Hydergine: Desire Better Brain-Power?

Q: Hydergine: Desire Better Brain-Power? What do you think of hydergine to boost mental powers?

A: Hydergine has been touted for some time as a "smart" drug for use in enhancing mental abilities and improving intelligence.

It has been around for more than 20 years and is marketed today as a nonspecific cerebral stimulant and prescribed to help relieve symptoms of age-related mental decline. Hydergine has been studied but found ineffective for the treatment of Alzheimer's disease.

Originally developed for the treatment of hypertension, hydergine didn't really help lower blood pressure and is no longer used for that purpose. However, some people who took it soon after its introduction noticed improvements in memory and mood, which they associated with use of the drug. At first, these changes were attributed to increased blood flow to the brain, but later research suggested that hydergine improved brain cell metabolism.

Today, hydergine is FDA approved only for the treatment of people over the age of 60 who show signs of mental decline. I'm told it is more widely used in Europe, and I understand that some in the anti-aging community advocate taking more than the 3 mg daily dose recommended by the FDA.

Frankly, I wouldn't bother. I tried hydergine myself some years ago to see what it could do, but I detected no benefits. While the drug seems safe enough, I don't see the point of using it - especially since it's expensive. I'm unconvinced that it makes good on the promises made for it by its Internet promoters.

Andrew Weil, M.D.

Folic Acid to Boost Memory?

Q: Folic Acid to Boost Memory?Is it true that folic acid can prevent Alzheimer's disease? I heard that it improves memory.

A: New findings do suggest that folic acid may slow the declines in memory that can occur with age. Dutch researchers recently presented compelling evidence from a three-year study that included 818 adults between the ages of 50 and 70, none of whom were having any memory problems.

During the study, the participants took either a placebo or 800 mg folic acid (twice the amount recommended for women of childbearing age to protect against birth defects).

Results showed that those who took the folic acid had memory scores equal to people five and a half years younger. The folic acid group in the study also did better in information processing and muscle skills. The study was conducted by researchers at Wageningen University in the Netherlands and reported at the Alzheimer's Association International Conference on Dementia Prevention.

Commentary on Nutritional Treatment

from Willam Walsh, Ph.D., Senior Scientist, Pfeiffer Treatment Center http://www.hriptc.org/
(The following information is taken from Dr. William Walsh's discussion on Safe Harbor's "Integrative Psychiatry" email list for professionals.

To preserve Dr. Walsh's wealth of information, we have posted his comments here, with the notation of added commentary [with the date] as discussion goes on.)

SAMe
SAMe is very promising for undermethylated persons and a bad idea for those who suffer from a genetic tendency for overmethylation. I don't particularly like the "allopathic" method you referred to which is simply trial & error. SAMe can do great harm if given to the wrong person.

I hate going to funerals. (17 Dec, 2002)The mechanisms of action of SAMe and TMG are quite different. Most of our methyl groups come from dietary methionine. The methionine is converted to SAMe in a reaction with magnesium, ATP, methionine-adenosyl-transferase, and water. SAMe is a relatively unstable carrier of methyl groups and is the primary source of methyl for most reactions in the body.

Once the methyl group has been donated, the residual molecule is s-adenosyl-homocysteine which converts to homocysteine. TMG (betaine) is a biochemical which can donate a methyl group to homocysteine, thus converting it back to methionine.

The TMG route is secondary to the 5-methyl-tetrahydrofolate/B-12 reaction which the primary route for restoring methionine. Methionine and SAMe supplements directly introduce new methyl groups into the body.

TMG can provide a methyl group only to the extent that there is insufficient folate/B-12 to do the job. In some persons, the methylation effect of TMG is very minimal. In addition, persons who are undermethylated have a SAM cycle which is "spinning very slowly", much like a superhighway with little traffic.

The answer for them is NOT to more efficiently convert the small amount of homocysteine to methionine (using TMG), but rather to directly introduce more methionine or SAMe into the body. A small percentage of persons with sufficient dietary methionine cannot efficiently produce SAMe --- These persons need supplemental SAMe, and not methionine or TMG and are the exception to the rule. In most other cases, methionine supplements alone are sufficient.

TMG is a great way to treat individuals with dangerously high homocysteine levels. TMG can be very useful in augmenting methionine therapy along with B-6/P-5-P , serine, etc. The challenge is to supply enough methyl groups to help the patient, without creating dangerously high levels of homocysteine. Use of TMG is an "insurance policy" against this happening. (Jan 22, 2003)

A quick way to test for need for methylation therapy is to carry out a cautious trial of SAMe.

