FW: more on virgin coconut oil defeating Alzheimer's

[Guest guest]

could virgin coconut oil (MCTs) of course with vitamin B6, zinc, also have

omega 3 (fish oil, salmon, flax) be a great help to feed the brains of the

children? from Kathy's information w/ more from willis

go to <http://livinlavidalowcarb.com/blog/?p=4181>

http://livinlavidalowcarb.com/blog/?p=4181 to read about it

to listen to this:

http://www.thelivinlowcarbshow.com/shownotes/wp-content/uploads/llvlc240-dr-

mary-newport.mp3 and turn up your computer speakers to listen.

after listening, I believe the cinnamon capsules would also be beneficial.

decreased glucose uptake? if you get cold sores, you should take coconut

oil

go to You must supplement vitamin B6, zinc, also have omega 3 (fish oil,

salmon, flax)

go to <http://coconutketones.com/> http://coconutketones.com/ for more

information

excerpt: In Episode

<http://www.thelivinlowcarbshow.com/dr-mary-newport-coconut-oil-alzheimers-c

ure-episode-240/> 240 of “The Livin’ La Vida Low-Carb Show with Jimmy

,” we are privileged to hear from Dr. Newport

<http://www.coconutketones.com/biography.html> who I first found out about

after reading this

<http://tampabay.com/news/aging/article879333.ece#comments> St. sburg

Times story about how feeding her husband coconut oil greatly IMPROVED his

Alzheimer’s. It was such an extraordinary story that I just HAD to book her

for an interview to tell this remarkable story to my listeners. She

correctly identifies the glucose connection to Alzheimer’s disease which is

now becoming well-known as Type 3 diabetes

<http://livinlavidalowcarb.com/blog/?p=3495> , how ketone bodies are the

preferred fuel for brain function, and why medium chain triglycerides (MTCs)

found in coconut oil are a miracle for her husband’s condition. This is one

of the most stunning personal testimonies of how a high-fat, low-carb

ketogenic diet can dramatically improve health. You can’t help but be a

believer after listening to Dr. Newport gush about her husband Steve is

overcoming his tremors, regain cognitive function, and DEFEATING his

Alzheimer’s.

Note: You must supplement vitamin B6(p5p), zinc, and magnesium when using

coconut oil. i get mine at iherb.com

Scroll down for more detailed information.

There are lots of ways to get coconut oil into the diet: stir coconut oil in

some tea; make macaroons; replace some of the butter in baking with coconut

oil; and use it in cooking/sautéing. 's oil blend (see below) is a good

way to incorporate coconut oil in cooking and salad dressings.

More detailed information from forum below.

What are MCT's?

Dear Doug:

This is an abbreviation for Medium Chain Triglycerides. This fatty acid

isn't digested in the manner of other fats, but is converted to ketones

which

the brain can use as fuel.

The recommended amounts of coconut oil is one tablespoon to three

tablespoons a day, depending upon the degree of insulin resistance. It is

said that

diabetics, whose bodies are already converting other fats to ketones may

need to be cautious. There are ketone strips to keep track. MCT oil may

cause diarrhea when it is consumed in large amounts (small amounts

throughout

the day promote greater tolerance).

To utilize these MCT oils requires coenzyme B6 (Pyridoxal 5' Phosphate,

often referred to as P5P), and magnesium. Some might have essential

fatty-acid

deficit symptoms, but the problem could really be a lack of vitamin B6 and

magnesium. You must supplement vitamin B6, zinc, and magnesium, especially

when using coconut oil. Remember, that a zinc deficiency adversely

influences coconut oils tending to a fatty liver. P5P is apt to be more

effective

because a large majority of " healthy " people do not convert the regular

vitamin B6 to its metabolite form. One study showed 19% were deficient in

one

or more B-vitamins, but 62% were deficient in the necessary metabolites.

Zinc deficiency can also look like a fatty acid deficiency, and children

with

milk intolerance have been shown to be deficient in EFAs.

MCTs can improve liver function and fat absorption. Unlike other fats and

oils, they are not transported through the lymphatic system during

digestion, but go directly to the liver where they are burned to provide

energy.

Burned like carbohydrates, MCTs are a good source of energy for athletes.

They

have been shown to lower cholesterol levels and help people with irritable

bowel problems

MCTs Promote Weight Loss

Several studies have shown that medium chain triglycerides (MCTs) promote

weight loss. One study showed that rats fed long chain fatty acids (LCTs)

stored body fat, while rats fed MCTs reduced body fat and improved insulin

sensitivity and glucose tolerance...(See June, 2003, Obesity Research) In

March of 2003, this same journal published findings that Medium-chain

triglycerides increase energy expenditure and decrease adiposity in

overweight

men. The study was conducted with twenty-four healthy, overweight men with

body mass indexes between 25 and 31 kg/m. They consumed diets rich in MCT or

LCT for 28 days, each in a crossover randomized controlled trial. Those

consuming MCTs lost more weight and had more energy than those consuming

LCTs

(in this case olive oil).

An earlier study in 2002, The Journal of Nutrition came to the same

conclusion. They reported that MCTs are more readily oxidized in the liver

than

LCTs, which leads to more energy and less weight gain. The study concluded

that MCTs increase energy expenditure, may result in faster satiety, and

facilitate weight control when included in the diet as a replacement for

fats

containing LCTs.

Scores of people have discovered the benefits of MCTs firsthand. Sharon

writes the following to the coconut discussion group:

I have had the same problem with sluggish metabolism and weight gain since

having children. Even a no-calorie diet (fast) for 5 days did not work. As

soon as I started taking Virgin Coconut Oil the fat began to melt and I

have lost 20 pounds. Over the same period of time, my 13- year- old daughter

who was very chubby and very worried about it, but could not bring up the

self-control to renounce some of her favorite fatty foods, lost about 10

pounds. She now has the perfect figure, to her great joy! Pants she was

bulging out of a year ago hang loose on her!

To obtain MCTs cook with a quality coconut oil and use if for salad

dressing. Mix it in a smoothie. Start with a very small amount.

I append a paper that elaborates on the subject.

Warmly,

Willis

Hello List mates:

Some have recently asked about MCT oils. Here are the answers.

Willis

From: <mailto:_kblanco%40mindspring.com> _kblanco@..._ (mailto:

<mailto:kblanco%40mindspring.com> kblanco@...) .

Uses of MCT Oils

By Darnley, RD

----------------------------------------------------------

Dietary fat and the fat stored on our body as adipose tissue are in the

form of triglycerides, which contain long-chain fatty acids (14 carbons or

more) [1]. The most prevalent fatty acids found in food are oleic (C18:1),

palmitic (C16:0), stearic (C18:0), and linoleic (C18:2). Due to molecular

distillation in the early 1960's, it became possible to prepare a mixture of

triglycerides that contain only medium-chain fatty acids (MCFA; 6-12

carbons). MCFA's are naturally found in coconut oil, palm kernel oil, and

milk.

