Quelling the Abstinential Forces of Devourance (Tripping into Thyrule)

[. . .] the whole creation will be consumed and appear infinite and holy whereas it now appears finite & corrupt.
This will come to pass by an improvement of sensual enjoyment.
But first the notion that man has a body distinct from his soul is to be expunged; this I shall do, by printing in the infernal method, by corrosives, which in Hell are salutary and medicinal, melting apparent surfaces away, and displaying the infinite which was hid.
If the doors of perception were cleansed every thing would appear to man as it is, infinite.
For man has closed himself up, till he sees all things thro' narow chinks of his cavern.

[. . .]

The Giants who formed this world into its sensual existence and now seem to live in it in chains, are in truth the causes of its life & the sources of all activity, but the chains are the cunning of weak and tame minds which have power to resist energy, according to the proverb, the weak in courage is strong in cunning.
Thus one portion of being is the Prolific, the other the Devouring: to the devourer it seems as if the producer was in his chains, but it is not so, he only takes portions of existence and fancies that the whole.
But the Prolific would cease to be Prolific unless the Devourer, as a sea, recieved the excess of his delights.
Some will say: 'Is not God alone the Prolific?' I answer: 'God only Acts & Is, in existing beings or Men.'
These two classes of men are always upon earth, & they should be enemies; whoever tries to reconcile them seeks to destroy existence.
Religion is an endeavour to reconcile the two.
Note: Jesus Christ did not wish to unite but to seperate them, as in the Parable of sheep and goats! & he says I came not to send Peace but a Sword.
Messiah or Satan or Tempter was formerly thought to be one of the Antediluvians who are our Energies.

[. . .]

Chorus.

Let the Priests of the Raven of dawn, no longer in deadly black, with hoarse note curse the sons of joy. Nor his accepted brethren, whom, tyrant, he calls free: lay the bound or build the roof. Nor pale religious letchery call that virginity, that wishes but acts not!
For every thing that lives is Holy.

As shown in Table I, the reduction of the riboflavin content of rat livers, which occurs after approximately 3 weeks on the deficient diet, is associated with a loss of the estradiol-inactivating ability. The animals showed, in the later stages of this deficiency, the gross morphological changes associated with riboflavin depletion. Further data on riboflavin-deficient animals are included in Table II. From the values in both tables, it is apparent that under these experimental conditions a riboflavin level of 13 to 14 y per gm. of liver is essential for estradiol inactivation by liver slices. Further, the activity, presumably enzymatic, lost by depletion can be restored by the feeding of the vitamin. The restoration of activity in these deficient animals following the administration of riboflavin is relatively slow and parallels the slow rise in the liver riboflavin content.

The effects of thiamine deficiency (Table III) demonstrate the dependence of estradiol inactivation, by liver slices, on the liver content of this vitamin. With a method of thiamine determination by which there is no differentiation between the free and combined forms of the vitamin, it was found that the thiamine content would return to the normal values in a period of not more than 2 hours under our conditions. The estradiol-inactivating ability was restored in the same period. The data on vitamin B complex deficiencies in the rat (Table IV) reflect changes mainly in the thiamine content. The failure of the liver to inactivate estradiol appears to be due to the loss in thiamine. Mouse liver slices, from mice depleted in riboflavin, thiamine, or the whole vitamin B complex, react in an entirely analogous manner to that of the rats (Table V).

[. . .]

The presence of excess free estrogen may be associated with a number of clinical syndromes. A relation of those manifestations to nutritional deficiency is supported by the work of Biskind and our findings. In this connection it is interesting to note that Ashworth and Sutton (14) have reported that estrogens either increase the demand for or suppress the utilization of members of the vitamin B complex in human patients. Biskind, Biskind, and Biskind (15) have recently presented evidence that certain gynecological conditions are associated with nutritional deficiencies and respond to vitamin B complex therapy.

RESULTS The expression of Icer/ICER was reduced in VAT and WAT of obese humans and mice, respectively. Diminution of Icer/ICER was restricted to adipocytes and was accompanied by a rise of Atf3/ATF3 and diminution of Adipoq/ADIPOQ and Glut4/GLUT4. Silencing the expression of Icer in 3T3-L1 adipocytes mimicked the results observed in human and mice cells and hampered glucose uptake, thus confirming the requirement of Icer for appropriate adipocyte function.

