A Tale of Two Indoleamines: Melatonin and Serotonin

[trouble]

Lets tie one loose end and establish a link between sleep, stress, ROS induced damage from lack of sleep and exertion and stress, glutatione protection against ROS in membranes, melatonin induced gluthathione enzyme and its recycle, and glutathione induced optimization of mitochrondrial respiration.
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Both Melatonin and a Putative Nuclear Melatonin Receptor Agonist CGP 52608 Stimulate Glutathione Peroxidase and Glutathione Reductase Activities in Mouse Brain In Vivo

by Marta I. Pablos, Juan M. Guerrero, Genaro G. Ortiz, Maria T. Agapito and Russel J. Reiter. Neuroendocrinology Letters. 1998; 18:49-58.

Melatonin is both a direct and indirect antioxidant. Thus, it scavenges a variety of free radicals and it stimulates the antioxidative enzyme glutathione peroxidase (http://en.wikipedia.org/wiki/Glutathione_peroxidase).

Melatonin has been shown to enter the brain and to accumulate in the nucleus of cells. A high-affinity nuclear binding site/receptor for melatonin has been tentatively identified. Using an agonist of the putative nuclear receptor, we show here that the agonist duplicates the stimulatory effect of melatonin on cerebral and cerebellar glutathione peroxidase activity in vivo.

We also report that both melatonin and the agonist stimulate glutathione reductase activity.

(this involves the regeneration of gluthtione to its reduced state, where it can once again participate in membrane protection against ROS oxidation)

The increases in both enzyme activities are time-dependent, but the stimulation in glutathione reductase activity is delayed compared to that of glutathione peroxidase.

--->The results indicate that melatonin's ability to protect the brain from oxidative damage may be in part be a consequence of a receptor-mediated stimulation of neural antioxidative enzymes.

Thus, the key tie between melatonin and its maintenance of glutathione scavenging of free radicalss (ROS) ths is critical to membrane protection in many tissues, specifically the brain.

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Another set of authors (http://www.fasebj.org/cgi/content/full/14/12/1677) went one step further, demonstrating that glutathione and NOT vitamin C, E or NAC was responsible for this membrane protection AND that glutathione upregulates mitochrondrial respiration.

I need you to understand this significance of this linkage.

Lack of sleep causes stress, and reduces melatonin. Stress causes glutathione suckout from liver. Loss of melatonin reduces the brains ability to recycle gluthathione to protect delicate membranes in mitochrondria, and lastely, stress reduces melatonin that reduces glutathione that keeps mito working at high gear.

Got it?

"Melatonin is a highly important antioxidant. Free radicals are chemical constituents that have an unpaired electron. If an electron is added to O2 then the superoxide anion radical O2- is formed. O2- is reduced by superoxide dismutase to H2O2 which is toxic at high concentrations and can be reduced to.OH. The hydroxyl radical (.OH) damages cells. Melatonin is an efficient neutraliser of.OH. (9)

Age related brain deterioration is extremely costly in terms of quality of life. One of the potential major causes of age-related destruction of neuronal tissue is toxic free radicals that are a natural result of aerobic metabolism. The brain is particularly susceptible to free radical attack.

Vitamin antioxidants.vitamin E (tocopherol) and vitamin C (ascorbate) aid in protecting the brain from oxidative stress by directly scavenging toxic radicals. The pineal hormone melatonin is rapidly taken up by the brain. In vitro melatonin is more effective than glutathione in scavenging the highly toxic (.OH) radical and also more efficient than vitamin E in neutralising the peroxyl radical. It also stimulates the main antioxidant enzyme of the brain, glutathione peroxidase. In vivo melatonin is a potent antioxidant."

Source: melatonin review (http://www.priory.com/mel.htm)

[trouble]

Links between their actions: an interesting science blog (http://circadiana.blogspot.com/2006/01/serotonin-melatonin-immunity-and.html) to read.

Now, onto the good stuff.