Within a week or two you should have your answer. If she clearly is improving on the SAMs (which is frightfully expensive)..... you can get usually the same benefits (albeit more slowly) using methionine plus calcium, magnesium, and B-6. This should be side-effect free unless (a) the methylation is begun too abruptly or (b) the patient has a rare genetic enzyme disorder which disrupts the SAM cycle. We've found that direct methylation is usually more successful than tinkering with the SAM cycle. The primary way humans receive most of their methyl groups is from dietary methionine. It's often hard to improve on Mother Nature. (Jan 20, 2003)

SAMe is likely to cause great worsening of symptoms, including mania, if given to an OVER-methylated person. The incidence of overmethylation in our patient database of 1,500 bipolar cases is about 18%. Bipolar disorder is not a single condition, but a collection of very different biochemical disorders under the same umbrella diagnosis. SAMe works great for truly undermethylated patients, but all hell breaks out if given to someone who is overloaded (genetically) with methyl groups. The right way to do this is to (a) first determine the person's innate methylation tendency & then (b) act accordingly. (Jan 31, 2003)

Schizophrenia
Severe wheat gluten intolerance can cause classic symptoms of schizophrenia, and amounts to about 4% of all schizophrenia diagnoses in the U.S. These persons usually become quite normal when placed on a gluten-free diet.I've done medical histories for more than 2,000 persons diagnosed with schizophrenia and have always been struck by the high frequency of schizophrenia in other relatives. Interestingly, the schizophrenia would often skip a generation.

NIMH data suggests that the overall incidence of schizophrenia in the USA is between 1% and 4%, depending on the definitions. However, the incidence of schizophrenia for children who have a schizophrenic parent is about 16%. This number doesn't change much for children of schizophrenics adopted at birth. I don't think there is "a schizophrenia gene", partly because this is a garbage term which encompasses several completely different conditions.

There are a number of biochemical ingredients which predispose to each phenotype of SZ..... these may be either genetic or acquired. However, I'm absolutely certain there is a genetic component in most cases.

Carl Pfeiffer was the first to develop meaningful chemical classifications of schizophrenia (and separate treatments for each phenotype). Carl Pfeiffer of Princeton, N.J. saw more than 20,000 schizophrenics in his lifetime. He found that 90% of all SZ patients could be classified into 3 large groups, with completely different etiologies & treatment approaches. These he termed "histapenia", "histadelia", and "pyroluria". The remaining 10% fit into several splinter groups.

One of the splinter groups was gluten intolerance, which represents 4% (1 case in 25). This is a rare form of schizophrenia, but if you've got it, it's everything!Multiple food & chemical sensitivities are also associated with histapenia (low histamine, overmethylation), the largest of all SZ groups, amounting to about 48% of all cases.

For this group, SZ symptoms often worsen if exposed to the offending substances, & nice improvements often occur if they are identified & avoided. However, the food sensitivities usually disappear after about 1 year of aggressive Folate/B-12/B-3 treatment, which is the primary route to a normal life for these patients.

We've known for more than 20 years that the metallothionein protein system does not perform well in most ADHD patients. About 68% of them exhibit very poor control of Cu & Zn, based on lab data from more than 6,000 patients diagnosed with ADD/ADHD. Autism is different in that about 90% of patients exhibit Cu/Zn imbalances that are generally much more severe than in ADHD.For several months, we have extended our metallothionein-promotion protocol to ADHD, behavior, depression, and schizophrenic patients who exhibit Cu/Zn imbalance.

