Re: Discouraged!

[Guest guest]

Don't be discouraged we have all been there and at times continue to

be.

From what I understand not all children that are autistic have

apraxia. However I have read that sometimes children are misdiagnosed

with autism when they are really apraxic.

Regarding the MRI, what does the doctor hope to find out?

Next I would approach the school district with the doctor's

recommendation that your child receive a more intense schedule. Hold

your ground and don't let them tell you what they think is

appropriate. Did the school also do a full evaluation?

If he has sensory issues then OT services would help that as well as

the speech.

Lastly have you had an evaluation done by a speech therapist? Is this

where you got the possible apraxia diagnosis. See if you can get into

the developmental neurologist before December.

Good luck.

--- In @y..., Kristi Olsen <kristi_olsen@e...>

wrote:

> Hi,

> I have just a few questions. I have a 3.5 year old son. I had been

told

> that he very likely had apraxia. (He is very vocal, but non

verbal.) I took

> him to a dr. that has experience with children and delays. She

does NOT

> think he has verbal apraxia, but did say he had autistic

tendencies, some

> sensory issues, and possible obsessive-compulsive problems. I left

not

> knowing what to think. We scheduled a MRI in Sept. Does anyone

know what

> this test reveals or if it is even worth going through? I have an

appt.

> with a Ped. Neurologist in Dec. and she warned me about a lot of

blood tests

> they could possibly do. I'm not sure what to think. I went in

thinking

> speech therapy was my goal for him and now does he need more?

starts

> Special Ed Preschool tomorrow. He'll go two days a week, but the

dr we saw

> recommeded asking for the 4 day a week schedule.

> Also, I thought that the reason some Autistic children don't talk

WAS

> basically apraxia, that they go hand-in hand.

> Anyway can you tell I am confused as to what to think.

>

> Any feelings on MRI's or autisim, I would really love to hear.

>

> Thanks,

> Kristi (mom to 3.5 yrs with WHO KNOW!!)

[Guest guest]

Hi Kristi,

My son, 5.1, has a lot of dx's also. His dev. ped. has him listed as

apraxia, hypotonia, and global delays. I have had some professionals tell

me that he is autistic. He had an MRI done in May, 2000. It was a tough

thing for both of us to go thru, since he had to be put to sleep with a

needle in his hand. He cried himself to " sleep " . The MRI showed nothing

abnormal in his brain. I'm not sure what exactly they are looking for. I

have my theories about , tho. Towards the end of my pregnancy it was

discovered that his heart rate was dropping to as low as 60 bpm. I believe

that his problems were caused by a lack of oxygen to his brain. gets

ABA therapy in my home every day for 3 hours. Soon they want to start an

afternoon session, in addition to the morning session. Getting all of this

therapy can only catch them up that much sooner! If you can get your son

more class time, I think that would be a good thing. When was 3 and

started his special preschool, I didn't think he could handle that, either.

There were times that he took a little cat nap in the classroom! But he

ended up really enjoying himself. I don't send him there anymore b/c he

wasn't working hard enough. He needs the 1x1 therapy to really progress.

Hope this helps!

~~

in PA

[ ] Discouraged!

> Hi,

> I have just a few questions. I have a 3.5 year old son. I had been told

> that he very likely had apraxia. (He is very vocal, but non verbal.) I

took

> him to a dr. that has experience with children and delays. She does NOT

> think he has verbal apraxia, but did say he had autistic tendencies, some

> sensory issues, and possible obsessive-compulsive problems. I left not

> knowing what to think. We scheduled a MRI in Sept. Does anyone know what

> this test reveals or if it is even worth going through? I have an appt.

> with a Ped. Neurologist in Dec. and she warned me about a lot of blood

tests

> they could possibly do. I'm not sure what to think. I went in thinking

> speech therapy was my goal for him and now does he need more?

starts

> Special Ed Preschool tomorrow. He'll go two days a week, but the dr we

saw

> recommeded asking for the 4 day a week schedule.

> Also, I thought that the reason some Autistic children don't talk WAS

> basically apraxia, that they go hand-in hand.

> Anyway can you tell I am confused as to what to think.

>

> Any feelings on MRI's or autisim, I would really love to hear.

>

> Thanks,

> Kristi (mom to 3.5 yrs with WHO KNOW!!)