Tryptophan is converted to sertotonin and then to melatonin in the pineal gland.


If we are low in melatonin, I get its linked to sertonin production, and that to tryptophan. I go looking and what do I find? The rate limiting condition to tryptophan synthesis:

Conversion of glutamine to glutamate, a side reaction that supply electrons for the synthesis of tryptophan!

Oh shit! If we have the conversion of glutamine to glutamate blocked by crappy hydrogen ion (thats pH) control, we DO NOT make tryptophan, sertotonin or melatonin very efficiently!

Aaiiiii! We have our stumbling block, in the those with glutamine/glutamate metabolism issues, and thats just about everyone who as chronic stress and stress induced lack of glutathione, since its the ion "mop" up, along with a few other antioxidants, that allows glutamine - glutamate conversion to occur.

The tryptophan conversion cascade is abbreviated:

Chorismate + L-Glutamine + 5-Phosphoribosylpyrophosphate (PRPP) + Serine ---> L-Tryptophan + L-Glutamate + Pyruvate + PPi + 2 H2O + CO2 + D-Glyceraldehyde-3-Phosphate

And you can view it its glory here (http://www.gwu.edu/~mpb/shikimate3.htm)

The common name for this problem is serotonin deficiency (http://tinnitusformula.com/infocenter/articles/treatments/trypto.aspx).

We can step back yet again and draw a very nice connection between methionine and glutathione driven serotonin production:

From LeMagazine 1997 (http://www.lef.org/magazine/mag97/march97-report.html)
SAMe Is Necessary for Melatonin

"One of the most exciting things about SAMe is that it is melatonin's daytime equivalent. The natural synthesis of melatonin during the night is dependent on the synthesis of SAMe during the day. SAMe is necessary for the biochemical reaction that converts serotonin into melatonin. (Serotonin is the neurotransmitter that drugs like Prozac elevate). SAMe and melatonin are entwined in a circadian rhythm that see-saws back and forth as the sun rises and sets. SAMe is melatonin's other half: when melatonin levels shoot up at night, SAMe stays low. But during the day, when melatonin falls, SAMe levels climb. Without adequate SAMe during the day, neither melatonin nor serotonin can be synthesized. And both are dependent on light and dark.

One of the most fascinating animal studies on SAMe and melatonin was published in the Journal of Neurochemistry in 1995. Researchers demonstrated in great detail the perfect orchestration that occurs between levels of SAMe and melatonin. The so-called "nyctohemeral" rhythm (pertaining to both day and night) was documented almost minute-by-minute. Data were translated onto graphs showing the see-saw relationship between melatonin and SAMe (Fig. 1).

Both melatonin and SAMe are controlled by an internal "clock" that knows lightness from darkness. In the evening, about 30 minutes before sunset, levels of SAMe shoot up to their highest level. They stay there for about an hour, and then suddenly drop. When this happens, melatonin kicks in. Melatonin increases for four hours, while SAMe drops. Five hours into the night, melatonin hits its high, and SAMe hits its low. Melatonin stays elevated until three hours before sunrise, when it abruptly falls. Meanwhile, SAMe builds up. Five hours into the day (around 11:00 A.M.), SAMe reaches its peak level again, then begins a gradual descent until evening.

Serotonin levels follow roughly the same pattern-higher during the day and lower at night. It appears that the serotonin synthesized during the day is used at night to make melatonin. SAMe is absolutely crucial for the natural synthesis of melatonin because it donates a methyl group molecule to the enzyme that converts the acetylated form of serotonin to melatonin."

So, we must goose up glutathione with both cysteine supplied from NAC and methionine, primarily from sam-e, before we can begin to repair the dysfunctional productio of our twins, serotonin and melatonin.

Makes nice line of logical sense, don't it?

[trouble]

First, some interesting background reading on linkages (http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1998001200002) between foods we eat and mood.