The informal results so far are very encouraging. However, we've not yet done a formal outcome study for these populations, and thus have no statistics yet.We are considering applying MT-Promotion to Alzheimers & Parkinsons patients in the near future. Both disorders involve serious oxidative stress and abnormal trace metal levels. In addition, recent research has revealed a striking metallothionein deficiency in the brains of Alzheimers patients. (Feb 25, 2003)I've evaluated more than 3,500 patients with a diagnosis of bipolar or schizophrenia. The predominance of auditory hallucinations, serious self abuse, aggressiveness, inability to continue school, and social isolation...... all point in the direction of classic "paranoid schizophrenia", although many of these patients are labeled "bipolar disorder with psychotic features". Most severely mentally ill persons with a history of exceptional artistic or musical talent test as overmethylated. The biochemical recipe for these patients usually consists of (1) overmethylation, (2) low folate levels, and (3) elevated blood copper levels. All three of these chemical imbalances impact dopamine and norepinephrine in the brain, and together can cause rather extraordinary abnormalities in these important neurotransmitters. In my opinion, the key to successful treatment is biochemical treatment to overcome these chemical imbalances...... fortunately this can be accomplished using aggressive therapy with nutrients to normalize the chemical factors.Most mental breakdowns are triggered by severe stress, but the underlying cause is genetic and involves brain chemistry. Many persons self-medicate with alcohol, marijuana, or other illegal drugs in a desperate attempt to feel better. Many patients and their families erroneously believe that the EtOH or drug experiences were the underlying cause of the condition. They are wrong! This adult-onset condition will strike eventually in most cases, even if substance abuse never occurs.Traditional medicine can provide medication support which can usually eliminate (temporarily) most/all psychosis symptoms. However, these patients are usually plagued by drug side effects and are a mere shadow of their original selves. Common side effects are (a) fatigue, (b) inability to focus/concentrate for more than a few minutes, (c) change in personality, (d) massive weight gain, etc. The most popular drugs for these patients are Zyprexa, Seroquil, Risperdal, Geodon, and Clozaril..... the so-called atypical antipsychotics. Since most patients hate these medications, poor compliance is a major problem.I've seen many young schizophrenics and bipolar patients achieve complete recoveries through biochemical (nutrient) therapy. This rarely occurs with traditional medication therapy. (May 12, 2003)Some of schizophrenics who spontaneously get better are those who experience a toxic psychosis. I have a friend who had a toxic psychosis after an accidental overdose of a medication during childbirth. For 6 hours she was a full blown paranoid schizophrenic..... No symptoms in the following 20 years. Also, schizophrenia comes in mild, moderate, and severe versions. Many persons with a very mild genetic tendency for SZ can experience an environmental insult which pushes them into a temporary mental illness. Most will become quite ok with or without therapy.The real problem is the millions of SZ persons who have moderate to severe SZ which does not go away easily. (May 27, 2003)

Taurine
Yes, I've read a few articles and a book that talked about Taurine's slow metabolism and tendency to build up over time. Because of this, I've believed that high doses of Taurine (1,000 to 2,000 mg/day) are ok in the beginning..... but that the dosages need to be reduced within 2 weeks to about 400 to 500 mg/day..... to achieve the same effect.I believe that Taurine is especially effective for (1) combating seizure tendency and (2) reducing liver stress in processing fats. There have been several reports of intolerances and side effects from use of Taurine, and I feel that indiscriminant high doses are unwise.About 12 months ago, there was a fad among several alternative practitioners in which high doses of Taurine were given to every autistic patient. One of the reasons given was "to assist the liver cope with stresses associated with toxic metal overload". This seems to be a poor reason, since Taurine's action in the liver appears to be limited to fat metabolism, and most autistics are slender malabsorbers with low lipid levels. (June 24, 2003)

Womb Trauma
There is an exquisite and fragile biological/biochemical process during gestation in which short, dense immature brain cells are pruned, grow into fully-developed brain cells, and then (remarkably) experience growth inhibition to complete the process. The molecular biology of this process is becoming very well defined, and it is clear that many environmental events can hinder or disrupt early brain development. The primary culprits are oxidative stress, teratological chemicals, and infections. The least appreciated of these harmful factors is oxidative stress which can deplete key proteins and enzymes required for normal brain development.Environmental harm to a developing fetus can result from (a) biochemical inadequacies of the mother, and (b) external environmental insults. We're all familiar with birth defects that can result from Thalidomide, Thorazine, Prolixin, Haldol, and other psychiatric medications. Also the dangers of mercury, lead, and other toxics are well established, and we know that a mother's improper diet (e.g. inadequate folic acid) can be harmful. Although lower on the radar screen, fetal oxidative stresses can be equally devastating.What I'm leading up to.... is the scientific fact that serious emotional or physical stresses experienced by the mother can impair early brain development, especially if the mother is not biochemically intact. For example high emotional stresses or physical trauma to the mother will weaken the activity of metallothionein (MT) and glutathione (GSH) proteins, andincrease oxidative stress in the brain. MT-1 and MT-2 are directly involved in growth of immature brain cells. MT-3 is a key protein required for pruning and growth inhibition. These proteins also have the job of defending against oxidative stress in the brain and are consumed in the process. Maternal emotional stresses and psychic traumae deplete the embryonic brain of MT proteins and can compromise brain development.Womb trauma is real and the concept of "a cry so deep" is not psycho-babble guesswork. Rather, it is solidly supported by scientific fields such as embryology and molecular biology. (Aug 1, 2003)If fetal or early infant traumae have resulted in a brain that hasn't completely matured..... therapies to promote MT and GSH appear very promising..... especially in tandem withbehavioral therapies which stimulate the development of new brain cells.If the net result of the traumae is biochemical or neurotransmitter differences, then biochemical therapy aimed at normalizing brain chemistry would be indicated.If the traumae resulted in diminished ability to tolerate environmental toxins (for example an incompetent blood-brain barrier), then avoidance of such toxins would be an important aspect of treatment.If the traumae resulted in an innate inability to cope with emotional stresses, then counseling or other psychological services could be very beneficial.If the traumae resulted in a brain that is structurally different, this may represent "brain damage" that may be refractory to all treatments. (Aug 1, 2003)