>

>

>

>

>

> _______________________________________________________

> Send a cool gift with your E-Card

> http://www.bluemountain.com/giftcenter/

>

>

>

>

>

> ****Official Statement from the 7/23,24/01 landmark apraxia conference is

NOW POSTED at http://www.apraxia.cc!!!!****

>

> Like information but not emails? Choose the option of " no emails web only "

to read, respond to, or post messages directly from the website. For all

the emails sent in one choose " digest. " If you need help with membership

options, please email , , or Rhonda at

-owner

>

> If you are looking for support in your own area, contact CHERAB's Outreach

Coordinator at nicole@...

>

> URL to the home page to change options/or to search the archives:

>

> Kaufman Kits & other products that may help:

http://shopinserviceinc.goemerchant2.com

>

> The opinions expressed on this forum are the opinions of the individuals,

not the CHERAB Foundation. Medical advice should be sought before

implementing any therapeutic treatment.

>

> Post message:

> List owner: -owner

> For more information: http://www.apraxia.cc http://www.omega3ri.org

>

>

>

[Guest guest]

Hi Kristie,

There is information from a Developmental Pediatrician on " what is

apraxia " with signs to look for that you can share with your child's

doctor at the CHERAB website http://www.apraxia.cc

If your child is nonverbal and three and a half years old it's

important to find out why. Seek evaluations from both medical and speech

professionals that are knowledgeable and experienced about apraxia and autism.

Not all professionals are, which is why we need to raise awareness.

As far as sensory issues, that is found in both autism and apraxia,

as well as other disorders, and can also be found to stand alone.

http://internalmedicine.medscape.com/IMNG/PediatricNews/2000/v34.n02/ped3402.42.\

01.html

There is a wealth of information/links at both http://www.apraxia.cc and in the

archives here. Just go to

childrenapraxianet

put key word(s) into the box that says " search archives " and then

when a page comes up, click on the messages of interest, and then

click on next at the bottom until you see all the messages that may

have information that can help you. Keep in mind that you may want

to use different types of words that mean the same thing: (IEP,

IEPs, school, advocacy, etc.) There is a huge amount of information

for example on amounts or types of therapy in the archives, and on

our website.

Here are two past messages from Developmental Pediatricians Dr. Agin and Dr.

Laveman that have information on apraxia and MRIs:

From: " Marilyn Agin M.D. "

Subject: re: aphasia vs. apraxia

I would like to respond to the questions that some parents are asking

re:aphasia vs. apraxia. One of the problems we have in discussing

childhood speech and language disorders is terminology.

I practiced speech pathology back in the 1970's. In graduate school

we had mostly learned about working with articulation disorders in

children, i.e. working on lisps, /th/ sound etc. There were groups

of research SLP beginning to talk about language disorders in

children separate from what we see in adults. The terminology

of " aphasia " and " apraxia " traditionally refers to older adults who

suffer strokes to the left side of the brain leaving them with

speech and language problems, and usually a paralysis of the right

side of the body called a hemiplegia. Adult aphasics may have

receptive (comprehension) and/or expressive (difficulty verbalizing)

language problems along with dysnomia (word finding problems), alexia

(reading problems) and agraphia(writing problems). They may also

have an apraxia with difficulty with the organization and sequencing

of speech sounds.

In attempts to describe what SLP researchers began seeing in

children, i.e. receptive/expressive language problems, and a motor

planning disorder involving the speech mechanism, they borrowed the

adult terminology and began to talk about childhood aphasia and

developmental apraxia. Purists will say you cannot have these

disorders in childhood because the term implies that the individual

had language and then had some brain insult (brain damage either due

to a stroke, head injury, or accident) that caused them to lose their

speech and language abilities. Others adopted the terminology

because the speech/language characteristics were so similar to the

adult model.

This is part of the reason why some neurologists do not acknowledge

apraxia as a diagnosis in children. There is a dilemma about what to

call children who are having difficulty developing speech and

language. I personally do not use the term childhood aphasia any

more and refer mostly to children having a receptive and/or

expressive language delay or disorder. Some therapists do and

that is ok as long as you define your terms.

Most children with

speech-language disorders have some neurologic reason for their

problems that is not easily identified in terms of time of onset.

Also it does not usually show up on MRI or CAT scan since it is more

subtle than the technology can show us. We will say they have

a " static (not progressing) encephalopathy (brain damage) of

probable prenatal origin of unknown etiology " . (What we are saying

is that something went wrong probably during the gestation period).