Note that consumption of vitamin D has an effect on reducing depression. And that serotonin production is correlated to light level, as is its conversion to melatonin in pineal gland.

And that linkage is through a very simple factor: sunlight. (http://www.bbc.co.uk/science/hottopics/sunshine/benefits.shtml)

The less we out in the sun (http://www.cnn.com/HEALTH/alternative/9907/12/sun.depression/index.html) the less pineal gland activity, and the less conversion of tryptophan to serotonin to melatonin, the first steps in liver and the last in brain, in the pineal gland.

Gloriously simple and elegant.

And now we have tie back to our liver, in the production of key amino acids, in the cholesterol cascade and its side path vitamin D biosynthesis, sunlight, serotonin and melatonin.

I'll take a break and back later to tie this into the endocannabinoid pathway in the brain.

[El_Animal]

Trouble,

How does one know if they have glutamine/glutamate metabolism issues?

What does SAMe stand for?

Is serotonin deficiency another name for depression?

Is there any link between energy levels or testosterone levels and the elvels of SAMe/melatonin in the body? I find that I ahve to most energy about 1 hour after waking up.

I supplement with melatonin and glutamine. Should I look into NAC?

[trouble]

El_Animal inquried:

>How does one know if they have glutamine/glutamate metabolism issues?

See this article (http://www.psychiatrist.com/pcc/brainstorm/br5806.htm)for a quasi-technical description of excitotoxicity. Also see this one (http://www.smart-drugs.com/ias-excitotoxins.htm) which talks about glutamate and aspartame, an eye opener, thats Equal.

In another thread, I revealed what may be the primary cause of hypoglycemia and hyperinsulinemia - thats a lack of GABA control over stimulation of the beta cells in the presence of glutamine. Got GABA? No excess release. Not got it, insulin release is turned and it stays on until a latent feedback mechanism shuts it off hours later.

>What does SAMe stand for?

S-adenosylmethionine, both methyl donor and source of methionone for the transulfuration pathway matrix.

>Is serotonin deficiency another name for depression?

Its believed to be one of the one causes, yes.

>Is there any link between energy levels or testosterone levels and the levels of SAMe/melatonin in the body? I find that I have to most energy about 1 hour after waking up.

That's cortisol, and rise in it, after the previous days damage from its excess, along with release of stored glucose, is the reason you feel good. Its what wakes you us, as melatonin, serotonins twin, is dwindling. At the same time, light levels are driving serotonin production via vitamin D.

Later, as both test and cortisol cause excess buildup of ROS, if you can't scavenge it, you get reduced energy from mitochondria, because glutathione fine tuning that increases its capacity for making energy is missing.

>I supplement with melatonin and glutamine. Should I look into NAC?

You just might want to rethink glutamine use.

Yes, you should look into NAC, but that last post clearly says, NAC is isn't the wonderhchild in brrain that it once was was thought to be, nor is vitamin C or E...its glutathione, and for that, you need vitamin B6 - in its most bioactive form.

As an experiment, I bought B6 the other day. After one day, I deliberately tested insulin induction.

Guess what? It did not jack up insulin when a mixture of fats and sugar is consumed. It rose, but its was much reasonable, and much more obvious that it was controlled than with ordinary B6 use. I tried it again with whey, a larger dose, as it can also set off blood sugar swings by hyperinsulin release. Again, it worked.

Regular B6 helps with insulin, as does chromium, vanadium, and ALA, but it was no comparison with the active form of B6. I thought was rather cool; the biochemical logic holds up in practical application.

[El_Animal]

El_Animal inquried:

>How does one know if they have glutamine/glutamate metabolism issues?

See this article (http://www.psychiatrist.com/pcc/brainstorm/br5806.htm)for a quasi-technical description of excitotoxicity. Also see this one (http://www.smart-drugs.com/ias-excitotoxins.htm) which talks about glutamate and aspartame, an eye opener, thats Equal.