Medium-chain triglyceride (MCT) oil is comprised of primarily caprylic

(C8:0) and capric (C10:0) acids with a very small percentage of caproic

(C6:0)

and lauric (C12:0) acids, which are esterified to a glycerol backbone. MCT

oil is a light yellow, translucent, odorless liquid at room temperature

(MCT's are also available in powder form). Although completely saturated, it

is not atherogenic [2] or solid in consistency like other saturated fats,

due to the shorter chain lengths of the fatty acids within the oil.

The energy value of MCT oil is approximately 7-9 Calories per gram, and

this fat is metabolized differently than long-chain triglycerides (LCT).

Complete hydrolysis to MCFA's and small amounts of monoglycerides occurs in

the

stomach with very little secretion of pancreatic lipase or bile acids.

After MCFA's are absorbed into the intestinal mucosal cells, they are not

resynthesized into triglycerides and incorporated into chylomicrons as are

long-chain fatty acids. MCFA's bypass the lymphatic system and are carried

by

the portal vein directly to the liver, where they are metabolized to produce

carbon dioxide, ketones, and acetate.

Therapeutic uses

Due to the unique properties of MCT's, they are used as a fat source in

many disease states. MCT oil can be used to add calories to a formula or

diet

in the case of malabsorption syndromes. Due to a more rapid digestion and

absorption, MCT's increase the osmolality of formulas. Since it requires

lower concentrations of bile or pancreatic lipase for digestion and

absorption, patients with bile acid and pancreatic lipase deficiencies

benefit from

adding this fat source to the diet. MCT's comprise the lipid component in

many infant formulas because infants rely on lingual lipase for lipid

digestion when pancreatic function is not fully developed.

MCT's are contraindicated for people with diabetes, due to the risk of

hyperketonemia. MCT's are also generally not recommended for people who have

compromised hepatic function because a diseased liver does not have the

ability to clear the increased levels of MCFA's. Essential fatty acids and

fat-soluble vitamins must be added to MCT oil if it is a significant source

of

fat in the diet.

MCT oil is also unpalatable for some people and may cause diarrhea when it

is consumed in large amounts (for people who experience GI distress, small

amounts throughout the day promote greater tolerance). The high cost of MCT

oil is another limitation to its use in the diet. These factors should be

addressed by the dietitian or physician after it is determined whether a

client or patient can benefit from MCT oil. Using coconut oil is more

economical.

Alternative uses

Besides being used to alleviate the effects of malabsorption syndromes,

MCT's have some nontraditional applications. The ketogenic diet has been

effective in treating chronic seizures. MCT's are used to induce ketosis in

these patients.

When MCT's are substituted for long-chain triglycerides in the diet,

animals gain less weight, store less adipose, and experience an increase in

metabolic rate [3, 4, 5]. MCT-fed mice also have been shown to possess

increased

endurance over that of LCT-fed mice [6]. It is probably these factors that

have brought MCT oil into the market of ergogenic aids and dietary

supplements. Due to the caloric value of MCT oil, it can be effective in

adding

energy to the diet.

There is far less research conducted in human subjects, and the results

from animal studies do not necessarily apply to humans. The amount of this

fat

that is consumed by animals to create a performance effect is far more

than the average human consumption of fat. Nevertheless, it could be

beneficial to substitute MCT oil for other oils that contain long-chain

fatty acids,

since scientific evidence indicates that MCT's may be less easily stored

as adipose. Recipes using MCT oil have been published [7], and MCT oil can

be substituted in place of most cooking oils.

_____

From: Williss [mailto:Williss ]

Sent: Thursday, May 13, 2010 7:35 AM

Williss

Subject: more on virgin coconut oil and alzherimers

A

<Williss;_ylc=X3oDMTJjYzY0cm84BF9TAzk3MzU5NzE1

BGdycElkAzM0Njg5NwRncnBzcElkAzE3MDUxMjYxNzEEc2VjA2hkcgRzbGsDaHBoBHN0aW1lAzEy

NzM3NTA0ODQ-> place to exchange ideas and experiences and find help for

Autistic and ADHD Kids, unrestricted by stringent *moni

Messages In This Digest (2 Messages)

1.

Re: [ARIsupport] Fwd: Coconut Oil and Alzheimer's <> Disease From:

WillissL@...

2.

Dopamine Excess, Risperdal, and natural <> treatment From: WillissL@...

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Re: [ARIsupport] Fwd: Coconut Oil and Alzheimer's Disease

<Williss/message/12225;_ylc=X3oDMTJxNzNrZGc1BF

9TAzk3MzU5NzE1BGdycElkAzM0Njg5NwRncnBzcElkAzE3MDUxMjYxNzEEbXNnSWQDMTIyMjUEc2

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Posted by: " WillissL@... " WillissL@...

<mailto:WillissL@...?Subject=

Re%3A%20%5BARIsupport%5D%20Fwd%3A%20Coconut%20Oil%20and%20Alzheimer%27s%20Di

sease> willissl1919 <willissl1919>

Wed May 12, 2010 12:15 pm (PDT)

In a message dated 5/12/2010 4:26:16 A.M. Pacific Daylight Time,

douglisaadam@ <mailto:douglisaadam%40dslextreme.com> dslextreme.com writes:

What are MCT's?

Dear Doug:

This is an abbreviation for Medium Chain Triglycerides. This fatty acid

isn't digested in the manner of other fats, but is converted to ketones

which

the brain can use as fuel.

The recommended amounts of coconut oil is one tablespoon to three

tablespoons a day, depending upon the degree of insulin resistance. It is

said that

diabetics, whose bodies are already converting other fats to ketones may

need to be cautious. There are ketone strips to keep track. MCT oil may

cause diarrhea when it is consumed in large amounts (small amounts

throughout

the day promote greater tolerance).

To utilize these MCT oils requires coenzyme B6 (Pyridoxal 5' Phosphate,

often referred to as P5P), and magnesium. Some might have essential

fatty-acid

deficit symptoms, but the problem could really be a lack of vitamin B6 and

magnesium. You must supplement vitamin B6, zinc, and magnesium, especially

when using coconut oil. Remember, that a zinc deficiency adversely

influences coconut oils tending to a fatty liver. P5P is apt to be more

effective

because a large majority of " healthy " people do not convert the regular

vitamin B6 to its metabolite form. One study showed 19% were deficient in

one

or more B-vitamins, but 62% were deficient in the necessary metabolites.

Zinc deficiency can also look like a fatty acid deficiency, and children

with

milk intolerance have been shown to be deficient in EFAs.

MCTs can improve liver function and fat absorption. Unlike other fats and

oils, they are not transported through the lymphatic system during

digestion, but go directly to the liver where they are burned to provide

energy.

Burned like carbohydrates, MCTs are a good source of energy for athletes.