I would like to see the use of SPECT scans which documents blood flow

in the brain used more, as one small study in 1989 found reduced

blood flow in the frontal area of the brain involving Broca's area.

That is the expressive language area of the brain. SPECT scans are

very expensive and are usually found in academic institutions. We may

incorporate using this technology as part of our EFA/apraxia research...

So in summary, those children identified as having an aphasia and

apraxia, will have a receptive and/or expressive language component

as well as a speech disorder related to motor planning and sequencing

sounds.

Hope this helps your understanding of the problem. Always ask the

professionals you see to define their terms (medical jargon!) to

comprehensible English!

Marilyn Agin, M.D

Medical Director CHERAB Foundation

http://www.apraxia.cc

From: " Lawrence Laveman " <laveman56@...>

Subject: MRI and role of developmental pediatrician

Hi Mitch:

Let's take your two questions individually

" Hi. My son is 5 years old, he has been dx with verbal

apraxia for 2 years now and has been receiving speech therapy for as

long. His neurologist is sending him for an MRI of the speech area of

his brain to rule out any lesions in that area. what to expect to

find from an MRI ( is there something that causes apraxia that will

show up on an MRI) "

An MRI of the brain will rule out several questions your neurologist

may have. First, is there any obvious structural malformation of

's brain that may be causing the apraxic findings. Second, is

there an immaturity, in the absence of malformation, of the brain

itself that may explain the delays in skills - if your brain is

delayed in its maturation, it is logical to assume that the skills it

is capable of handling will also be delayed. Third, is there any

vascular (blood vessel - related) changes in his brain - any areas of

decreased blood supply, scar tissue, etc.

" His neurologist has suggested we make an appointment for him to see

an developmental Pediatrician, which we did with great effort, the

developmental pediatrician couldn't understand why we wanted him to

see , after describing his problems and being referred to him

by a neurologist that works with him, it took several phone calls to

the neurologist, the neurologist office to the pediatrician, the

pediatrician to us to finally get him an appointment in the middle of

August? Also should I consider looking for a different pediatrician

since their seems to be a lack of interest in my sons case already

with the unwillingness of them to give us an appointment. "

Unfortunately, there are more ped neurologists than DBP's, and it is

sad but not surprising that there is a greater delay in getting an

appointment with one. Don't view this as a " lack of interest " - on

the contrary, you are doing the best you can given the circumstances.

I would advise you to call around - other developmental peds

specialists may have a shorter waiting list. Your general

pediatrician is most likely not disinterested in 's case, but

more likely not well-informed enough to respond to the issues you

raise. That is why people like myself and Dr. Agin do what we

do.

" And what does a developmental pediatrician do different than that of

a regular pediatrician? "

Ah, my friend, that would take a dissertation (and in fact a talk I

often give...). In summary, we have gone on from pediatric residency

to spend two to three additional years working with children having

developmental disabilities in a supervised training program at a

center where evaluations are done. The two training programs in New

Jersey are at UMDNJ-NJMS (Hackensack) and at UMDNJ-RWJMS (New

Brunswick), two of the largest centers for evaluation of children in

the state. Most of us continue to be affiliated with hospital-based

programs in developmental disabilities - often in state-funded Child

Evaluation Centers (there are nine in NJ). So, in essence, you see a

lot, you do a lot, you deal with these issues day in and day out,

something that general pediatricians don't necessarily do. Just as

endocrinologists know more about your glands, and nephrologists your

kidneys, a developmental pediatrician can help you navigate the maze

of services your child may need, and create a " medical home " , as the

American Academy of Pediatrics refers to it, for your child.

Email me if you have any further questions.

Larry Laveman, MD

Consultant, CHERAB Fdn.

http://www.apraxia.cc

--- In @y..., Kristi Olsen <kristi_olsen@e...>

wrote:

Hi,

I have just a few questions. I have a 3.5 year old son. I had been

told that he very likely had apraxia. (He is very vocal, but non

verbal.) I took him to a dr. that has experience with children and

delays. She does NOT think he has verbal apraxia, but did say he had

autistic tendencies, some sensory issues, and possible obsessive-

compulsive problems. I left not knowing what to think. We scheduled

a MRI in Sept. Does anyone know what this test reveals or if it is

even worth going through? I have an appt. with a Ped. Neurologist in

Dec. and she warned me about a lot of blood tests they could possibly

do. I'm not sure what to think. I went in thinking speech therapy

was my goal for him and now does he need more? starts Special

Ed Preschool tomorrow. He'll go two days a week, but the dr we saw

recommeded asking for the 4 day a week schedule. Also, I thought

that the reason some Autistic children don't talk WAS basically

apraxia, that they go hand-in hand. Anyway can you tell I am

confused as to what to think.

