Tuesday, August 26, 2008

Simply Bread

Simple bread
For this bread you need a 4-6 quart dutch oven, the heavier the better. You can use a dutch oven that is wide and shallow, but if you can use one that is deep rather than wide your bread will rise more and the loaf being higher it may be more suitable for sandwiches. However, use what you have; it will probably work.

4 cups bread flour, more for dusting
1/2 teaspoon instant yeast
2 tablespons kosher salt or 1 tablespoon table salt
1 tablespoon Accent (MSG)
Cornmeal or wheat bran as needed.
  • In a large bowl combine flour and water and stir until blended; dough will be shaggy and sticky. Let stand 1/2 to 1 hour. Add salt, MSG and yeast and mix enough to distribute.Cover bowl with plastic wrap. Let dough rest at least 12 hours, preferably about 18, at warm room temperature, about 70 degrees, possible. The use of MSG makes the length of rise less important. A lot of the yeasty flavor of good bread is secondary to yeast's natural formation of glutamate which is MSG. Refrigerate if you are going out or to sleep. Just let it warm up and proceed when ready
  • Dough is ready when its surface is dotted with bubbles. Lightly flour a work surface and place dough on it; sprinkle it with a little more flour and fold it over on itself once or twice.
  • Using just enough flour to keep dough from sticking to work surface or to your fingers, gently and quickly shape dough into a ball. Generously coat a cotton towel (not terry cloth) with flour, wheat bran or cornmeal. Place towel in a big enough bowl and put dough seam side down on towel and dust with more flour, bran or cornmeal. Cover with another cotton towel and let rise for about 2 hours. When it is ready, dough will be more than double in size and will not readily spring back when poked with a finger.
  • At least a half-hour before dough is ready, heat oven to 450 degrees. Put large dutch oven and lid in oven as it heats. When dough is ready, carefully remove pot from oven. Slide your hand under towel and turn dough over into pot, seam side up; it may look like a mess, but that is O.K. Shake pan once or twice if dough is unevenly distributed; it will straighten out as it bakes. Cover with lid and bake 30 minutes, then remove lid and bake another few minutes until loaf is browned to your satisfaction. The New York Times original recipe said this would take 15 to 40 minutes. I think this is way too long.
Flip over on to a rack to cool. When cool, use dutch oven as a custom bread box.

Thursday, August 7, 2008

Wordle's collation of "Pietr's Diary: Searching for Balance"

Click on image then select "Open in Window"

Wednesday, August 6, 2008

Superstimulation and the derangement of tryptophan metabolism

Streptococcus pyogenes may cause tonsillitis, scarlet fever and so-called “streptococcal toxic shock-like syndrome” (STSS). These streptococci produce exotoxins which are implicated as superantigens in the pathogenesis of STSS and scarlet fever. Such toxins were shown to induce neopterin production and tryptophan (TRP) degradation and cause hyperstimulation of the Kynurenic pathway. The production of the enzyme IDO (indoleamine (2,3)-dioxygenase) is promoted by interferon-gamma. IDO promotes TRP being shunted down the kynurenic pathway and the production of excitatory dopaminergic neurotoxins such as Quinolinate. Furthermore, since inadequate amounts of TRP are not passing down the serotonin pathway, decreased serotonin production lessens its ability to inhibit Interferon-gamma, also stimulated

Both generations of the CODAS protocol, fen/phen and PURSOR have been successful in remitting acute viral syndromes including the flu. REMEMBER, 5-HT inhibits INF-gamma and the resulting paucity prevents sufficient production of IDO which trips off TRP degradation.

The same basic concept is central in HIV’s ability to initiate immunodeficiency by superstimulating the immune system thru INF-gamma and the production of IDO and the subsequent immunodeficiency and neurotoxic metabolite of the kynurenic pathway, Quinolinic acid. CODAS has remitted terminal HIV.

The most widely propagated etiology for winter colds is because more people from outside the community commingle at such times. I believe that the immune system in winter is weakened by monoamine deficiencies associated with less light.

Getting rid of hyperlinks

When I provide a block quote I will no longer provide hyperlinks. Let Google find the reference.

The YIN YANG (DA/5-HT) duality

the Monoamines Dopamine and Serotonin are Antipodal in Nature.
Yin (陰 or 阴 "shady place, north slope, south bank (river); cloudy, overcast"; Japanese: in or on; Korean: 음, Vietnamese: âm) qualities are characterized as soft, slow, substantial, water, cold, conserving, tranquil, gentle, and corresponds to the night.

Yang (陽 or 阳 "sunny place, south slope, north bank (river), sunshine"; Japanese: yō; Korean: 양, Vietnamese: dương) qualities are characterized as hot, fire, restless, hard, dry, excitement, non-substantial, rapidity, and corresponds to the day.
Dopamine is Yang while Serotonin is Yin