In another thread, I revealed what may be the primary cause of hypoglycemia and hyperinsulinemia - thats a lack of GABA control over stimulation of the beta cells in the presence of glutamine. Got GABA? No excess release. Not got it, insulin release is turned and it stays on until a latent feedback mechanism shuts it off hours later.

>What does SAMe stand for?

S-adenosylmethionine, both methyl donor and source of methionone for the transulfuration pathway matrix.

>Is serotonin deficiency another name for depression?

Its believed to be one of the one causes, yes.

>Is there any link between energy levels or testosterone levels and the levels of SAMe/melatonin in the body? I find that I have to most energy about 1 hour after waking up.

That's cortisol, and rise in it, after the previous days damage from its excess, along with release of stored glucose, is the reason you feel good. Its what wakes you us, as melatonin, serotonins twin, is dwindling. At the same time, light levels are driving serotonin production via vitamin D.

Later, as both test and cortisol cause excess buildup of ROS, if you can't scavenge it, you get reduced energy from mitochondria, because glutathione fine tuning that increases its capacity for making energy is missing.

>I supplement with melatonin and glutamine. Should I look into NAC?

You just might want to rethink glutamine use.

Yes, you should look into NAC, but that last post clearly says, NAC is isn't the wonderhchild in brrain that it once was was thought to be, nor is vitamin C or E...its glutathione, and for that, you need vitamin B6 - in its most bioactive form.

As an experiment, I bought B6 the other day. After one day, I deliberately tested insulin induction.

Guess what? It did not jack up insulin when a mixture of fats and sugar is consumed. It rose, but its was much reasonable, and much more obvious that it was controlled than with ordinary B6 use. I tried it again with whey, a larger dose, as it can also set off blood sugar swings by hyperinsulin release. Again, it worked.

Regular B6 helps with insulin, as does chromium, vanadium, and ALA, but it was no comparison with the active form of B6. I thought was rather cool; the biochemical logic holds up in practical application.

Thanks for the replies.

So I take it, it is better to train in the morning for me?

[Odium]

Regular B6 helps with insulin, as does chromium, vanadium, and ALA, but it was no comparison with the active form of B6. I thought was rather cool; the biochemical logic holds up in practical application.


Pyridoxal-5-Phosphate?

[jumpman]

Found this part interesting

Both undernutrition and overnutrition in preweaning rats result in long-lasting functional changes in the brain. The effects of protein undernutrition on behavior, brain development, and intellectual function are well known (2,44). Unfortunately, there are far fewer studies on the effect of long-term excess consumption of any macronutrient - particularly protein - on the brain. Some reported studies on the effect of protein overnutrition on behavior are not rigorous in design and data analysis. For example, it has been reported that adult rats consuming a high-protein diet become more easily frightened and "snappish" (45). A few years ago, we undertook a series of studies to evaluate the effect of long-term (20-36 weeks) consumption of isocaloric high (50% of total calories; HP)-, moderate (20% of total calories; MP)-, and low-protein (5% of total calories; LP) diets on a variety of behavioral measures. These included the adhesive patch test and negative geotaxis commonly used to evaluate sensorimotor function; locomotor activity and stereotypy as measures of ambulatory and searching behavior; the tail-flick test for nociception, and the elevated plus-maze test as a measure of anxiety and aversive behavior. The HP group was more responsive compared with the MP or LP groups in sensorimotor function, negative geotaxis, and spontaneous locomotor activity (46). In addition, the HP group exhibited reduced aversion as measured by the elevated plus-maze test of anxiety and hyperalgesia as shown by tail-flick reaction time (46). These data suggested that long-term consumption of an HP diet may lead to hyperactivity and hyperresponsiveness to the environment, a change that may not always be desirable. In a separate study, we examined whether the HP diet had any effect on learning, memory, and sensory discrimination. The results of these studies showed the following: in the swim cylinder of Porsolt, which tests adaptation to stress, HP rats were significantly less able than was the control group (MP rats) to develop an effective coping strategy (47); during the recording of auditory-evoked responses to deviant tones, short-term auditory memory traces degraded more quickly in the HP rats (47), and finally, in the Morris water maze, diet had no significant effect on acquisition and recall of spatial information (47). These data suggest that a long-term HP diet may precipitate a deficit in short-term but not long-term memory and a diminution in the ability to cope with acute stress.

