Another source for cystein : the Whey !
 

Another source for cystein : the Whey ! and it is natural. Pls see following link which I partially quote. It claims it gets through BBB ...:rolleyes:
FEEDBACK GREATLY APPRECIATED

http://64.233.169.104/search?q=cache...lnk&cd=5&gl=jo
"WHEY PROTEIN & GLUTATHIONE Whey Protein contains essential amino acids which are noted to provide overall health benefits. More specifically, whey protein is very beneficial because whey protein drinks increase Glutathione (GSH) concentration in a number of tissues. Whey-based peptide studies have shown that whey protein may reduce hypertension which contributes to cardiovascular diseases. In fact, one of whey protein’s major benefits is to assist in the building of collagen. Therefore, by supplementing whey protein to your diet, it helps to accelerate the healing of fractures as well as provide overall health benefits. Whey protein is also helpful in the prevention and treatment of Osteoporosis. American Journal of Clinical Nutrition, June 2000.Whey protein increases Glutathione levels. Glutathione (GSH) is a powerful antioxidant. It is a tripeptide protein (made within the body) from three key amino acids; Cysteine, Glutamic Acid, and Glycine. The benefits of Glutathione include detoxifying many toxic chemicals and heavy metals from the body such as lead, mercury, aluminum, arsenic and cadmium, as well as the effects of alcohol and tobacco smoke. In the Immune System, Glutathione inhibits the excessive production of Cytokines that are implicated in Autoimmune Disease. Glutathione combats Free Radicals that cause allergies and aids in Chronic Fatigue. In regards to aging and life extension, old cells contain 20% less Glutathione compared to young cells, indicating it may be beneficial. In the Cardiovascular System, Atherosclerosis patients generally exhibit reduced Glutathione, indicating it may be beneficial. Brink; Life Ext., 6(2), 2000"
--
"THE EFFECTS OF WHEY PROTEIN ON NEUROTRANSMITTER FUNCTION Essential Amino Acids, the building blocks that make up proteins, play a large part in every living cell in the body. Each group of amino acids is tailored for a specific need. It is actually the amino acids rather than the proteins that are the essential nutrients. Amino acids act as neurotransmitters to carry information from one nerve cell to another. The neurotransmitter dysfunction is caused by the lack of amino acids. The dysfunction of the neurotransmitters results in depression and obesity with further results in diabetes, heart diseases, hypertension (high blood pressure), and lack of emotional control. “Essential amino acids are primarily responsible for the amino acid stimulation of muscle protein anabolism in healthy elderly adults,” Elena Volpi, Hisamine Kobayaski, Melinda Sheffield-Moore, Bettina Mittendorfer, and Robert R. Wolfe, Am J Clin Nutr 2003;78:250-8. Amino acids also act as neurotransmitters to carry information from one nerve cell to another. Amino acids enable vitamins and minerals to do their jobs properly, but if there is a deficiency in amino acids, nerve cells can’t function. There are approximately 28 amino acids. The liver produces 19 amino acids while the other 9 must be obtained from the diet which is called the essential amino acids. Prescription for Nutritional Healing, James F. Balch, M.D., Phyllis A. Balch, CNC, 1997, Page 34-35.Plainly, the neurotransmitter dysfunction is caused by the lack of amino acids. The dysfunction of the neurotransmitters results in depression and obesity with further results in diabetes, heart diseases, hypertension (high blood pressure), and lack of emotional control. The neurotransmitters are fat soluble and cannot cross the blood/brain barrier. Therefore, the amino acids that made up the neurotransmitters must cross the blood/brain barrier and then the body makes the neurotransmitters out of the amino acids and the appropriate vitamins and minerals necessary. Neurotransmitter Testing and Amino AcidTherapy, Marty Hinz, MD, NeuroResearch, Morgan Park Clinic, Duluth, Minnesota, 2002, Pages 22-24.Nutritional deficiency is a major cause of neurotransmitter dysfunction, as well as drugs such as Zoloft and Prozac. These drugs inhibit the reuptake of serotonin and so cause a loss of serotonin. Neurotoxic effects are permanent. They are caused by heavy metals, chemicals and drugs. The main drug that causes neurotoxicity is amphetamines. Neurotoxic effects are in the post-synaptic neurons. The treatment is the same as deficiency of amino acids, but it takes more of these amino acids forming serotonin to be effective at the post-sympathic neuron. Neurotransmitter Testing and Amino Acid Therapy, Marty Hinz, MD, NeuroResearch, Morgan Park Clinic, Duluth, Minnesota, 2002, Pages 22-24"

I drink whey protein. It's my favorite protein drink. I'd read that whey helps diabetics stabilize blood sugar, even when ingested with a high carb meal. I posted the study on the old board. My friend is diabetic, and the whey protein definitely helps her.