DA and 5-HT have been antipodal in their activities for more than a billion years. Here, for example, the prostostomes, who according to Dawkins, went their particular way and parted from us 500M years ago are using the monoamines to decide whether to move or not.
The effect of dopamine on [snail] command neurons is significantly reduced in the presence of serotonin. In the presence of dopamine, the efficacy of serotonin action on the size of the response elicited in command neurons is reduced. Based on the data obtained, it was concluded that the interrelation of dopamine and serotonin concentrations could be the basis for the formation of behavioral choice in snails
Dopamine is the Reward Neurotransmitter
When the cortex has received and processed a sensory stimulus indicating a reward, it sends a signal announcing this reward to a particular part of the midbrain–the ventral tegmental area (VTA)–whose activity then increases. The VTA then releases dopamine not only into the nucleus accumbens, but also into the septum, the amygdala, and the prefrontal cortex.The nucleus accumbens then activates the individual’s motor functions, while the prefrontal cortex focuses his or her attention.
These regions are connected by what is called the pleasure or reward bundle. In neuroanatomical terms, this bundle is part of the medial forebrain bundle (MFB), whose activation leads to the repetition of the gratifying action to strengthen the associated pathways in the brain.
First described by James Olds and Peter Milner in the early 1960s, the MFB is a bundle of axons that originates in the reticular formation, crosses the ventral tegmental area, passes through the lateral hypothalamus, and continues into the nucleus accumbens as well as the amygdala, the septum, and the prefrontal cortex.
The MFB is composed of ascending and descending pathways, including most of the pathways that use monoamines as a neurotransmitter. The mesocorticolimbic dopaminergic system is one of its main components.
But Serotonin inhibits Reward and Stops Excessive Behavior

Serotonin plays a major role in the behavioural inhibition system (BIS).
This system was identified by Henri Laborit in the early 1970s. It is associated with the septo-hippocampal system, the amygdala, and the basal nuclei. It receives inputs from the prefrontal cortex and transmits its outputs via the noradrenergic fibres of the locus coeruleus and the serotininergic fibres of the medial Raphe nuclei.
The BIS is activated when both fight and flight seem impossible and the only remaining behavioural option is to submit passively. The pathological consequences of this behavioural inhibition have provided an understanding of how destructive chronic stress can be to people’s health.
Substantial evidence suggests that the functional status of the mesocorticolimbic dopamine (DA) system originating in the ventral tegmental area is under a phasic and tonic inhibitory control by the 5-HT system that acts by stimulating 5-HT(2C) receptor subtypes. Serotonin within the nucleus accumbens may play an important role in mediating incentive motivation by modulating dopaminergic neurotransmission.

Several hypotheses regarding physiopathology of major psychiatric diseases exist. Attention has been focused on cerebral monoaminergic systems, the dysfunction of which is thought to underlie various aspects of their symptomatology. There are reports describing the involvement of serotonergic and dopaminergic systems in the mechanism of action of psychotropic drugs. This article reviews current knowledge on interaction between 5-hydroxytryptamine (5-HT), acting at 5-HT2C receptors in the central dopamine (DA) systems. Since 90s, a growing body of behavioural, neurochemical and electrophysiological evidence from animal studies have demonstrated a clear role for 5-HT2C receptors in modulation of activity of dopamine neurones.
The blockade of serotonin receptors potentiates behavioral effects of dopamine agonists. It is concluded that central serotonin may play an inhibitory role, antagonistic to that of catecholamines
Increasing 5-HT activity in the nucleus accumbens inhibits dopamine-dependent behaviour, and further indicate that activation of 5-HT(1B) receptors is particularly important in this regard

T helper cell I and II Duality of the Immune System are under the Control of Dopamine and Serotonin

Devoino wrote seminal articles in the early 1980s that dealt with the monoamines regulation of the immune system. She wrote prior to the discovery of the T helper cell and its differentiation into Th1 and Th2 subsets. However, interpolating her articles forward she was clearly stating that DA promotes Th1 and suppresses Th2 cytokines and serotonin does the converse. She wrote in 1984:
The monoamine systems take part in the mechanisms of immunomodulation: the dopaminergic one accelerates and the serotoninergic system inhibits the development of immune response, the final result being determined by their interaction.
The combined use of a combined dopamine and serotonin agonist protocol (CODAS) such as PURSOR can titrate DA and serotonin into sufficiency and balance and remit addictive craving and immune disorders.

Does depression decrease cholesterol? Apparently

In the CODAS model, depression is associated with a decrease in DA/5-HT. One would, therefore, postulate that depression would be associated with decreased cholesterol.

Biochemical markers of anxiety and depression

The results of research into a biochemical marker for depression are presented. The research was carried out on a normal population in a primary care setting. Cholesterol levels were identified as the blood marker for anxiety and depression. The Hamilton Rating Scale for Depression was chosen to identify depression. Those with low cholesterol scored significantly higher on the Hamilton Rating Scale for Depression

Tuesday, August 5, 2008

LDL lowered to level compatible with CAD regression

Cholesterol levels markedly improved. Three months ago, LDL was 102. Today, 72. This is a highly significant drop.

Since stent for LAD lesion in May '07, intensive lipid lowering pharmacologic therapy (statin and niacin) had been successful. However, LDL had stabilized at ~100. Last evaluation had been 5/08 (102). While improved from pre-stent levels still not sufficiently decreased to expect regression of CAD lesions or even stabilization.

I expected an improvement in LDL levels. I did not expect results would take place in less than a month. To my surprise, LDL drawn 8/2 was 72. This is a statistically highly significant decrease with a p < 0.01.

An increase in 5-HTP, glutamate supplements and Canola oil are the only changes in Rx. Dr. Kashi may be finally impressed.

Delta Weight in Kashi's office since 5/08 8 lbs.

Saturday, August 2, 2008