Any feelings on MRI's or autisim, I would really love to hear.

Thanks,

Kristi (mom to 3.5 yrs with WHO KNOW!!)

[Guest guest]

My diet is 100% better, my calories are lower..and yet, my weight loss seems to have stalled and bounces within a two lb range and has done so for the last 6 weeks.

How do the rest of you keep on the path when this type of thing happens?

Thanks!

[Guest guest]

Try a new strategy.

Is your goal health and longevity, or weight loss qua weight loss?

>From: bernadettepawlik@...

>Reply-

>

>Subject: [ ] Re: Discouraged!

>Date: Wed, 28 Jul 2004 12:43:44 EDT

>

>My diet is 100% better, my calories are lower..and yet, my weight loss

>seems

>to have stalled and bounces within a two lb range and has done so for the

>last

>6 weeks.

>

>How do the rest of you keep on the path when this type of thing happens?

>

>Thanks!

[Guest guest]

Or stick to the same strategy and revise your thinking.

I remember plateauing for what seemed like MONTHS while losing. But that

was normal. After a few months I started losing again. So have patience.

In any case, if you are on a CRON diet, focusing on weight is not the goal.

Better health is. So keep to your healthier diet and focus on that. In

fact the mice that lost the least weight on CRON lived the longest.

One tip: are you using high fiber (with meals) such as guar? That seems to

aid in weight loss.

Also, you don't give us any stats. How tall are you? How much do you

weigh? Often, we THINK we should weigh less (our society's images of

fashion models etc) when such weight is unattainable for most people.

on 7/28/2004 12:50 PM, Dowling at dowlic@... wrote:

> Try a new strategy.

>

> Is your goal health and longevity, or weight loss qua weight loss?

>

>

>> From: bernadettepawlik@...

>> Reply-

>>

>> Subject: [ ] Re: Discouraged!

>> Date: Wed, 28 Jul 2004 12:43:44 EDT

>>

>> My diet is 100% better, my calories are lower..and yet, my weight loss

>> seems

>> to have stalled and bounces within a two lb range and has done so for the

>> last

>> 6 weeks.

>>

>> How do the rest of you keep on the path when this type of thing happens?

>>

>> Thanks!

>

>

[Guest guest]

Hi Bernadette:

Do you weigh yourself every morning AND THEN PLOT THAT WEIGHT ON A

CHART SOMEWHERE? (Fitday.com for example)

I doubt you or anyone else ever 'plateaus' when consuming a CR diet.

In my case FOR CERTAIN, while it may look like a plateau the problem

is not plateauing. The problem is that everyone's weight varies so

much from day to day and week to week for many reasons, that it is

very difficult to see the trend.

By far the single largest reason for these fluctuations in weight is

the diuretic/anti-diuretic content of the foods we eat. This causes

HUGE fluctuations in weight because of the amount of water retained

or discarded by your body in response to those foods. (In my case

the fluctuations in the past six months have been from five pounds

below the trend to five pounds above it. Yes. A ten pound range.

But my trend weight has fallen about thirteen pounds as planned. Yet

that is barely more than the fluctuation!)

For example, when you drink tea you lose a large amount of water and

lose weight, artificially. If you drink wine, or a salty (japanese,

perhaps) meal, your body will retain all the water it can, and you

artificially gain weight. In the case of salt (ever wonder why

establishments that sell beer provide SALTY pretzels FOR FREE?) the

reason for it is that your body makes you thirsty as a means of

trying to dilute the salt concentration in your body until it has had

time to excrete the excess, which takes a few days.

Take some of my numbers as an example. Had I not been plotting the

data daily, and had I not understood the 'diuretic issue', I could

easily have been fooled into thinking that my weight had not only

plateaued, but gone UP sharply!

Around 17th February my weight was 164 pounds (an aberration on the

low side). On 12th June it was 169½ pounds. Apparently a five pound

weight GAIN in nearly four months!!! But on 19th July I was 157!!!

I am now back up to ~161.

The reason was that the February number was a completely unrealistic,

lots-of-tea recently, low point, five pounds below trend. Similarly

my mid-June number was a totally unrealistically high number, five

pounds above trend, because of a weekend where I drank wine and had a

lot of (very healthy but always salty) japanese food.