Zinc
There have been several recent published articles which indicate that zinc and zinc metallothionein proteins (1) tend to prevent brain strokes, (2) tend to assist brain recovery after strokes, and (3) that deficiency of Zn or Zn-MT is associated with increased stroke likelihood. An occasional test for plasma Zn could help identify the proper dosage. Most adults can safely start with 25 to 50 mg/day of Zn. Without indication of B-6 deficiency, it might be a good idea to limit pyridoxine hydrochloride (usual form of B-6) to about 200 mg/day. B-6 is very helpful in enhancing the utilization of Zn.After use of these nutrients with thousands of persons, I'm not aware of a single case of harm. However, it is a good idea to introduce zinc gradually & to take Zn during the PM only. (June 3, 2003
Every 5 years or so, the zinc experts of the world convene for a symposium in which they share new advances in Zn technogy & research..... It's usually headed up by the eminent Prof. Prasad.One of the topics is laboratory testing to indicate an individual's Zn status. They consider about 10 different methods including packed cells, taste tests, etc...... The last two symposia resulted in the consensus that none of the testing options is wonderful, but that the best of the commercially available tests is plasma zinc. Taste tests didn't make the top three methods.However the Zn experts also stated that the most definitive determination of zinc depletion is the presence of symptoms of Zn depletion which disappear after Zn supplementation.My organization has evaluated the Zn status of 18,000 patients and we've tried all of these methods. Our standard protocol involves plasma Zn, being careful to use acid-etched, trace-metal-free tubes.We find that virtually all treatment-naive ASD persons are very Zn depleted and overloaded in "free" (unbound by ceruloplasmin) copper. Our patient population for ASD is 2,800. Our database of 5,600 ADHD patients indicates that about 75% are depleted in Zn. The remaining 25% have problems associated with pyrrole disorders, methylation disorders, EFA disorders, toxic overloads, etc. (July 22, 2003)

The high level of zinc depletion in ASD appears to stem from a genetic weakness in the metallothionein protein system.Cu/Zn ratios in hair are very helpful in ADHD and behavior disorders..... but far less useful in ASD, depression, and schizophrenia. Tracking plasma Zn, serum Cu and serum ceruloplasmin levels can be very helpful in guiding dosages aimed at normalizing Zn.

Management of Zn & Cu levels is a challenging problem in ASD. Sometimes rather extraordinary Zn dosages are required to normalize blood Zn levels.Virtually all ASD persons are Zn depleted., but not all exhibit an elevated Cu/Zn ratio. A minority of ASD patients exhibit normal or low Cu levels in serum, but have vastly inadequate levles of ceruloplasmin. Thus, the level of "unbound" Cu can be very high, even though all standard measures of Cu appear to be low. Some of these patients seem to have a mild version of Wilson's Disesase. (July 24, 2003)

Weight Loss May Yield Alzheimer's Clues

MONDAY, July 17 (HealthDay News) -- Gradual weight loss can precede dementia and begin as early as 10 years prior to memory loss, concludes a Mayo Clinic study involving women with and without dementia.

The findings may provide clues to the origins of dementia, say the researchers, who were expected to present the findings Sunday at the International Conference on Alzheimer's Disease and Related Disorders, in Madrid, Spain.

The Mayo team compared the long-term medical records of 560 people diagnosed with the onset of dementia between 1990 and 1994. These patients were compared to a group of patients who did not have dementia.

Both groups averaged about the same weight -- 140 pounds -- at the beginning of the study. Women who did not develop dementia maintained that weight over the next 30 years.

In contrast, "The women who later developed dementia started off at the same weight as those who didn't develop dementia, but their weight drifted downward to 136 pounds 10 years before symptom onset and 128 pounds at symptom onset," Dr. David Knopman, lead researcher and neurologist, said in a prepared statement.

He and his colleagues said it's unclear what caused the weight loss in the women who later developed dementia, but they have some theories.

"The weight loss findings raise scientific questions about the cause or causes of the weight loss. This points to changes in the brain that develop years before the actual memory loss. We think that there are several possible explanations," Knopman said.

"The women might have less initiative and lose interest in eating, they might develop a duller sense of taste and smell, or they might experience an earlier sense of satiety (feeling full). Also, because, we didn't observe the anticipatory weight loss in men, the weight loss could have something specific to do with postmenopausal hormonal changes," he said.

Pinpointing the brain mechanisms that influence weight loss in women who develop dementia may help researchers better understand how it develops, Knopman said.

More information
The American Medical Association has more about dementia.

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