CONCLUSIONS Impaired expression of ICER contributes to elevation in CREB target genes and, therefore, to the development of insulin resistance in obesity.

At night, clock-driven norepinephrine release activates pineal-adrenergic receptors, which stimulate adenylate cyclase and cause an increase in intracellular levels of cAMP (Fig. 2). At the same time, norepinephrine also activates cal-adrenergic receptors, which cause an activation of the phosphoinositide pathway and a consequent elevation of intracellular Ca2+ levels. Activated protein kinase C (PKC) then dramatically potentiates the stimulatory effects of receptors positively coupled to adenylate cyclase. Ultimately, this combined- and al-adrenergic receptor stimulation causes a synergistic elevation of intracellular cAMP levels [10].

In 1963, P.J. Randle clearly described the inhibition of glucose oxidation by free fatty acids. Later, when lipid emulsions came into use for intravenous feeding in hospitals, it was found that they blocked glucose oxidation, lowered the metabolic rate, suppressed immunity, and increased lipid peroxidation and oxidative stress.
Estrogen and stress are both known to create some of the conditions of diabetes, while increasing fat oxidation and inhibiting glucose oxidation. Emotional stress, overwork, trauma, and infections have been known to initiate diabetes. Estrogen increases free fatty acids and decreases glycogen storage, and when birth control pills were becoming popular, some researchers warned that they might cause diabetes. But the food oil industry and the estrogen industry were satisfied with the medical doctrine that diabetes was caused by eating too much sugar.

[. . .]

Free fatty acids suppress mitochondrial respiration (Kamikawa and Yamazaki, 1981), leading to increased glycolysis (producing lactic acid) to maintain cellular energy. The suppression of mitochondrial respiration increases the production of toxic free radicals, and the decreased carbon dioxide makes the proteins more susceptible to attack by free radicals. The lactate produced under the influence of excessive fat metabolism stimulates the release of endorphins, which are lipolytic, releasing more free fatty acids from the tissues. Acting through cytokines such as interleukin-6, lactate shifts the balance toward the catabolic hormones, leading to tissue wasting.

Lactic acid itself, and the longer chain fatty acids, inhibit the regulatory enzyme pyruvate dehydrogenase (which is activated by insulin), reducing the oxidative production of energy. Drugs to activate this enzyme are being studied by the pharmaceutical industry as treatments for diabetes and cancer (for example, DCA, dichloroacetate).

[. . .]

The importance of the fats in causing type-2 diabetes is coming to be accepted, for example Li, et al., recently (2008) said "The cellular link between fatty acids and ROS (reactive oxygen species) is essentially the mitochondrion, a key organelle for the control of insulin secretion. Mitochondria are the main source of ROS and are also the primary target of oxidative attacks."
But much earlier (Wright, et al., 1988) it had been demonstrated that a deficiency of the "essential fatty acids" prevents toxin-induced diabetes and greatly increases resistance to inflammation (Lefkowith, et al., 1990). The lack of those so-called "essential fatty acids" also prevents autoimmune diabetes in a strain of diabetic mice (Benhamou, et al., 1995),

Suppressing fatty acid oxidation improves the contraction of the heart muscle and increases the efficiency of oxygen use (Chandler, et al., 2003). Various drugs are being considered for that purpose, but niacinamide is already being used to improve heart function, since it lowers the concentration of free fatty acids.

[. . .]

In every type of tissue, it is the failure to oxidize glucose that produces oxidative stress and cellular damage. Even feeding enough sucrose to cause fat deposition in the liver can protect the liver from oxidative stress (Spolarics and Meyenhofer, 2000), possibly by mechanisms such as those involved in the treatment of alcoholic liver disease with saturated fats.

The active thyroid hormone, T3, protects the heart by supporting the oxidation of glucose (Liu, et al., 1998). The amount of T3 produced by the liver depends mainly on the amount of glucose available.

[. . .]

The GABA system (GABA is highly concentrated in the beta-cells) is involved in regulating blood sugar, inhibiting the release of glucagon when glucose isn't needed, and apparently allowing the beta cells to discriminate between amino acids and glucose (Gu, et al., 1993) and acting as a survival and growth factor for neighboring cells (Ligon, et al., 2007).