The simple fact is that the TREND in my weight has been down at a

pretty steady rate of half a pound a week for six months. But the

fluctuations above and below that trend make it difficult to see what

the trend is unless you plot it and recognize the aberrations for

what they are. That is, understand what causes the aberrations and

when they happen, recognize them.

There is a simple solution. It is in the second half of the very

first paragraph of this post.

Rodney.

> My diet is 100% better, my calories are lower..and yet, my weight

loss seems

> to have stalled and bounces within a two lb range and has done so

for the last

> 6 weeks.

>

> How do the rest of you keep on the path when this type of thing

happens?

>

> Thanks!

[Guest guest]

Hi folks:

If anyone can tell me how to link up in some way to the chart of my

weight at Fitday.com so that people here can see it, I would be happy

to do so.

It really would demonstrate, I think, how easy it is to be tricked

into believing one is 'plateaued'. When the real explanation is the

difficulty in discerning the gradual down trend from the substantial

noise in the data.

Anyway, if you know approximately how many calories you are burning

and how many you are eating and convert that information into an

approximation of your weekly weight loss, and recognize the things in

your diet that cause the fluctuations, it should help discern the

trend.

Rodney.

> > My diet is 100% better, my calories are lower..and yet, my weight

> loss seems

> > to have stalled and bounces within a two lb range and has done so

> for the last

> > 6 weeks.

> >

> > How do the rest of you keep on the path when this type of thing

> happens?

> >

> > Thanks!

[Guest guest]

This is completely normal. The body has an amazing ability to adapt

to different metabolic states in terms of preserving body fat,

negating an obvious calorie deficit for periods of time. The effect

is more pronounced in women, than in men. You can either wait it out

or you could consider the below to " unstuck " you:

1. 50% protein, 25%-30% carbohydrates, 20%-25% fat. But keep net

carbohydrates at least 130 grams a day for brain function.

2. 7-Keto DHEA (normalizes thyroid) & Synephrine (increases

metabolism).

Logan

> My diet is 100% better, my calories are lower..and yet, my weight

loss seems

> to have stalled and bounces within a two lb range and has done so

for the last

> 6 weeks.

>

> How do the rest of you keep on the path when this type of thing

happens?

>

> Thanks!

[Guest guest]

And where do you get this information?

on 7/29/2004 9:35 PM, loganruns73 at loganruns73@... wrote:

> This is completely normal. The body has an amazing ability to adapt

> to different metabolic states in terms of preserving body fat,

> negating an obvious calorie deficit for periods of time. The effect

> is more pronounced in women, than in men. You can either wait it out

> or you could consider the below to " unstuck " you:

>

> 1. 50% protein, 25%-30% carbohydrates, 20%-25% fat. But keep net

> carbohydrates at least 130 grams a day for brain function.

>

> 2. 7-Keto DHEA (normalizes thyroid) & Synephrine (increases

> metabolism).

>

> Logan

>

[Guest guest]

This is anecdotal evidence from the field of sports nutrition,

specifically body-building. I'm not aware of any published,

empirical research specificing addressing the protocol.

The purpose of 7-Keto DHEA is to safely upregulate the thyroid gland

to increase thermogenesis, i.e. the uncoupled oxidation of fatty

acids contained within brown adipose tissue. Hypothyroidism is one

of the symptoms of calorie restriction as well as the " normal " age-

onset hormonal decline.

Synephrine is one of several beta3-adrenoceptor agonists which

triggers one of the pathways for fat loss, but is not a strong

nervous system stimulator. So while guarana and other stimulants can

and do work, the problem with stimulating directly via the nervous

system is the weight-gaining rebound effect when the stimulation is

ceased (not to mention the potential for physical addiction!). It is

better and safer to rely on CRON as a foundation for creating an

energy deficit.

And while I'm at it, CLA shrinks the size of fat cells but doesn't

reduce their number at all.

Logan

7-KETO DHEA

Relationship of dehydroepiandrosterone and its 7-hydroxylated

metabolites to thyroid parameters and sex hormone-binding globulin

(SHBG) in healthy subjects.

Hampl R, Hill M, Bilek R, Starka L.

Institute of Endocrinology, Prague, Czech Republic. rhampl@...

Clin Chem Lab Med. 2003 Aug;41(8):1081-6.