They

have been shown to lower cholesterol levels and help people with irritable

bowel problems

MCTs Promote Weight Loss

Several studies have shown that medium chain triglycerides (MCTs) promote

weight loss. One study showed that rats fed long chain fatty acids (LCTs)

stored body fat, while rats fed MCTs reduced body fat and improved insulin

sensitivity and glucose tolerance...(See June, 2003, Obesity Research) In

March of 2003, this same journal published findings that Medium-chain

triglycerides increase energy expenditure and decrease adiposity in

overweight

men. The study was conducted with twenty-four healthy, overweight men with

body mass indexes between 25 and 31 kg/m. They consumed diets rich in MCT or

LCT for 28 days, each in a crossover randomized controlled trial. Those

consuming MCTs lost more weight and had more energy than those consuming

LCTs

(in this case olive oil).

An earlier study in 2002, The Journal of Nutrition came to the same

conclusion. They reported that MCTs are more readily oxidized in the liver

than

LCTs, which leads to more energy and less weight gain. The study concluded

that MCTs increase energy expenditure, may result in faster satiety, and

facilitate weight control when included in the diet as a replacement for

fats

containing LCTs.

Scores of people have discovered the benefits of MCTs firsthand. Sharon

writes the following to the coconut discussion group:

I have had the same problem with sluggish metabolism and weight gain since

having children. Even a no-calorie diet (fast) for 5 days did not work. As

soon as I started taking Virgin Coconut Oil the fat began to melt and I

have lost 20 pounds. Over the same period of time, my 13- year- old daughter

who was very chubby and very worried about it, but could not bring up the

self-control to renounce some of her favorite fatty foods, lost about 10

pounds. She now has the perfect figure, to her great joy! Pants she was

bulging out of a year ago hang loose on her!

To obtain MCTs cook with a quality coconut oil and use if for salad

dressing. Mix it in a smoothie. Start with a very small amount.

I append a paper that elaborates on the subject.

Warmly,

Willis

Hello List mates:

Some have recently asked about MCT oils. Here are the answers.

Willis

From: _kblanco@mindspring <mailto:_kblanco%40mindspring.com> .com_

(mailto:kblancomindspring (DOT) <mailto:kblanco%40mindspring.com> com) .

Uses of MCT Oils

By Darnley, RD

----------------------------------------------------------

Dietary fat and the fat stored on our body as adipose tissue are in the

form of triglycerides, which contain long-chain fatty acids (14 carbons or

more) [1]. The most prevalent fatty acids found in food are oleic (C18:1),

palmitic (C16:0), stearic (C18:0), and linoleic (C18:2). Due to molecular

distillation in the early 1960's, it became possible to prepare a mixture of

triglycerides that contain only medium-chain fatty acids (MCFA; 6-12

carbons). MCFA's are naturally found in coconut oil, palm kernel oil, and

milk.

Medium-chain triglyceride (MCT) oil is comprised of primarily caprylic

(C8:0) and capric (C10:0) acids with a very small percentage of caproic

(C6:0)

and lauric (C12:0) acids, which are esterified to a glycerol backbone. MCT

oil is a light yellow, translucent, odorless liquid at room temperature

(MCT's are also available in powder form). Although completely saturated, it

is not atherogenic [2] or solid in consistency like other saturated fats,

due to the shorter chain lengths of the fatty acids within the oil.

The energy value of MCT oil is approximately 7-9 Calories per gram, and

this fat is metabolized differently than long-chain triglycerides (LCT).

Complete hydrolysis to MCFA's and small amounts of monoglycerides occurs in

the

stomach with very little secretion of pancreatic lipase or bile acids.

After MCFA's are absorbed into the intestinal mucosal cells, they are not

resynthesized into triglycerides and incorporated into chylomicrons as are

long-chain fatty acids. MCFA's bypass the lymphatic system and are carried

by

the portal vein directly to the liver, where they are metabolized to produce

carbon dioxide, ketones, and acetate.

Therapeutic uses

Due to the unique properties of MCT's, they are used as a fat source in

many disease states. MCT oil can be used to add calories to a formula or

diet

in the case of malabsorption syndromes. Due to a more rapid digestion and

absorption, MCT's increase the osmolality of formulas. Since it requires

lower concentrations of bile or pancreatic lipase for digestion and

absorption, patients with bile acid and pancreatic lipase deficiencies

benefit from

adding this fat source to the diet. MCT's comprise the lipid component in

many infant formulas because infants rely on lingual lipase for lipid

digestion when pancreatic function is not fully developed.

MCT's are contraindicated for people with diabetes, due to the risk of

hyperketonemia. MCT's are also generally not recommended for people who have

compromised hepatic function because a diseased liver does not have the

ability to clear the increased levels of MCFA's. Essential fatty acids and

fat-soluble vitamins must be added to MCT oil if it is a significant source

of

fat in the diet.

MCT oil is also unpalatable for some people and may cause diarrhea when it

is consumed in large amounts (for people who experience GI distress, small

amounts throughout the day promote greater tolerance). The high cost of MCT

oil is another limitation to its use in the diet. These factors should be

addressed by the dietitian or physician after it is determined whether a

client or patient can benefit from MCT oil. Using coconut oil is more

economical.

Alternative uses

Besides being used to alleviate the effects of malabsorption syndromes,

MCT's have some nontraditional applications. The ketogenic diet has been

effective in treating chronic seizures. MCT's are used to induce ketosis in

these patients.

When MCT's are substituted for long-chain triglycerides in the diet,

animals gain less weight, store less adipose, and experience an increase in

metabolic rate [3, 4, 5]. MCT-fed mice also have been shown to possess

increased

endurance over that of LCT-fed mice [6]. It is probably these factors that

have brought MCT oil into the market of ergogenic aids and dietary

supplements. Due to the caloric value of MCT oil, it can be effective in

adding

energy to the diet.

There is far less research conducted in human subjects, and the results

from animal studies do not necessarily apply to humans. The amount of this

fat

that is consumed by animals to create a performance effect is far more

than the average human consumption of fat. Nevertheless, it could be

beneficial to substitute MCT oil for other oils that contain long-chain

fatty acids,

since scientific evidence indicates that MCT's may be less easily stored

as adipose. Recipes using MCT oil have been published [7], and MCT oil can

be substituted in place of most cooking oils.

For More Information

Search the HCRC and NCAHF Web Sites References

Babayan, VK (1987) Medium chain triglycerides and structured lipids.

Lipids, 22(6), 417. Blackburn, GL et al. (1989) A reevaluation of coconut

oil's

effect on serum cholesterol and atherogenesis. J. Phil. Med. Assoc., 65(1),

144. Hashim, SA (1967) Medium chain triglycerides: Clinical and metabolic

aspects. J. Amer. Diet. Assoc., 67(9), 221. Baba, N et al. (1982) Enhanced

thermogenesis and diminished deposition of

fat in response to overfeeding with diet containing medium chain

triglyceride. Amer. J. Clin. Nutr., 35(4), 678, Geliebter, A et al. (1983)

Overfeeding with medium-chain triglyceride diet results in diminished

deposition of fat. Amer. J. Clin. Nutr., 37(1), 1.

