Addressing the french fry factor again(insulin-seratonin)

[Guest guest]

sorry to be so obsessive about the french fry question, but thought

you might find it relative to what I've been reading.

In regards to autism, children with ASD (from what I've been

reading) have extra serotonin and lack a transporter to actually be

able to use the serotonin. So, really they are deficient in

serotonin? So truly, a person with an inborn seratonin (transport)

error might try to compensate by using foods to increase seratonin

which tend to be carbs and sweets, which then tend to make a person

insulin resistant and then you have even less insulin for

transporting seratonin, which becomes a vicious cycle? I guess I

wonder now why do some people get seizures (if this is the case with

the seratonin transporter) or then some people just get anxiety

disorder instead? Or maybe the 30% of kids with epilepsy and autism

have the usual insults of autism injury AND this blood brain sugar

thing...leading to a starving brain, leading to seizures?

******************************************************

http://www.doctorezrin.com/pages/464980/

The chief clinically relevant symptoms of serotonin deficiency are:

1. Sleep disturbances, e.g. insomnia, middle-of-the-night

awakening, snoring, sleep apnea, and daytime fatigue. 2.

Carbohydrate cravings which temporarily provide a brief burst of

serotonin via an insulin-mediated increased transfer of tryptophane

(the precursor of serotonin) across the blood-brain barrier.

Although the comfort produced by the surge of serotonin is short-

lived, the calories consumed to produce it are more lasting.

*************************************************************

What really caught my eye was the carbohydrate vehicle of

transporting serotonin.

from:

http://www.shtup.com/naar/naarative2/hunt.htm

The Serotonin Gene

The serotonin transporter gene has been a puzzler. Cook and his team

looked at genes controlling serotonin in the first place because one

of the most robust findings in the biochemistry of autism has been

that approximately one quarter to one third of people with autism

show abnormally high levels of serotonin in the blood. And sure

enough, Cook and his team found, in three separate studies, a

statistically significant association between autism and a shortened

version of the promoter of the serotonin transporter gene, HTT.

However, while it was no surprise to find a serotonin gene involved

in autism, it did surprise everyone involved that the short form of

HTT turned up in all three studies. In simple terms,

the " transporter " portion of the gene transports serotonin inside

blood cells-and the long form is better at doing this than the

short. Thus if people with autism have more serotonin inside their

blood cells than average, which they do, you would expect that

people with autism would also have higher levels of the long

transporter than typical people. But this is not what Cook's three

studies found.

The precise relationship between serotonin in the blood and

serotonin in the brain is complicated, of course, but basically

blood cells are analogous to brain cells-which means that the long

form of the transporter would lead to more serotonin inside the

brain cells, and less serotonin outside the brain cells. Generally

speaking (and again this is a simplification) we want good levels of

serotonin outside our brain cells where it is free to work its

magic. All of the " SSRIs " (selective serotonin reuptake

inhibitors), -Prozac, Paxil, Zoloft and Luvox-are thought to work by

increasing the level of serotonin in the spaces, or synapses,

between brain cells.

*******************************************************************

from

http://www.hypoglycemia.asn.au/articles/serotonin_connection.html

1) A extended period of physical or psychological stress, will

produce stress hormones such as cortisol and adrenaline, that can

interfere with the synthesis of the brain neurotransmitter,

Serotonin.

2) A neurotransmitter is any one of numerous chemicals that occupy

the gap (synapse) between two or more nerve cells (neurons) and

thereby allows the triggering of a tiny electrical currents in

adjacent cells. Each neurotransmitter fits into a unique receptor -

like a key fitting into a lock - thus allowing messages to be

carried along nerve pathways

3) Serotonin is a neurotransmitter that conveys the positive

sensations of satiety, satisfaction and relaxation. It regulates

appetite and when converted to melatonin helps us to sleep.

4) A deficiency of Serotonin in the brain can cause endogenous

depression, upsets the appetite mechanism and may lead to obesity or

other eating disorders such as anorexia and bulimia nervosa and may

be responsible for insomnia. Doctors usually prescribe Selective

Serotonin Reuptake Inhibitors (SSRIs) which have the effects of

increasing the amount Serotonin and thereby medically treat the

above conditions. Unfortunately, SSRIs may have side effects in some

patients.

5) Serotonin is produced from an essential amino acid (protein

unit), called tryptophan, obtained from food and then converted to

Serotonin under the influence of vitamin B6

(Pyridoxine). " Essential " amino acids are sources of protein, that

the body cannot produce and must obtain from food!

6) If here is a deficiency of vitamin B3 (niacin),the body will use

dietary tryptophan to synthesize niacin. It takes 60 mg of

tryptophan to produce 1 mg of niacin. Hence, niacin deficiency may

also be responsible for depression.