The concentrations of four immunomodulatory steroids, namely

dehydroepiandrosterone (DHEA), its sulfate and its 7-hydroxylated

metabolites, and sex hormone-binding globulin (SHBG) and major

laboratory parameters of thyroid function were determined in sera

from 104 healthy females and 48 males, screened for iodine deficiency

in one region of the Czech Republic. The mutual relationships of the

laboratory parameters were investigated by using four statistical

approaches: correlation analysis, principal component analysis,

canonical correlation and linear model relationship. In addition to

expected correlations among thyroid parameters and substrate-product

relationships among the steroids, several new relationships were

revealed: The only thyroid parameter tightly correlating with SHBG

was free triiodothyronine. The latter hormone was also associated

with one of the 7-OH-DHEA epimers, namely with 7beta-OH-DHEA. Thyroid

hormones are known to possess thermogenic properties, as does another

7-oxygenated DHEA metabolite, 7-oxo-DHEA, the major metabolite of

which is 7beta-OH-DHEA. It may indicate a link between the two

thermogenic factors. The results should serve for further

investigation of changes in the thyroid hormone concentrations,

together with SHBG and dehydroepiandrosterone metabolites, under

various pathological situations.

---

7-oxo-DHEA and Raynaud's phenomenon.

Ihler G, Chami-Stemmann H.

Department of Medical Biochemistry and Medical Genetics, Texas A & M

College of Medicine, College Station 77843, USA. gmihler@...

Med Hypotheses. 2003 Mar;60(3):391-7.

Patients with Raynaud's phenomenon have abnormal digital

vasoconstriction in response to cold. The pathogenesis remains

unknown but may involve a local neurovascular defect leading to

vasoconstriction. Diagnosis of primary Raynaud's phenomenon is based

on typical symptomatology coupled with normal physical examination,

normal laboratory studies and lack of observable pathology by nail

fold capillaroscopy. Secondary Raynaud's phenomenon is known to occur

associated with several connective tissue diseases, vascular injury

due to repeated vibrational trauma, and other causes which produce

demonstrable vascular and microcirculatory damage. Treatment of

Raynaud's symptoms is conservative and aimed at prevention of

attacks. Patients are advised to remain warm and, if possible, to

live in warm climates. We suggest that an ergogenic (thermogenic)

steroid, 7-oxo-DHEA (3-acetoxyandrost-5-ene-7,17-dione), which is

available without prescription as the trademarked 7-keto DHEA, may be

very helpful in prevention of primary Raynaud's attacks by increasing

the basal metabolic rate and inhibiting vasospasm.

---

The effects of the ergosteroid 7-oxo-dehydroepiandrosterone on

mitochondrial membrane potential: possible relationship to

thermogenesis.

Bobyleva V, Bellei M, Kneer N, Lardy H.

Dipartimento di Scienze Biomediche, Universita di Modena, Italy.

Arch Biochem Biophys. 1997 May 1;341(1):122-8.

Administered 3 beta-hydroxyandrost-5-ene-7,17-dione (7-oxo-DHEA) is

more effective than 3 beta-hydroxyandrost-5-en-7-one (DHEA) as an

inducer of liver mitochondrial sn-glycerol-3-phosphate dehydrogenase

and cytosolic malic enzyme in rats. Like DHEA, the 7-oxo metabolite

enhances liver catalase, fatty acylCoA oxidase, cytosolic sn-glycerol-

3-phosphate dehydrogenase, mitochondrial substrate oxidation rate,

and the reconstructed sn-glycerol 3-phosphate shuttle. The

mitochondrial adenine nucleotide carrier is diminished by

thyroidectomy and is restored to normal activity by administering 7-

oxo-DHEA. The relationship between respiratory rate and proton motive

force across the mitochondrial membrane was measured in the

nonphosphorylating state. When treated with increasing concentrations

of respiratory inhibitors liver mitochondria from rats treated with 7-

oxo-DHEA or thyroid hormones show a more rapid decline of membrane

potential than do normal liver mitochondria. Thus 7-oxo-DHEA induces

an increased proton leak or slip as has been reported for the thyroid

hormone by M.D. Brand [(1990) Biochem. Biophys. Acta 1018, 128-133].

This process may contribute to the enhanced thermogenesis caused by

ergosteroids as well as by thyroid hormones.

SYNEPHRINE

Selective activation of beta3-adrenoceptors by octopamine:

comparative studies in mammalian fat cells.