The damaged beta-cells lose the enzyme (glutamate dehydrogenase) that makes GABA, and their ratio of linoleic acid to saturated and monounsaturated fat increases, a change that corresponds to a decreased metabolism of glucose.

Are you drinking too much water?
[link to www.slideshare.net]

Are you crushing your metabolism?
[link to www.slideshare.net]

Sugar does not cause diabetes
[link to www.slideshare.net]

Check out GLA. Essential fatty acid deficient in modern diet, lifestyle, nutritive condition, etc.

Multiple roles apparently - hormonal, inflammation, and as energy precursor (cAMP related), etc. The government wanted to put this in milk to get it back into our diets years ago but it won't stay stable exposed to air even with vitamin E from what I remember seeing years back.

Hemp seeds are the only nutritively viable seed for consumption. They also have an excellent nutritive profile ration that matches closer to our bodies apparently as well.

Hmm. Regarding EFA deficiency:

Effects of prolonged use of extremely low-fat diet on adult human subject
[link to jn.nutrition.org]


I've looked up some pretty nasty things about CREB (transcription factor promoted by cAMP) that you can find on this thread.
Found yours: Thread: Thoughts on Insulin Resistance Diabetes

The cAMP-elevator forskolin greatly exacerbated my anhedonia. And I'm sure chronic coffee consumption would ramp cAMP levels up, too, and that would be the prime reason it no longer felt sustainable. Blood sugar levels were certainly hard to keep down few days after.

Thiamine and magnesium seem to make a great team for glucose intolerance.

Following the finding that fluoxetine and paroxetine and other SSRIs increase the content of allopregnanolone in several rodent brain structures (34), we hypothesized that normalization of brain allopregnanolone levels may underlie the pharmacological effects of the so called “selective serotonin reuptake inhibitors” or SSRIs in mood disorders. To test this hypothesis, we conducted experiments using the socially isolated mouse as an animal model of anxiety disorders and PTSD (16; 35-38). The socially isolated mouse expresses a robust decrease of corticolimbic allopregnanolone levels, which are associated with anxiety-like behaviors, fear, resistance to sedation, and heightened aggression (16; 35; 39). These behavioral deficits can be ameliorated by administration of fluoxetine and other SSRIs that upregulate allopregnanolone levels. Interestingly, fluoxetine’s pharmacological effects resulted to be independent from the ability of this drug to inhibit serotonin reuptake (35; 36).

Our experiments support a selective and novel mechanism whereby SSRIs, acting as selective brain steroidogenic stimulants (SBSSs), increase brain corticolimbic allopregnanolone levels and improve PTSD, anxiety, and depression behavioral symptoms.

[. . .]

Biosynthesis of neurosteroids in the brain is independent from adrenals, ovaries, and testis (40-44). Neurosteroids are functionally active in modulating gene expression and neurotransmitter systems (45-52). Allopregnanolone exerts pharmacological actions, such as anticonvulsant, anxiolytic, antidepressant, and even sedative-hypnotic (53-60). These pharmacological actions are similar to those elicited by barbiturates and benzodiazepines (52; 61; 62). Allopregnanolone potently (nM affinity), positively, and allosterically modulates the action of GABA at GABAA receptors (45-51). The endogenous physiological relevance of allopregnanolone is substantiated by its facilitation and fine-tuning of the efficacy of direct GABAA receptor activators and positive allosteric modulators of GABA action at GABAA receptors (43; 47; 48; 63). The demonstration that allopregnanolone potentiates GABA responses via two binding sites in the GABAA receptor that, respectively, mediate the potentiation and the direct activation of the GABAA receptor by allopregnanolone has been pivotal in neurosteroid pharmacology (64). Also, GABAA receptors incorporating a4, a6, and [delta] subunits in combination with y and B subunits show higher affinity (nM range) for allopregnanolone (45; 46; 51; 64; 65). Relevant for pharmacological strategies to overcome behavioral deficits resulting from GABAA receptor signal transduction deficits, allopregnanolone allosteric modulation of the action of GABA at GABAA receptors is much less selective than that of benzodiazepines, which are relatively inactive at a4- or a6-containing GABAA receptors (4; 45; 46; 66).