7) The absorption of tryptophan competes with the absorption of

other amino acids in the digestive process.

8) The absorption of tryptophan can be accelerated by consuming

refined carbohydrates, such as sugar.

9) Sugar consumption stimulates the body to produce insulin, a

hormone which transports glucose, fatty acids and amino acids

(except tryptophan) into body cells. Thus insulin speeds up the

absorption of amino acids other than tryptophan.

10) This leaves tryptophan available for absorption and conversion

to Serotonin (via 5-hydroxytryptophan, 5-HTP) in the presence of

vitamin B6, and presto we feel happy.

11) A person low in Serotonin will be inclined to consume greater

amounts of sugar in an attempt to increase Serotonin production and

this may lead to sugar addiction.

12) Sugar addiction can lead to insulin resistance. High levels of

insulin cause receptors for insulin to shut down by means of `down-

regulation'.

13) Insulin resistance starts first as mild insulin resistance

leading to hypoglycemia (low blood sugar level also

called `hyperinsulinism'), then reactive hypoglycemia, more severe

insulin resistance which causes unstable concentrations of blood

glucose, and finally more complete insulin resistance, causing

diabetes over time. Thus there is a range of insulin resistance from

low to severe which causes erratic and unpredictable sugar levels in

the blood and to the brain. This explains some of the

variable `psychological' and physical symptoms of hypoglycemia.

14) High levels of insulin - hyperinsulinism - blocks the

utilization of fat cells (adipocytes) as a source of energy, thus

causing obesity. It also causes to dump magnesium into the urine,

upsetting the delicate balance of intracellular magnesium and

calcium ions that regulate blood pressure, thereby contributing to

hypertension.

15) In hypoglycemia wild fluctuations in blood sugar levels causes

the body to produce excess adrenaline, which functions to convert

glycogen (stored sugar) into glucose in an attempt to stabilize the

supply of glucose to the brain. The brain normally has no other

source of energy than glucose and needs a stable supply.

16) Treatment of hypoglycemia is achieved by adopting a hypoglycemic

diet accompanied with vitamin and mineral supplements (Vitamin C,

Zinc, Chromium picolinate, Thiamine (B1) and other B-complex

vitamins, see The Hypoglycemic Diet ). This helps to stabilize the

blood sugar levels, even out mood swings, rebalance the appetite

mechanism, equalize energy intake and expenditure; and halt if not

reverse obesity.

17) The overproduction of adrenaline, known as the fight/flight

hormone, can cause nervousness, panic attacks, anxiety, phobias,

extreme mood swings and bouts of aggression and many other symptoms

of hypoglycemia, described in the article " What is Hypoglycemia? "

18) Depressant drugs, such as alcohol, tranquilizers,

benzodiazepines, sleeping pills may temporarily counteract the

effects of adrenaline, these are however very addictive and this

helps to explain how hypoglycemia may lead to alcohol or drug

addiction. Most drug addicts have been found to be hypoglycemic!

19) It is suggested that insulin resistance may also interfere with

the absorption of other essential amino acids such as phenylalanine

and tyrosine, which are forerunners of important brain

neurotransmitters, such as dopamine and norepinephrine.

20) Norepinephrine (closely associated with dopamine) is believed to

be a neurotransmitter that blocks out any irrelevant information

from the brain and helps a person (usually young children) to

concentrate on the task at hand. An error in norepinephrine

synthesis has been associated with Attention Deficit and

Hyperactivity Disorder (ADHD), because the person is bombarded with

irrelevant information and cannot concentrate. Thus ADHD is

considered another consequence of insulin resistance and

hypoglycemia.

21) Hypoglycemia and/or insulin resistance is believed to result in

a dysfunction of dopamine metabolism. Dopamine conveys the sensation

of pleasure and many addictive drugs such as heroin and cocaine

increase the amount of dopamine, by blocking (inhibiting) the

reabsorption (reuptake) of dopamine by brain cells. This causes

increased levels of dopamine which is felt by the addict as a high

and as a feeling of great pleasure.

22) The presence of excess dopamine in the brain causes the down-

regulation of dopamine receptors as a defence against superfluous

dopamine. Receptors for dopamine are reduced and the person becomes

dependent on the heroin, cocaine or any other addictive drug to

artificially obtain `normal' levels of dopamine. Treatment aims at

rebuilding natural dopamine receptors through abstinence from drugs

and with nutritional aids, such as omega-3 essential fatty acids

(fish oil) which is thought to help restore brain cell membranes.

23) Treatment aims at reversing the Serotonin Connection by

correcting the chemical imbalance of the various neurotransmitters.

It is essential that the patient adopt the hypoglycemic diet

together with nutrient supplements, vitamins and minerals, omega-3

fatty acids, neurotransmitter precursors, exercises and so on as

explained in the article