Carpene C, Galitzky J, Fontana E, Atgie C, Lafontan M, Berlan M.

Institut National de la Sante et de la Recherche Medicale (INSERM),

Unite 317, Institut Federatif de Recherches 31, CHU Rangueil,

Toulouse, France. carpene@...

Naunyn Schmiedebergs Arch Pharmacol. 1999 Apr;359(4):310-21.

Numerous synthetic agonists selectively stimulate beta3-adrenoceptors

(ARs). The endogenous catecholamines, noradrenaline and adrenaline,

however, stimulate all the beta-AR subtypes, and no selective

physiological agonist for beta3-ARs has been described so far. The

aim of this study was to investigate whether any naturally occurring

amine can stimulate selectively beta3-ARs. Since activation of

lipolysis is a well-known beta-adrenergic function, the efficacy and

potency of various biogenic amines were compared with those of

noradrenaline, isoprenaline, and beta3-AR agonists 4-(- inverted

question mark[2-hydroxy-(3-chlorophenyl)ethyl]-amino inverted

question mark propyl)phenoxyacetate (BRL 37,344) and (R,R)-5-(2-

inverted question mark[2-(3-chlorophenyl )-2-hydroxyethyl]-amino

propyl)-1,3-benzo-dioxole-2,2-dicarboxylate (CL 316,243) by testing

their lipolytic action in white fat cells. Five mammalian species

were studied: rat, hamster and dog, in which selective beta-AR

agonists act as full lipolytic agents, and guinea-pigs and humans, in

which beta3-AR agonists are less potent activators of lipolysis.

Several biogenic amines were inefficient (e.g. dopamine, tyramine and

beta-phenylethylamine) while others (synephrine, phenylethanolamine,

epinine) were partially active in stimulating lipolysis in all

species studied. Their actions were inhibited by all the beta-AR

antagonists tested, including those selective for beta1- or beta2-

ARs. Octopamine was the only amine fully stimulating lipolysis in

rat, hamster and dog fat cells, while inefficient in guinea-pig or

human fat cells, like the beta3-AR agonists. In rat white fat cells,

beta-AR antagonists inhibited the lipolytic effect of octopamine with

a relative order of potency very similar to that observed against CL

316,243. Competitive antagonism of octopamine effect resulted in the

following apparent pA2 [-log(IC50), where IC50 is the antagonist

concentration eliciting half-maximal inhibition] values: 7.77

(bupranolol), 6.48 [3-(2-ethyl-phenoxy)-1[(1 S)-1,2,3,4-

tetrahydronaphth-1-ylaminol]-(2S)2-propanol oxalate, SR 59230A, a

beta3-selective antagonist], 6.30[erythro-D,L-1(7-lethylindan-4-

yloxy)-3-isopropylamino-+ ++butan-2-ol, ICI 118,551, a beta2-

selective antagonist] and 4.71 [(+/-)-[2-(3-carbomyl-4-

hydroxyphenoxy)-ethylamino]-3-[4-(1- methyl-4-trifluoromethyl-2-

imidazolyl)-phenoxy]2-propanolmethane sulphonate, CGP 20712A, a beta1-

selective antagonist]. Octopamine had other properties in common with

beta3-AR agonists: stimulation of oxygen consumption in rat brown fat

cells and very low affinity in displacing [3H]CGP 12,177 binding to

[beta1- or beta2-ARs in dog and rat adipocyte membranes. In Chinese

hamster ovary (CHO) cells expressing human beta3-ARs, octopamine

inhibited [125I]ICYP binding with only twofold less affinity than

noradrenaline while it exhibited an affinity around 200-fold lower

than noradrenaline in CHO cells expressing human beta1- or beta2-ARs.

These data suggest that, among the biogenic amines metabolically

related to catecholamines, octopamine can be considered as the most

selective for beta3-ARs.

>

> > This is completely normal. The body has an amazing ability to

adapt

> > to different metabolic states in terms of preserving body fat,

> > negating an obvious calorie deficit for periods of time. The

effect

> > is more pronounced in women, than in men. You can either wait it

out

> > or you could consider the below to " unstuck " you:

> >

> > 1. 50% protein, 25%-30% carbohydrates, 20%-25% fat. But keep net

> > carbohydrates at least 130 grams a day for brain function.

> >

> > 2. 7-Keto DHEA (normalizes thyroid) & Synephrine (increases

> > metabolism).

> >

> > Logan

> >