Fushiki, T et al. (1995) Swimming endurance capacity of mice is increased

by chronic consumption of medium chain triglycerides. J. Nutr., 125(3),

531. Schizas, AA et al. (1967) Medium chain triglycerides: Use in food

preparation. J. Amer. Diet. Assoc., 67(9), 228

Sincerely,

Willis

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Dopamine Excess, Risperdal, and natural treatment

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<mailto:WillissL@...?Subject=

Re%3ADopamine%20Excess%2C%20Risperdal%2C%20and%20natural%20treatment>

willissl1919 <willissl1919>

Thu May 13, 2010 12:27 am (PDT)

In a message dated 5/11/2010 4:34:20 A.M. Pacific Daylight Time,

ritzywright@ <mailto:ritzywright%40> writes:

Dear Drissia:

When I get my son's issues under control I will worry about what's going

on with me.

I know this is a common view, but it is likely to be a misguided one :-(.

What if that is long coming? What if we fall by the wayside before it

arrives? Do we not owe it to ourselves and to our family to care for ourself

FIRST? What does the Stewardess say on preparation for takeoff? " Mother's,

put

the oxygen mask on yourself first, then put one on your children " . This

makes sense. Who will put the mask on the children if you pass out? Please,

consider your worth and the need to care for yourself first.

You said there were supplements he could take in the place of the

Risperdal. Can they be taken in addition to the Risperdal and used as an

adjunct

to keep him from needing a larger dose?

Yes, to all those questions. I would never suggest your stopping Risperdal

without the help of your doctor in reducing dosage as you wean off. To

quit these type drugs cold turkey can be disastrous. These are some of the

side effects of continued usage. I realize you are taking half milligram,

whereas the normal dose is up to 6 mg, nevertheless, I know one adult who,

on

the low dose, had to change drugs because of elevated liver enzymes.

>>>Risperdal has been linked to diabetes and, more specifically, Type 2

diabetes. Other serious side effects include Neuroleptic Malignant Syndrome

(NMS), a potentially fatal syndrome involving muscle rigidity, liver damage,

and irregular blood pressure and pulse.[vii] >>>

>>>risperidone is often used; however, a major study followed children for

only 8 wk; some patients develop tardive dyskinesia after several months.

>>>

Risperidone is usually thought to antagonize the overactive serotonin and

dopamine receptors, but it also affects norepinephrine:

>>>risperidone (0.5 mg/kg), the 5-HT (serotonin) syndrome was completely

inhibited, and the Noradrenaline (NA) level increased to 6.5 times the

pre-administration level. >>>

Dopamine antagonists, such as Risperdal, can be very effective in

controlling Exposure anxiety, panic attacks, and OCD. Dopamine increases

proportionately to the amount of stress. 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. >>>

In addition to caffeine and stress induced adrenaline raising dopamine

levels, mercury is a known inducer of excess dopamine levels.

>>>Citation: Faro LR, do Nascimento JL, Alfonso M, et al. Protection of

methylmercury effects on the in vivo dopamine release by NMDA receptor

antagonists and nitric oxide synthase inhibitors. Neuropharmacology. 2002

Sep42(5)612-8. PMID:11985818.

Abstract: The possible protective effects of NMDA receptor antagonists

dizocilpine (MK-801) and D(-)-2-amino-5-phosphonopentanoic acid (AP5), and

nitric oxide synthase (NOS) inhibitors L-nitro-arginine methyl ester

(L-NAME)

and 7-nitro-indazol (7-NI) on the methylmercury (MeHg)-induced dopamine

(DA) release from rat striatum were investigated using in vivo

microdialysis.

Intrastriatal infusion of 400 microM or 4 mM MeHg increased the

extracellular DA levels to 1941+/-199 and 7971+/-534% with respect to basal

levels.

Infusion of 400 microM or 4 mM MeHg in 400 microM MK-801 pretreated animals,

increased striatal DA levels to 677+/-126 and 2926+/-254%, with respect to

basal levels, these increases being 65 and 63% smaller than those induced

by MeHg in non-pretreated animals. Infusion of 400 microM or 4 mM MeHg in

400 microM AP5 pretreated animals, increased striatal DA levels to 950+/-234

and 2251+/-254% with respect to basal levels, these increases being 51 and

72% smaller than those induced by MeHg in non-pretreated animals. Infusion

of 400 microM MeHg in 100 microM L-NAME or 7-NI pretreated animals,

increased the extracellular DA levels to 1159+/-90 and 981+/-292%, with

respect

to basal levels, these increases being 40 and 50% smaller than those induced

by MeHg in non-pretreated animals. In summary, MeHg acts, at least in

part, through an overstimulation of NMDA receptors with possible NO

production

to induce DA release, and administration of NMDA receptor antagonists and

NOS inhibitors protects against MeHg-induced DA release from rat striatum.

>>>

<<<Elevated dopamine levels are closely linked to schizophrenia.

Excess dopamine may cause sleep disorders and Insomnia. >>>

>>>dopamine(DA). Low levels of dopamine are vasodilatory (can be blocked

by nimodipine and hydergine). High doses are vasoconstrictive. <<<

>>>One therapeutic approach in the treatment of patients with infantile

autism involves the use of dopamine antagonists. The dopaminergic system of

the brain affects motor behaviors. Its abnormalities involve excess motor

activity and stereotypes similar to those observed in autistic patients.

Intellectually subnormal autistic children, particularly those with severe

hyperactivity and stereotypes, were found to have excess dopaminergic

activity

as measured by high levels of homovanillic acid in the CSF (Cohen, et al)

Note: Low dose Risperdal™ (0.5 mg) has freed one adult from OCD, Exposure

Anxiety, and panic attacks apparently through its effect in reducing

dopamine activity.

Why not build acetylcholine by supplementing lecithin, or choline, or CDP

Choline, or N-acetylcholine, or perhaps better, DMAE?

Omega-3 fatty acids of cod-liver oil are more effective than drugs used

for schizophrenia according to studies done at Harvard medical School. See

" Mastering Autism " , Section " Managing Fatty acids " for the correct way to

introduce fatty acids.

>>>The N-Methyl d Aspartate receptor (NMDA is activated mainly to amplify

the effect of glutamate during periods of especially intense excitation.

Since the blockade of NMDA receptors in the cerebral cortex enhances the

release of dopamine from lower brain regions, reduced glutamate transmission

could be the ultimate cause of excessive dopamine activity in the brains of

schizophrenic patients.

High levels of another NMDA receptor blocking agent, kynurenic acid, are

found in the spinal fluid of patients with AIDS dementia and in many

autistic children. The amino acid glycine and (at much lower doses) its

chemical

relative, the antitubercular drug D-cycloserine, indirectly activate NMDA

receptors and may reduce apathy, withdrawal, and cognitive impairment in

schizophrenic patients. >>>

The natural NMDA receptor blocking agent (calcium channel blocker) is

magnesium, manganese, and zinc. We normally need a blocker not an activator.

The schizophrenic and those with a dopamine overload need an NMDA activator.

>>>Excess dopamine is typically caused by a vitamin B6, zinc, and/or

acetylcholine deficiency, or a Clostridia overgrowth (produces dopamine).