I don't understand that. I thought those AD's increased serotonin which is a good thing for depression. :confused:

I'm sure there are other reasons!

: Anticancer Res. 2003 Mar-Apr;23(2B):1411-5.
The antioxidant system.
Bounous G, Molson JH.



The glutathione (GSH) antioxidant system is the principal protective mechanism of the cell and is a crucial factor in the development of the immune response by the immune cells. Experimental data demonstrate that a cysteine-rich whey protein concentrate represents an effective cysteine delivery system for GSH replenishment during the immune response.

Animal experiments showed that the concentrates of whey protein also exhibit anticancer activity. They do this via the GSH pathway, the induction of p53 protein in transformed cells and inhibition of neoangiogenesis.

PMID: 12820403 [PubMed - indexed for MEDLINE]

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

Elevated glutathione as a therapeutic strategy in Alzheimer's disease -
DA Butterfield, CB Pocernich, J Drake - Drug Development Research, 2002

GSH levels are increased with strict adherence to a diet rich in whey proteins. ....whether they're increased in the brain is probable but needs demonstration.

....The bioavailability of NAC given orally is less than 20%.

Lots of good info here:

http://www3.interscience.wiley.com/c...17480/PDFSTART

Wow. Nice to see such an avid discussion about this. I have MS and posted about this on an MS forum (not the board here) -- not one response! :eek:

I look forward to reading all the back and forth more carefully -- hope you don't mind that I poked my head in here. :)

Anytime!

paula

Bioavailability
 

Thanks IMark, must find a source of whey protein in the UK.
If NAC is used as a source of cysteine since NAC is more readily absorbed by the body, yet according to ZF's reference, "....The bioavailability of NAC given orally is less than 20%", then there must be a natural substance in whey protein to assist bioavailability.
Looks like natural sources are often best, so whey protein rather than NAC, and Mucuna pruriens instead of sinemet, (since mucuna P. seems to contain a natural decarboxylation inhibitor, rather than the synthetic carbidopa in sinemet)
Like Zuchini Flower, I found a couple of strange comments in IMarks paper,
"The neurotransmitters are fat soluble and cannot cross the blood/brain barrier." The more fat soluble (lipophilic) a molecule is, the easier to cross the BBB.
I also feel that "Neurotoxic effects are permanent" is wrong, look at Rick's example of AD patients regaining their memory in minutes. If the damage is permanent, we can never be cured.
Ron

Nac Bbb Etc
 

Dr. Russell Blaylock (author of "Excitotoxins: the Taste that Kills" and son of a PD victim) says that NAC is probably good for the brain but that cysteine is dangerous in the same way as MSG/glutamate is. It depends on where you are talking about and what the concentrations are. MSG knocks me for a loop. I go completely off with freezing for 4 to 8 hours and it takes a couple of days to recover. Nasty stuff.

From http://www.whale.to/a/blaylock5.html

In this brief discussion of a most complicated and evolving subject, I have had to omit several important pieces of the puzzle. For example, I have said little about the functional components of the receptor systems, the glutamate transporter and its relation to ALS and Alzheimer's dementia, receptor decay with aging and disease, membrane effects of lipid peroxidation products, membrane fluidity, effects of chronic inflammation on the glutamate/free radical cycle, stress hormones and excitotoxicity, the role of insulin excess on the eicosanoid system, or the detailed physiology of the glutamatergic system. I have also only briefly alluded to the toxicity of aspartame and omitted its strong connection to brain tumor induction.

But, I have tried to show the reader that there is a strong connection between dietary and endogenous excitotoxin excess and neurological dysfunction and disease. Many of the arguments by the food processing industry have been shown to be false. For example, that dietary glutamate does not enter the brain because of exclusion by the blood-brain barrier, has been shown to be wrong, since glutamate can enter by way of the unprotected areas of the brain such as the circumventricular organs. Also, as we have seen, chronic elevations of blood glutamate can breech the intact blood-brain barrier. In addition, there are numerous conditions under which the barrier is made incompetent.

