic receptor characteristics in the hippocampus and of the receptor affinity in the striatum and hypothalamus in comparison with control rats. The Bmax values were decreased in the cerebral cortex, striatum and hypothalamus when compared with control animals. The differences observed were slighter than those determined after the comparison of medazepam treated rats with control rats. 5. The results obtained afford an opportunity to suggest that the nootropic agent meclofenoxate acts to moderate the effect of the benzodiazepine tranquilizer medazepam on the activity of rat brain muscarinic receptors.
PMID: 2279692 [PubMed - indexed for MEDLINE]


These results suggest that using centrophenoxine along with benzodiazepines eliminates the benzo memory loss with respect to muscarinic receptor antagonism. These receptors deal with acetylcholine which is implicated with memory, and they also protect from apoptosis (read: programmed cell death), meaning benzos may make the user more susceptible to apoptosis (a form of brain damage). So centrophenoxine could prevent memory loss and possible brain damage.

[lulz]

It's a month to the day since I started this thread, and I've been in touch with old Joe.

First off - for him, valium has by far created the absolute worst memory problems he has ever experienced. Valium bad! For him that is...

Clonazepam (Ristoril, Roche brand, Klonopin in USA) has been far more useful. Little to no memory loss experienced so far.

It seems to me that most people seem to react to valium vs. ristoril/klonopin in radically different ways. One benzo works perfectly for some people, the other benzo works perfectly for other people, and the only way to find out which suits SWIY is to experiment (sensibly) with each to determine which suits SWIY.

Anyhow, the nootropic coctail that Joe has ultimately found to work the best is:

1) DMAE + choline
2) Piracetam added if available
3) Low doses of caffeine in Joe's case. Your mileage may vary.
4) Nicotine. Nicotine. Nicotine!

Just Joe's input.