Cadmium toxicity suppresses norepinephrine, serotonin, and acetylcholine,

but not

dopamine. Removal of heavy metals allows restoration of near-normal levels

of acetylcholine. High estrogen levels from soy foods and from flax-oil

tend to cause increased absorption of copper and cadmium. Cadmium affects

verbal ability more and lead affects performance measures more. The high

estrogen and/or excess dopamine can create anxiety in the child.

When anxious and fearful, the sympathetic nervous system kicks in and or

having been made predominant, anxiety is the result. It's sort of a Chicken

or egg question. The Sympathetic Nervous System is balanced by the

Parasympathetic Nervous System. The overactive Sympathetic is suppressed by

magnesium and the diminished Parasympathetic function is stimulated by

potassium.

Here we see a need for magnesium and potassium supplementation to restore a

balance. Magnesium deficiency keeps potassium from being replenished in

the cell.

Cigarette smoke (including secondhand smoke) reduces MOA (, an enzyme

needed to break down dopamine and other chemicals, compromising the body's

ability to detoxify itself of many harmful substances. Smoking (and eating

white flour) builds cadmium toxicity and also depletes the amino acid

cysteine needed to make metallothionein, sulfates, and glutathione necessary

to

detoxify the body of heavy metals, phenols, amines, and other poisons.

The result may be an out-of-control, panic-stricken child suffering

Environmental Anxiety. This behavior is often dramatically controlled by ¼

to ½

mg Risperdal™. It's better to correct the above problems and to build

acetylcholine, though the latter may be difficult in view of cadmium

suppressing

the needed enzyme.

Magnesium, calcium, selenium, zinc, melatonin, and metallothionein protect

the cells against cadmium and mercury, and germanium protects the liver

against damage from cadmium. Heavy metals can be chelated by oral

supplements

of Ambrotose AO™, IP-6 (phytic acid), zinc, manganese, selenium,

N-acetylcysteine (NAC), serine, melatonin, Cilantro, transdermal or oral

glutathione, and vitamins B6, C, and E. The initial treatment must be

gradual to avoid

a sudden dumping of metal toxins from tissues, which could cause kidney

damage and a worsening of symptoms.

Choline (Lecithin) is antidopaminergic, as is anything that will build

acetylcholine. See " Mastering Autism " for several ways to build

acetylcholine.

Supplementing DMAE (crosses the BBB and supplies choline) will work well

for the overmethylated person. >>>

I have mentioned building Acetylcholine several times. That seems the

logical and effective way to balance excess dopamine, which is often an

imbalanced ratio with acetylcholine, but this won't work for the

undermethylated

(55%) of Autistic children. See Dr. Walsh's explanation below. See

" Mastering Autism " for details of undermethylation.

What would Gaba do, if I tried it along with the Risperdal? It is logical

that the lower dose he can take the better off he will be. Yesterday was

his 3 day on the .5mg. He had 1 episode; milder than the others. The day

before he had none. The doctor said to increase on day 5 to 1 mg. if he

showed

no side effects and his behaviors were not under control.

I would certainly ask the doctor about the use of low dose GABA. Should

you decide to use it, start at a low amount and increase as you observe his

response. Too much will make him lethargic.

I have wondered for a while if some of the issue is the MSG in the KFC

strips. He has been eating them daily since he was 9 and seems to crave

them.

He increased from 3 to 6 about a month before these behaviors got really

out of control. Is that a possibility?

This is typical allergic response. When this occurs, there is only one

solution: Tough Love! You have to remove all KFC foods. Frequently the

addiction is to their French Fries. No, he won't starve. After a couple of

days

for the allergens to clear, he will begin eating a more normal diet.

He was also taking Bentyl and Allegra.

The interaction of these two is possible. They are listed on the handout

as likely to interact.

The pharmacist said that possible side effects from Bentyl was psychosis

and Allegra, panic attacks.

Isn't that just Lovely?

When we stopped the medication the episodes did not go away, however.

Also, he has antibodies to gluten. Could the little bit of gluten in the

breading for the strips and a hotdog bun send him over the edge like this?

If he

doesn't eat the 2nd 3 strips, he eats a hotdog with ketchup in the evening.

The time of day these start is about 4-5 hours after he has eaten his

lunch(3 Crispy Strips & mashed potatoes and gravy-also full of msg.) Problem

is

he refused to eat anything else.

That is only a problem for a tenderhearted Mother! He must be denied all

these foods until he is free from the allergens and ready to eat normally. T

his diet will not long sustain health or normal function. The hotdogs are

loaded with phosphates which bind calcium and magnesium. Ketchup is loaded

with sugar and salicylates. the chicken strips are loaded with MSG, as you

said, and with oxidized fats, probably hydrogenated soy oil. The bread and

breading is loaded with gluten. When one is gluten sensitive, it only takes

the use of a utensil used with gluten in preparing non gluten meal to

cause a reaction. Remember how the Jews use a new plate for certain things

to

avoid cross contamination? Yes, those exposures to gluten are deadly to

those sensitive.

Thanks again.

Drissia

I append a discussion of controlling dopamine.

Summarized these are points of interest:

The following things enhance dopamine levels:

1. Stress, and these kids are stressed to the breaking. High adrenaline

levels promote high dopamine levels that, among other things, is

vasoconstrictive.

2. Mercury and cadmium toxicity, and probably other metals. Cadmium

suppresses norepinephrine and serotonin, but not dopamine. Soy and flax oils

and

bleached flours increase cadmium and lower acetylcholine, leading to

anxieties and stereotypes of Autism.

Magnesium, calcium, selenium, zinc, melatonin, and metallothionein protect

the cells against cadmium and mercury, and germanium protects the liver

against damage from cadmium. Heavy metals can be chelated by oral

supplements

of Ambrotose AO™, IP-6 (phytic acid), zinc, manganese, selenium,

N-acetylcysteine (NAC), serine, melatonin, Cilantro, transdermal or oral

glutathione, and vitamins B6, C, and E. The initial treatment must be

gradual to avoid

a sudden dumping of metal toxins from tissues, which could cause kidney

damage and a worsening of symptoms.

3. Caffeine and nicotine. Avoid all exposure to second-hand smoke.

Cigarette smoke prevents the breakdown of dopamine.

4. Blocking of the NMDA receptors reducing glutamate transmission.

The NMDA receptors can affect different persons differently. Typically,

activating of the NMDA activates a signal for a body function. Repeatedly

signaling for that activity can cause overactivity (excitotoxity),

hyperactivity, and even neuronal death. If overactivity is evident, then

blocking

needs to be promoted. If underactivity is evident, then activation is

desired.

These snips present the dilemma of determining what is needed.

>>> N-Methyl d Aspartate receptor (NMDA is activated mainly to amplify the

effect of glutamate during periods of especially intense excitation. Since

the blockade of NMDA receptors in the cerebral cortex enhances the release

of dopamine from lower brain regions, reduced glutamate transmission could

be the ultimate cause of excessive dopamine activity in the brains of

schizophrenic patients.