As our knowledge of the pathophysiology and biochemistry of the neurodegenerative diseases increases, the connection to excitotoxicity has become stronger.(21) This is especially so with the interrelationship between excitotoxicity and free radical generation and declining energy production with aging. Several factors of aging have been shown to magnify this process. For example, as the brain ages its iron content increases, making it more susceptible to free radical generation. Also, aging changes in the blood brain barrier, microvascular changes leading to impaired blood flow, free radical mitochondrial injury to energy generating enzymes, DNA adduct formation, alterations in glucose and glutamate transporters and free radical and lipid peroxidation induced alterations in the neuronal membranes all act to make the aging brain increasingly susceptible to excitotoxic injury.

Over a lifetime of free radical injury due to chronic stress, infections, trauma, impaired blood flow, hypoglycemia, hypoxia and poor antioxidant defenses secondary to poor nutritional intake, the nervous system is significantly weakened and made more susceptible to further excitotoxic injury. We know that a loss of neuronal energy generation is one of the early changes seen with the neurodegenerative diseases. This occurs long before clinical disease develops. But, even earlier is a loss of neuronal glutathione functional levels.

A word about ascorbic acid: Few are aware of the importance of adequate ascorbate levels for CNS function and neural protection against excitotoxicity. We are finding out that ascorbic acid plays a vital role in neurobehavioral regulation and the dopaminergic system as well, which may link ascorbate supplementation to improvements in schizophrenia.

Our knowledge of this process opens up new avenues for treatment as well as prevention of excitotoxic injury to the nervous system. For example, there are many nutritional ways to improve CNS antioxidant defenses and boost neuronal energy generation, as well as improve membrane fluidity and receptor integrity. By using selective glutamate blocking drugs or nutrients, one may be able to alter some of the more devastating effects of Parkinson's disease. For example, there is evidence that dopamine deficiency causes a disinhibition (overactivity) of the subthalamic nucleus and that this may result in excitotoxic injury to the substantia nigra.(22) By blocking the glutamatergic neurons in this nucleus, one may be able to reduce this damage. There is also evidence that several nutrients can significantly reduce excitotoxicity. For example, combinations of coenzyme Q10 and niacinamide have been shown to protect against striatal excitotoxic lesions. Methylcobolamine, phosphotidylserine, picnogenol and acetyl-L-carnitine all protect against excitotoxicity as well.

Of particular concern is the toxic effects of these excitotoxic compounds on the developing brain. It is well recognized that the immature brain is four times more sensitive to the toxic effects of the excitatory amino acids as is the mature brain. This means that excitotoxic injury is of special concern from the fetal stage to adolescence. There is evidence that the placenta concentrates several of these toxic amino acids on the fetal side of the placenta. Consumption of aspartame and MSG containing products by pregnant women during this critical period of brain formation is of special concern and should be discouraged. Many of the effects, such as endocrine dysfunction and complex learning, are subtle and may not appear until the child is older. Other hypothalamic syndromes associated with early excitotoxic lesions include immune alterations and violence dyscontrol.

Over 100 million American now consume aspartame products and a greater number consume products containing one or more excitotoxins. There is sufficient medical literature documenting serious injury by these additives in the concentrations presently in our food supply to justify warning the public of these dangers. The case against aspartame is especially strong.

Oral NAC 100% effective as a Cys precursor
 

Hi,

I recently found an article at the Journal of Animal Science that dealt specifically with this issue of NAC bioavailability that I think might be insightful.

Oral N-acetyl-L-cysteine is a safe and effective precursor of cysteine
R. N. Dilger and D. H. Baker

"It is apparent that considerable confusion exists with regard to the meaning of the term "NAC bioavailability." Previous pharmacokinetic studies (Borgström et al., 1986Go; Olsson et al., 1988Go; De Caro et al., 1989Go) have focused on the amount of an oral NAC dose that reaches the bloodstream as NAC itself. Little emphasis has been placed on the chemical modification of NAC (i.e., deacetylation) within the gut lumen and enterocyte during absorption. Therefore, pharmacokinetic studies suggesting that less than 10% of oral NAC is absorbed into portal blood as NAC per se are misleading. Our approach, however, was based on the assumption that beneficial effects of NAC do not result from NAC itself, but rather from NAC delivering Cys for in vivo functions (e.g., glutathione synthesis). Thus, the ability of NAC (the test precursor) to provide Cys relative to Cys itself (the standard nutrient) was assessed in assay 2. The results of this study (Table 3Go) clearly showed that oral NAC was 100% effective as a Cys precursor."

*to read more please go to http://jas.fass.org/cgi/content/full/85/7/1712

Thank you for a great discussion!

In health,

Paul