At the end of the 19th century, scientists Bohr and Verigo discovered what seemed a strange law: a decreased level of carbon dioxide in the blood leads to decreased oxygen supply to the cells in the body including the brain, heart, kidneys etc. Carbon dioxide (CO2) was found to be responsible for the bond between oxygen and haemoglobin. If the level of carbon dioxide in the blood is lower than normal, then this leads to difficulties in releasing oxygen from haemoglobin. Hence the Verigo-Bohr law.

The method of Konstantin Buteyko is based on the above law as to how carbon dioxide acts on the body. His drug-free treatment is beginning to spread around the world. Fifty years ago, he found a major cause of bronchial asthma and many other chronic diseases to be a deficiency of carbon dioxide in the alveolus of our lungs, and this, in turn, was found to be caused by deep breathing or hyperventilation.

[. . .]

Public opinion tends to think of carbon dioxide as a waste product or even a poison. (It is sometimes confused with carbon monoxide, which is a poison). During the last century, there was a particular interest as to the functional importance of carbon dioxide in the animal and the human body. Physiologists and chemists, such as Albitzkiy, Bohr, Verigo and Henderson, found that carbon dioxide has an important role as a regulator of the processes of metabolism. Buteyko called carbon dioxide "the main hormone of all hormones and the main vitamin of all vitamins". Carbon dioxide may truly be the 'breath of life'.

[. . .]

"Relations of Carbon Dioxide and Oxygen in the Body. Carbon dioxide is, in fact, a more fundamental component of living matter than is oxygen. Life probably existed on earth for millions of years prior to the carboniferous era, in an atmosphere containing a much larger amount of carbon dioxide than at present. There may even have been a time when there was no free oxygen available in the air.

"Another natural misconception is that oxygen and carbon dioxide are so far antagonistic that a gain of one in the blood necessarily involves a corresponding loss of the other. On the contrary, although each tends to raise the pressure and thus promote the diffusion of the other, the two gases are held and transported in the blood by different means; oxygen is carried by the haemoglobin in the corpuscles, while carbon dioxide is combined with alkali in the plasma. A sample of blood may be high in both gases, or low in both gases. Under clinical conditions, low oxygen and low carbon dioxide generally occur together. Therapeutic increase of carbon dioxide, by inhalation of this gas diluted in air, is often an effective means of improving the oxygenation of the blood and tissues".[3]

Stress has to be understood as a process that develops in time, and the brain (especially the neocortex and the frontal lobes) organizes the adaptive and developmental processes in both the spatial and temporal dimensions. The meaning of a situation influences the way the organism responds. For example, the stress of being restrained for a long time can cause major gastrointestinal bleeding and ulcerization, but if the animal has the opportunity to bite something during the stress (signifying its ability to fight back, and the possibility of escape) it can avoid the stress ulcers.

The patterning of the nervous activity throughout the body governs the local ability to produce carbon dioxide. When the cortex of the brain is damaged or removed, an animal becomes rigid, so the cortex is considered to have a “tonic inhibitory action” on the body. But when the nerves are removed from a muscle (for example, by disease or accident), the muscle goes into a state of constant activity, and its ability to oxidize glucose and produce carbon dioxide is reduced, while its oxidation of fatty acids persists, increasing the production of toxic oxidative fragments of the fatty acids, which contributes to the muscle's atrophy.

[. . .]

In the 1960s, a Russian researcher examined hospital records of measurements of newborn babies, and found that for several decades the size of their heads had been increasing. He suggested that it might be the result of increasing atmospheric carbon dioxide.

The experiences and nutrition of a pregnant animal are known to affect the expression of genes in the offspring, affecting such things as allergies, metabolic rate, brain size, and intelligence. Miles Storfer (1999) has reviewed the evidence for epigenetic environmental control of brain size and intelligence. The main mechanisms of epigenetic effects or “imprinting” are now known to involve methylation and acetylation of the chromosomes (DNA and histones).

Certain kinds of behavior, as well as nutrition and other environmental factors, increase the production and retention of carbon dioxide. The normal intrauterine level of carbon dioxide is high, and it can be increased or decreased by changes in the mother's physiology. The effects of carbon dioxide on many biological processes involving methylation and acetylation of the genetic material suggest that the concentration of carbon dioxide during gestation might regulate the degree to which parental imprinting will persist in the developing fetus. There is some evidence of increased demethylation associated with the low level of oxygen in the uterus (Wellman, et al., 2008). A high metabolic rate and production of carbon dioxide would increase the adaptability of the new organism, by decreasing the limiting genetic imprints.