High levels of another NMDA receptor blocking agent, kynurenic acid, are

found in the spinal fluid of patients with AIDS dementia and in many

autistic children. The amino acid glycine and (at much lower doses) its

chemical

relative, the antitubercular drug D-cycloserine, indirectly activate NMDA

receptors and may reduce apathy, withdrawal, and cognitive impairment in

schizophrenic patients. >>>

The natural NMDA receptor blocking agent (calcium channel blocker) is

magnesium, manganese, and zinc. We normally need a blocker not an activator.

The schizophrenic/autistic who is apathetic apparently need glycine as an

activator. <<<

5. A deficiency of vitamin B6, zinc, and/or acetylcholine. Yet building

acetylcholine may be contraindicated. DMAE is the best way to supply choline

and build acetylcholine, but that is very damaging to anyone who is

undermethylated.

6. Clostridia overgrowth. They produce dopamine in the gut and it is

absorbed.

7. Subclinical PKU enhances dopamine levels. One suffering high dopamine

should test for PKU.

8. Amphetamines and cocaine greatly increase dopamine levels. Addicts are

self-medicating.

9. Excitotoxic conditions tend to diminish GABA. The tetanus virus

inhibits GABA. A cautious supplementation of GABA may be indicated.

10. Phenolics prolong the life of and intensify cellular responses to

catecholamines (epinephrine, norepinephrine, etc.). They each act as cardiac

stimulants. Nicotine (and probably caffeine) was observed to have a

pronounced effect on biological membranes, that is, it increases the

permeability of

these membranes to certain pharmacologically active substances, such as

norepinephrine, epinephrine, dopamine, etc. Peristalsis is increased in the

intestine and distribution of blood is altered by these phenolics because

of sensitizing smooth muscles to epinephrine, norepinephrine, and other

physiological stimulants. This is particularly vital to those diagnosed as

PST.

There must be an aggressive effort to " unload the donkey " .

Love,

Willis

I came across these bits of information that offer a new insight into

controlling dopamine without drugs. If you wish, we can talk about it. (Some

of

this is a repeat of some of the above.)

>>>Experiments on mice at Massachusetts General Hospital showed that

caffeine could maintain levels of dopamine in the brain, a neurotransmitter

that

allows brain cells to communicate.>>>

Additionally:

>>>Dopamine and norepinephrine levels can be raised by eating a high

protein meal and by using a supplement of the amino acid phenylalanine or

tyrosine. >>>

It would appear that one should avoid caffeine and high protein meals or

dopaminergic supplements if taking dopamine antagonists like Zyprexa, or

Risperdal.

A lack of zinc (a widespread lack among us) will cause over-activity of

these catecholamine neurotransmitters (dopamine, epinephrine, and

norepinephrine).

>>>Citation: Faro LR, do Nascimento JL, Alfonso M, et al. Protection of

methylmercury effects on the in vivo dopamine release by NMDA receptor

antagonists and nitric oxide synthase inhibitors. Neuropharmacology. 2002

Sep42(5)612-8. PMID:11985818.

Abstract: The possible protective effects of NMDA receptor antagonists

dizocilpine (MK-801) and D(-)-2-amino-5-phosphonopentanoic acid (AP5), and

nitric oxide synthase (NOS) inhibitors L-nitro-arginine methyl ester

(L-NAME)

and 7-nitro-indazol (7-NI) on the methylmercury (MeHg)-induced dopamine

(DA) release from rat striatum were investigated using in vivo

microdialysis.

Intrastriatal infusion of 400 microM or 4 mM MeHg increased the

extracellular DA levels to 1941+/-199 and 7971+/-534% with respect to basal

levels.

Infusion of 400 microM or 4 mM MeHg in 400 microM MK-801 pretreated animals,

increased striatal DA levels to 677+/-126 and 2926+/-254%, with respect to

basal levels, these increases being 65 and 63% smaller than those induced

by MeHg in non-pretreated animals. Infusion of 400 microM or 4 mM MeHg in

400 microM AP5 pretreated animals, increased striatal DA levels to 950+/-234

and 2251+/-254% with respect to basal levels, these increases being 51 and

72% smaller than those induced by MeHg in non-pretreated animals. Infusion

of 400 microM MeHg in 100 microM L-NAME or 7-NI pretreated animals,

increased the extracellular DA levels to 1159+/-90 and 981+/-292%, with

respect

to basal levels, these increases being 40 and 50% smaller than those induced

by MeHg in non-pretreated animals. In summary, MeHg acts, at least in

part, through an overstimulation of NMDA receptors with possible NO

production

to induce DA release, and administration of NMDA receptor antagonists and

NOS inhibitors protects against MeHg-induced DA release from rat striatum.

>>>

Apparently, mercury can be a cause of excess dopamine activity.

Many drugs control " excess " dopamine, whether Ritalin for ADHD or Zyprexa

for psychosis. Unfortunately, they have horrendous side effects. Nutrients

can be balanced by avoiding certain substances or by supplementing the

right natural-food substances, without the side effects. This from Dr. Wm.

Walsh of Pfeiffer Treatment Center is vital to understanding this:

Choline adds methylation to DNA and would seem the " right " thing for

building acetylcholine to balance the effects of dopamine. This letter shows

why

this is not necessarily true:

Kathy,

The benefits for choline are very significant for overmethylated persons,

but can harm undermethylated persons. This seems counter-intuitive since

choline enhances methylation. Here’s the reason: Choline supplements

increase

the production of acetylcholine, a dominant neurotransmitter in the brain.

Acetylcholine is anti-dopaminergic, meaning it reduces brain dopamine

levels. Undermethylated persons tend to be depressed in dopamine & the net

effect of choline is to make it worse. We learned this the hard way in our

early clinical practice – Undermethylated patients had nasty side effects

from

choline, but the overmethylated persons thrived on it. We now give DMAE to

all overmethylated persons --- Choline can’t pass the blood/brain barrier,

but DMAE readily passes into the brain. DMAE is a “vitamer” that converts

to choline, and helps reduce excess dopamine. This is especially potent in

helping overmethylated ADHD space cadets. There is a published study that

indicates DMAE is more effective than Ritalin for ADHD and LD kids.

Bill Walsh, MD,

Pfeiffer Treatment Center

Overmethylated, according to other communications with Dr. Walsh comprise

about 15% while undermethylated comprise about 55% of patients. That leaves

about 30% " normal " .

Bolte notes that tetanus infection of the intestines leads to the

formation of toxic compounds called phenols. As a corrosive substance,

phenol (also

known as carbolic acid) denatures proteins and generally acts as a

protoplasmic poison. Studies of autistic individuals have detected markedly

elevated levels of the phenolic metabolite of tyrosine (precursor of

dopamine)

called 3-(3-hydroxyphenyl) - 3-hydroxypropionic acid (HPHPA). Several

autistic children with high HPHPA levels, " have shown a significant

reduction in

stereotyped behaviors when treated with antimicrobials effective against

intestinal Clostridia " -a genus of bacteria that includes tetanus. " When

certain bacteria of the CLOSTIRIDUM family (genus) are present in high

numbers,

phenylpropionic acid or 3-hydroxytrosine may be formed in the intestinal

tract. Either of these compounds may then be converted to

3-hydroxphenyl-propionic acid that is, in turn, converted to HPHPA by the

enzymes in the human

mitochondria that break down fatty acids " - Shaw, Great Plains

Laboratory.