A review of the literature indicates that a number of food constituents (e.g., dietary macronutrients and neurotransmitter amino acid precursors) as well as food deprivation may modulate development of tolerance and physical dependence and influence self-administration of several drugs of abuse in animals (48). In an effort to examine further the nature of neuronal changes responsible for perturbation of spontaneous unprovoked motor behavior in animals consuming the HP diet, we examined the sensitivity of HP, MP, and LP mice to a variety of neurotropic agents such as amphetamine, apomorphine, haloperidol, etc. The following is a summary of our studies on amphetamine. Adult ICR mice were put on HP, MP, or LP diets for 35 weeks. At the end of this period, all mice were tested for spontaneous locomotor activity (SLA) and stereotypic behavior (SB) after administration of vehicle or amphetamine (0.1 or 1.0 mg/kg). Both SLA and SB, in the absence of amphetamine, increased with increasing levels of protein in the diet (49). Mice on the LP but not the MP or HP diets increased SLA and SB on low-dose (0.1 mg/kg) amphetamine. Mice on HP but not LP or MP diets, however, failed to respond to high-dose amphetamine (1 mg/kg). These data suggest that long-term consumption of an HP diet not only may lead to hyperactivity and hyperresponsiveness to the environment but may attenuate neuronal sensitivity to amphetamine and possibly other drugs of abuse. It is generally accepted that amphetamine-induced locomotion is mediated by mesolimbic DAergic neurons, whereas stereotypy is associated with nigrostriatal neurons (49). Furthermore, there is abundant evidence that DA alone is largely responsible for the effect of amphetamine on SLA and SB. Therefore, it seems that a long-term HP diet may modulate multiple DAergic pathways in the brain; it is not clear how the HP diet may affect other neuronal systems. To gain further insight into the effect of dietary protein on the neurochemical make-up of the brain, we examined the distribution of DA, DA-metabolites (dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA)), norepinephrine (NE), serotonin (5-HT), and 5-hydroxyindolacetic acid (5-HIAA) in the brains of rats consuming LP, MP, and HP diets for 36 weeks. Here I discuss only the data on DA and its metabolites.

In the substantia nigra, the striatum, and the dentate gyrus, DA levels decreased and increased, respectively, with a decrease and increase in dietary protein (P<0.05 compared with the MP diet) (50). The nigrostriatal system is important to a number of behaviors related to sensorimotor integration and response initiation, including extrapyramidal movement, aphagia and adipsia, emesis, and stereotypy (51-55). Our behavioral studies have shown that the HP diet produces hyperactivity. These neurochemical data suggest that an increase in DA in the nigrostriatal system may contribute to behavioral hyperactivity in HP rats. In the mesolimbic system, dietary manipulation had the most marked effect on DA metabolism. There was a diminution in amygdala DOPAC/DA and HVA/DA ratios in the rats on the HP diet, suggesting a decrease in the firing of DAergic neurons in this region. DA transmission in this region is implicated in emotion, sexual behavior, and the reward properties of many drugs of abuse (56-59). Therefore, it is conceivable that reduced sensitivity to SLA and SB after amphetamine administration to HP rats may be related to changes in DA metabolism.

In addition to its neurochemical and behavioral effects, the level of protein in the diet has also been shown to have a profound effect on food intake, body weight, and body composition. For example, White et al. (60) have recently shown that rats given a low-protein (5%) diet for only 11 days, compared with those on a 20%-protein diet, increased NPY gene expression in the hypothalamus, resulting in augmented caloric intake. In rats on 5% protein, while their average daily food intake was increased by 20%, their body weight gain was severely attenuated, and body composition analysis revealed increased water retention, decreased body protein, and increased body fat. While these studies underscore the effect of a low-protein diet-mediated increase in NPY gene expression on appetite, other behavioral consequences associated with increased NPY remain to be elucidated.