[. . .]

With aging, DNA methylation is increased (Bork, et al., 2009). I suggest that methylation stabilizes and protects cells when growth and regeneration aren't possible (and that it's likely to increase when CO2 isn't available). Hibernation (Morin and Storey, 2009) and sporulation (Ruiz-Herrera, 1994; Clancy, et al., 2002) appear to use methylation protectively.

Parental stress, prenatal stress, early life stress, and even stress in adulthood contribute to “imprinting of the genes,” partly through methylation of DNA and the histones.

Methionine and choline are the main dietary sources of methyl donors. Restriction of methionine has many protective effects, including increased average (42%) and maximum (44%) longevity in rats (Richie, et al., 1994). Restriction of methyl donors causes demethylation of DNA (Epner, 2001). The age accelerating effect of methionine might be related to disturbing the methylation balance, inappropriately suppressing cellular activity. Besides its effect on the methyl pool, methionine inhibits thyroid function and damages mitochondria.

[. . .]

Thinking about the long dormancy of frogs reminded me of a newspaper story I read in the 1950s. Workers breaking up an old concrete structure found a dormant toad enclosed in the concrete, and it revived soon after being released. The concrete had been poured decades earlier.

Although systematic study of frogs or toads during their natural buried estivation has been very limited, there have been many reports of accidental discoveries that suggest that the dormant state might be extended indefinitely if conditions are favorable. Carbon dioxide has antioxidant effects, and many other stabilizing actions, including protection against hypoxia and the excitatory effects of intracellular calcium and inflammation (Baev, et al., 1978, 1995; Bari, et al., 1996; Brzecka, 2007; Kogan, et al., 1994; Malyshev, et al., 1995).

[. . .]

Birds have a higher metabolic rate than mammals of the same size, and live longer. Their tissues contain fewer of the highly unsaturated fatty acids. Queen bees, which live many times longer than worker bees, have mainly monounsaturated fats in their tissues, while the tissues of the short-lived worker bees, receiving a different diet, within a couple of weeks of hatching will contain highly unsaturated fats.

Bats have a very high metabolic rate, and an extremely long lifespan for an animal of their size. While most animals of their small size live only a few years, many bats live a few decades. Bat caves usually have slightly more carbon dioxide than the outside atmosphere, but they usually contain a large amount of ammonia, and bats maintain a high serum level of carbon dioxide, which protects them from the otherwise toxic effects of the ammonia.

[. . .]

Several diseases and syndromes are now thought to involve abnormal methylation of genes. Prader-Willi sydrome, Angelman's syndrome, and various “autistic spectrum disorders,” as well as post-traumatic stress disorder and several kinds of cancer seem to involve excess methylation.

Moderate methionine restriction (for example, using gelatin regularly in the diet) might be practical, but if increased carbon dioxide can activate the demethylase enzymes in a controlled way, it might be a useful treatment for the degenerative diseases and for aging itself.

The low carbon dioxide production of hypothyroidism (e.g., Lee and Levine, 1999), and the respiratory alkalosis of estrogen excess, are often overlooked. An adequate supply of calcium, and sometimes supplementation of salt and baking soda, can increase the tissue content of CO2.

Entire thread is 'bot bait.

Next thing you know, BSZ will show up...

YIOLAS MELECH

My throbber is dangling dizzy from softly skimming surrounding surfaces un-soundly...

YIOLAS MELECH

:sayhuhcow:

Hey man, great thread, a lot of info (too much! )... how'd you learn so much medical stuff?? I'm interested! Also what kind of food diet are you on & recommend?

I've got health problems and trying to get back in line physically. Overrun with candida, fatigue, inflammation, neurological issues, cramps, pain, aches, etc... I'm currently on a water fast.

I was doing a raw till 4 diet with lots of fruit. And I really liked it but it was messing up my teeth!! All the sugar/fruit acids I reckon

Also what do u recommend for expanding brain like yours Quickly? I'm familiar with and done much stuff... but not in your level. Thank you