" We have noticed that the molar ratio of the urinary concentration of the

dopamine metabolite homovanillic acid (HVA) to that of the

epinephrine/norepinephrine (adrenaline/noradrenaline) metabolite

vanillylmandelic acid

(VMA) in urine is commonly elevated when HPHPA is elevated. This appears to

indicate that a by-product involved in the formation of HPHPA likely

inhibits

the conversion of dopamine to norepinephrine, leading to relative dopamine

excess. Animal studies indicate that dopamine neurons mediate behaviors

such as hyperactivity and stereotypical behaviors common in autism. Of

course,

the drugs such as the phenothiazines and Haloperidol (and Risperdal),

commonly used to treat autism and schizophrenia, are well known to block the

action of excessive dopamine at the receptor level " -Biological Treatments

for

Autism and PDD, Wm. Shaw. It is noted that excess dopamine contributes to

tics, OCD, and Exposure Anxiety that keeps the Autistic child in constant

fight-or-flight mode.

Additionally, phenolics prolong the life of and intensify cellular

responses to catecholamines (epinephrine, norepinephrine, etc.). They each

act as

cardiac stimulants which accounts for the accelerated pulse that Dr. Arthur

F. Coca so wisely deduced was symptomatic of an allergenic response.

Nicotine (and probably caffeine) was observed to have a pronounced effect on

biological membranes, i.e., it increases the permeability of these membranes

to certain pharmacologically active substances, such as norepinephrine,

epinephrine, dopamine, etc. Peristalsis is increased in the intestine and

distribution of blood is altered by these phenolics because of sensitizing

smooth muscles to epinephrine, norepinephrine, and other physiological

stimulants. There is evidence for increased entry of potassium ions into the

cell

under the influence of epinephrine. This could account for the electrolyte

imbalances and water retention (edema) noted in allergies.

Now the $64.00 question is, what raises HPHPA and interferes with the

neurotransmitters? That is a well-known answer. It is from the amino acid

phenylalanine! Now, why would this essential amino acid be a problem? Two

reasons: 1) you inherited a problem with metabolizing it called

Phenylketonuria

(PKU). This is a condition tested for today at birth, and if found, a diet

free of phenylalanine is prescribed, but it is notorious that the guidelines

for treating what I will call subclinical phenylketonuria is allowing many

to have the problem without being treated. This could be you. 2)

Clostridia overgrowth. When these are present in high numbers, the

phenylpropionic

acid or 3-hydroxytyrosine may be formed by these bacteria from phenylalanine

in the intestinal tract. What is the chance you have clostridia? You might

want to have an OAT and a stool test by Great Plains Laboratory to

determine if you have the gut problem, and you could have your GP run a test

for

Phenylketonuria. If one or both of these prove to be a cause of high

dopamine, then you are drug free! If your PKU test shows a value 5 or higher

treat for PKU (restrict phenylalanine). If suffering Clostridia, kill them

off.

The children treated for clostridia (usually with Flagyl™) become more

sociable, speak more, improve their eye contact, and are less hyperactive

and

hypersensitive. It should be noted that very high doses of L. Acidophilus

GG is usually equally effective as metronidazole (Flagyl™). Additionally,

Flagyl™ has a lot of side effects, and can upset the ecological balance in

the gastrointestinal tract and lead to a yeast overgrowth. Dr. Shaw warns

that the die-off effect can be even more severe than that of Candida. Some

combination of AlkaSeltzer Gold™, bentonite clay, and charcoal, should be

used

to minimize the die-off effect and protect from damage.

Bolte adds, " Parents also noted that regression occurred very quickly "

after treatment was discontinued. Given these findings, Bolte says,

" Parents,

doctors, and researchers must combine efforts to determine if some people

diagnosed as autistic are actually suffering from unrecognized forms of

sub-acute tetanus. " This is very significant to that large block of children

who do not handle phenol well (PST). The use of ORGANIC ACID TESTING (OAT)

can provide a valuable tool guiding therapy so that harmful microorganisms

may be eliminated before treatments with amino acids like phenylalanine that

might actually cause neuropsyciatric symptoms to worsen. It is most

interesting to note that phenol poisoning, as suffered by the PST child,

deadens

the nerves endings much as does aspirin (a phenol), thereby masking pain.

In addition, she notes, inhibitory neurons that release the

neurotransmitter GABA are a preferred target for tetanus neurotoxins-and the

Purkinje

cells of the cerebellum, that often appear highly abnormal in autistic

individuals, are inhibitory neurons that release GABA. Additionally, GABA is

reported to stimulate the brain to release human growth hormone (HGH), and

to

stimulate the anterior pituitary function.

Glutamine, a precursor of GABA, readily passes through the blood-brain b

arrier and is a good supplement to take if one wants to increase brain

levels

of GABA, since glutamine, once it is in the brain, converts into GABA,

however, excess glutamine can become excitotoxic. Due to that possibility,

GABA may be the preferred supplement. GABA activity is found in glands

controlled by the sympathetic nervous system, namely: the pancreas and

thymus. It

is estimated that 30-40% of all CNS neurons utilize GABA as their primary

neurotransmitter! Glutamic acid decarboxylase (GAD) the active enzyme

capable of decarboxylating glutamate to GABA requires pyridoxal 5-phosphate

(P5P)

as cofactor. This enzyme found in the liver is often the target of

autoimmune attack in type I diabetics and when inhibited, can lead to

excitotoxicity from unused glutamate.

When there is not enough GABA a person can have a seizure because

receiving neurons can be flooded with signals that say, " pass on this

message. " A

different type of neurotransmitter that promotes message transfer triggers

the " go " messages. The charged signals they set off are positive. This time,

more positively charged sodium particles (Na+) enter the neuron, which

tells the receiving neurons to pass on the message. Valproic Acid

(Depakote™),

on the other hand, blocks GABA transaminase activity, thereby elevating

GABA levels, thus alleviating seizures. Why depend on a drug that robs the

body of L-carnitine and folic acid, and probably vitamin E and

alpha-ketoglutaric acid, when GABA can be increased nutritionally with

glutamine, zinc,

and P5P (or GABA)? Further, Depakote™ (Epilum) is a bad choice of

anticonvulsants due to the risk of fatal hepatotoxicity, and it acts on the

metabolic

pathways, which could further lower the platelet levels. The

hepatotoxicity is probably due to valproate-induced carnitine deficiency.

Drug induced tremors and tics are common, and Depakote™ can cause them. To

prevent, use at least 333 mg each of vitamins C and niacinamide, and 66 mg

each of vitamins B6 and E with a good broad-based, vitamin-mineral

supplement. In one ten-year study, not a single case occurred! If already

suffering the devastating effects of this doctor-induced condition, use 5 to

10

times as much, and pray. I believe Ambrotose® and PhytoAloe®, and PLUS by

Mannatech, Inc. would be mandatory. Of course, when using Depakote™,

supplement

Carnitine and folic acid also.