[jumpman]

And for those who advocate raw foods
These amines comprise a family of bioactive substances in food that are not endogenous to food but are produced during its preparation or processing. Earlier I talked about the high levels of CHP in protein-derived nutritional supplements like Ensure Plus that are produced by a combination of enzymatic hydrolysis of proteins and heat treatment. I also must mention two heterocyclic amines (18) that are products of tryptophan pyrolysis and that are present in meat and fish cooked on an open flame; these were identified as 3-amino-1,4-dimethyl-5H-pyridol[4,3-b] indole (Trp-P-1) and 3-amino-1-methyl-5H-pyridol[4,3-b] indole (Trp-P-2). These compounds are related to ß-carbolines with structures similar to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a man-made agent known to cause Parkinson's disease. Functionally, however, they are quite opposite to MPTP. Systemic administration of Trp-P-1 and Trp-P-2 to mice caused a marked increase in the neurotransmitter dopamine (DA) and a decrease in DA metabolites in the brain, suggesting inhibition of enzyme monoamine oxidase in vivo. These data suggest the possibility of altering DA-dependent behaviors following consumption of foods containing these heterocyclic amines.

[jumpman]

In regards to the first part I posted seems very interesting -
Seems like there are drawbacks in terms of stress response with HP diets which are very serious- It seems they may be able to be modified however with raw protein sources due to less MAOI activity -

[jumpman]

Trouble What about K-ALA for its glutathione enhancing properties-?
Now in regards to compounds which modulate gaba we have taurine and magnesium-
Anything Else?

[jumpman]

Hmmmm Well gaba and glycine and anything else?
How to modulate this glutamine toxicity seems to be the most important point of all so maybe you could delve into even more detail than you have in the past or refine your ideas even further -

[trouble]

Couple points.

Ever seen rat chow? Its compressed pellets of Difco cheap ass protein, from a variety of sources. Lets put it this way; one of the primary sources is offal from slaughterhouses.

Get it?

Problem here is the carnitine and possibly the glutamine levels in the feed are are sky high, plus you're getting mostly PC and I guess PE in the phospholipids. I doubt the rats are fed much vegetable protein, so their intake of PS and PI is probably suboptimal.

Can you get hyperexcitation from this high protein diet?

Depends on your protein sources and what macronutrients constitute the rest of the diet.

I already told you got a problem with choline and inositol balance. Inositol is the "I" in phosphoinositol.

I always love it when folks write to me for help; they excitable types are always wanting to pound down choline or lethicin. I want to say to them, you're PLs (phospholipid) intake in food is screwed up...but that necessitates a longass discourse on phospholipid biochemistry...

Jumpman, you got these same folks wanting to take tyrosine.

What does that do in these hyperexcitable types?

BTW, the carbinol type pyrido-indoles that inhibit MAO...

How about them maybe also inhibiting tryptophan biochemistry in the body?

[jumpman]

Ok then well yeah the tyrosine will drive em nutty in most cases especially seeing it will be competing with trytophan for the same carriers into the brain -
So lets see what else -
In regards to the raw proteins causing problems here is a new idea -Not only does whey protein cause problems due to the amino acid content and glutamate issues but due to it being altered and producing the same substance which inhibit MAOI and maybe also cause tryptophan issues as you pointed out - This alteration however is due to it being heated the same as any cooked protein -
This is why I was able to ingest copious amounts of raw protein in the past - Whatever the exact chemistry is which is beyond my present knowledge to explain the raw proteins do not stimulate the "nuttiness" that the cooked ones do - Well I guess they definitely do to some degree but it feels completely different -