>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>

Dopamine increases proportionately to the amount of stress. 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.

Caffeine 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.

>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>..

dopamine

Dopamine is a chemical naturally produced in the body. In the brain,

dopamine functions as a neurotransmitter, activating dopamine receptors.

Dopamine is also a neurohormone released by the hypothalamus. Its main

function as

a hormone is to inhibit the release of prolactin from the anterior lobe of

the pituitary.

Dopamine can be supplied as a drug which acts on the sympathetic nervous

system, producing effects such as increased heart rate and blood pressure.

However, since dopamine cannot cross the blood-brain barrier, dopamine given

as a drug does not directly affect the central nervous system. To increase

the amount of dopamine in the brain of patients with diseases such as

Parkinson's disease, a synthetic precursor to dopamine such as L-DOPA can be

given, since this will cross the blood-brain barrier. (DMAE would be

contraindicated for it will cross the barrier and generate acetylcholine.)

Biochemistry

Dopamine molecule

Enlarge

Dopamine molecule

Dopamine has the chemical formula (C6H3(OH)2-CH2-CH2-NH2). Its chemical

name is 4-(2-aminoethyl)benzene-1,2-diol and it is abbreviated " DA. "

As a member of the catecholamine family, dopamine is a precursor to

epinephrine (adrenaline) and norepinephrine (noradrenaline) in the

biosynthetic

pathways for these neurotransmitters. Arvid Carlsson won a share of the 2000

Nobel Prize in Physiology or Medicine for showing that dopamine is not

just a precursor to these, but is a neurotransmitter as well.

Dopamine is synthesized in the body (mainly nervous tissue and adrenal

glands) by the decarboxylation of DOPA by aromatic-L-amino-acid

decarboxylase.

In neurons, dopamine is packaged after synthesis into vesicles, which are

then released in response to the presynaptic action potential. The

inactivation mechanism of neurotransmission are 1)uptake via a specific

transporter; 2) enzymatic breakdown; and 3) diffusion. Uptake back to the

presynaptic

neuron via the dopamine transporter is the major role in the inactivation

of dopamine neurotransmission. The recycled dopamine will face either

breakdown by an enzyme or be re-package into vesicles and reused.

Functions of Dopamine in the Brain

Role in Movement

Dopamine is critical to the way the brain controls our movements and is a

crucial part of the basal ganglia motor loop. Shortage of dopamine,

particularly the death of dopamine neurons in the nigrostriatal pathway,

causes

Parkinson's disease, in which a person loses the ability to execute smooth,

controlled movements.

Role in Cognition and Frontal Cortex Function

In the frontal lobes, dopamine controls the flow of information from other

areas of the brain. Dopamine disorders in this region of the brain can

cause a decline in neurocognitive function, particularly those linked to

memory, attention, and problem solving. This function is particularly

related to

the mesocortical dopamine pathway.

Role in Pleasure and Motivation

Dopamine is commonly associated with the 'pleasure system' of the brain,

providing feelings of enjoyment and reinforcement to motivate us to do, or

continue doing, certain activities. Certainly dopamine is released

(particularly in areas such as the nucleus accumbens and striatum) by

naturally

rewarding experiences such as food, sex, use of certain drugs and neutral

stimuli that become associated with them. This theory is often discussed in

terms of drugs (such as cocaine and amphetamine) which seem to directly or

indirectly related to increase dopamine in these areas, and in relation to

neurobiological theories of addiction, which argue that these dopamine

pathways

are pathologically altered in addicted persons. The mechanism of cocaine

and amphetamine is different. Cocaine is acting as dopamine transporter

blocker to competitively inhibit dopamine uptake to increase the lifetime of

dopamine in synapse, while amphetamine is acting as a dopamine transporter

substrate to competitively inhibit dopamine uptake (sic) and increase the

dopamine efflux via dopamine transporter.

However, the idea that dopamine is the 'reward chemical' of the brain now

seems too simple as more evidence has been gathered. Dopamine is known to

be released when unpleasant or aversive stimuli are encountered, suggesting

that it is not only associated with 'rewards' or pleasure. Also, the firing

of dopamine neurons occurs when a pleasurable activity is expected,

regardless of whether it actually happens or not. This suggests that

dopamine may

be involved in desire rather than pleasure. Drugs that are known to reduce

dopamine activity (e.g. antipsychotics) have been shown to reduce people's

desire for pleasurable stimuli, despite the fact that they will rate them

as just as pleasurable when they actually encounter or consume them. It

seems that these drugs reduce the 'wanting' but not the 'liking', providing

more evidence for the desire theory.

Other theories suggest that the crucial role of dopamine may be in

predicting pleasurable activity. Related theories argue that dopamine

function may

be involved in the salience ('noticeableness') of perceived objects and

events, with potentially important stimuli (including rewarding things, but

also things which may be dangerous or a threat) appearing more noticeable or

more important. This theory argues that dopamine's role is to assist

decision making by influencing the priority of such stimuli to the person

concerned.

Dopamine and Psychosis

Disruption to the dopamine system has also been strongly linked to

psychosis and schizophrenia. Dopamine neurons in the mesolimbic pathway are

particularly associated with these conditions. This is partly due to the

discovery of a class of drugs called the phenothiazines (which block D2

dopamine

receptors) that can reduce psychotic symptoms, and partly due to the finding

that drugs such as amphetamine and cocaine (which are known to greatly

increase dopamine levels) can cause psychosis. Because of this, all modern

antipsychotic medication is designed to block dopamine function to varying

degrees.

See the article on the dopamine hypothesis of psychosis for a wider

discussion of this topic.

Major Dopamine Pathways

* mesocortical pathway

* mesolimbic pathway

* nigrostriatal pathway

* tuberoinfundibular pathway

See also

* addiction

* amphetamines

* antipsychotic

* catecholamine

* catechol-O-methyl transferase

* cocaine

* dopamine hypothesis of schizophrenia

* neurotransmitter

* Parkinson's disease

* schizophrenia

Phenethylamines

{2C-B} {2C-C} {2C-D} {2C-E} {2C-I} {2C-N} {2C-T-2} {2C-T-21} {2C-T-4}

{2C-T-7} {2C-T-8} {3C-E} {Amphetamine} {Bupropion} {Cathine} {Cathinone}

{Dimethylcathinone} {DOB} {DOI} {DOM} {Dopamine} {Br-DFLY} {Ephedrine}

{Epinephrine} {Escaline} {Fenfluramine} {MBDB} {MDA} {MDMA} {MDEA}

{Mescaline}

{Methamphetamine} {Methcathinone} {Methylphenidate} {Norepinephrine}

{Phentermine} {Salbutamol} {Tyramine}

This entry is from Wikipedia, the leading user-contributed encyclopedia.

It may not have been reviewed by professional editors (see full disclaimer)

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