Now it would be interesting to have more in depth research on specific chemical changes which occur in the cooking of food and specifically what neurotransmitters they affect and how they affect body chemistry in general

In regards to the phospholipids your pshychic powers are working well today ( must be the residuals from full moon)
Cuz just yesterday I scribbled down phosholipids and did research on em -
I realized that eggs can both lift my depression and drive me nutty as well and I think it has to do with all the phospholipids in them but I am in the dark on this and well you can see it in your posts -

So yes I am in need of a thourough education on phospholipids biochemistry -
Now we all need to learn how to balance the phospholipids and knowing the best sources of them would help as well

[jumpman]

You know when I am thinking about it the nuttiness from whey protein or other proteins feels more to me like a toxic reaction - kind of like taking in a chemical or any toxin that basically means a fuck up in the system - I think there is much more to it than simply the makeup of amino acids present - It HAS to have something to do with the form of it-
I may do an experiment - I can get raw whey as a byproduct of cheese manufacture directly from a farm so................................................ .........................

[trouble]

Raw whey has far too little protein and far too much lactose to be of benefit in assessing the actions of various fractions.

If you were ingesting large quantities of the concentrate, with its lower (80%) and higher lactose content, it could be a simple fact that your intracellular buffering capacity is crappy (but we already know this to be true, else the ammonia supression of GABA and glutathione in brain, liver, pancreas wouldn't be a problem).

No, this whey excitation problem is insulin and cortisol related. Use the fiber I recommend in the protein pudding thread started by Halfway.

(What a little gem that thread has turned out to be. Bless Halfway for starting it.)

[trouble]

Phosphatidyl-serine and phosphatidyl-inositiol, they have neurological effects.

From what food sources are they derived, Jumpman?

[jumpman]

Uga Buga
Well seems like vegetable protein from what u said above -
Specific foods gonna have to look for em' .....................

[jumpman]

Hmmmm I wonder if Avocado Oil is a good source
Have to look into it
What about OO-
Coconut maybe?

[jumpman]

Cow brain seems to be best for PS-
Hmmmm that sounds tasty
Cow brains and monkey eyeballs
"You cheat Dr. Jones"
Never mind Never Mind

Hey trouble can ya think of any safety issues in regards to eating liver and adrenal glands and shit maybe even brain etc of grass fed organic cows?
Oh and kidneys too -
Damn I acually have a craving right now for............................................... ...............

[ljefe15]

Trouble, would you recommend supps, that help in restful sleep or for people who have problems getting rest, for people who do not have problems getting a restful nights rest? Simply put, is serotonin and melatonin for example, for everyone?

Would one have trouble sleeping if he/she gets off it?

Thanks!

[ljefe15]

bump!

[startingserious]

jumpan -

that nuttiness you speak of - I find that on a day with very high protein and low carbs/fats I have trouble sleeping. After introducing large amounts (say 80 grams per day, I way ~ 150lbs) of processed whey protein sources I had more noticeble stress-induced fat gain over a period and generally slept less well.

hmmm...im really starting to come around to this whole balance thing. even things like 8 eggwhites a day, two cans of tuna - all this just doesnt seem healthful

[Grassroots]

When you say a day of high protein, how many grams are you speaking of?

[startingserious]

say approx 150 - 160 grams, but important is the %calories from protein

Nattyness is pronounced when protein makes up the bulk of the diet; currently I'm on a higher fat diet still consuming ~ 150grams protein and feel better.

[juggernaut333]

sorry if i missed it completely in here somewhere but

"I'll take a break and back later to tie this into the endocannabinoid pathway in the brain."

did u ever get back to this?the endoc system has recently started to utterly fascinate me

[~David~]

sorry if i missed it completely in here somewhere but

"I'll take a break and back later to tie this into the endocannabinoid pathway in the brain."

did u ever get back to this?the endoc system has recently started to utterly fascinate me

haha
long story,
short answer is no.

I would love to see her posting again.