Nightshade Vegetable Allergies

In response to:
[Bess Rhoades has left a new comment on your post "Why I'm a Fan of Copper": 
Dr. A- I do not know how to enter a question on this blog, so this is the best I could do. Could you please address what you believe about nightshade vegetable allergies- and their possible role in inflammatory process and perhaps even arthrities in certain individuals. I thought this was far fetched until I began reading. This article in particular caught my interest: 
https://www.westonaprice.org/health-topics/food-features/nightshades/
Thank you] 
Looking at your reference.
Paragraph 1: Claiming sensitivity to these plants without delineating a causal pathophysiology is always concerning to me and makes the content lack credibility.
Paragraph 3: If you have as claimed a sensitivity to a certain food, I don’t think it would be harmful to avoid them for a month or two, and monitor the improvement or lack thereof. I doubt with pretty good logic and science that nightshade plants "cause" heartburn. They may exacerbate symptoms but don’t cause relaxation of the lower esophageal sphincter, as far as I know at this time. (One of these days I will write up the causes of alluded to relaxation).
Paragraph 5: Potatoes causing dropsy. Anytime a human relies on a high carbohydrate low protein diet in tandem with a  deficiency of other important nutrients, expect there to be body swelling.
I stopped reading after paragraph 6 as the author's arguments and evidence presentation were excessively weak and lacking in logic and definite pathophysiological cause, not to mention heavily infused with loose associations being put forth as evidence. Also the author, although listing references, didn’t associate them with the facts being quoted and therefore very difficult to verify his studies/articles/references.
Notes: Tomatoes have evidence of being anticancer.
In summary I would say that it's possible some people may have increased sensitivities to certain foods, but I would hesitate to say that 'nightshade' plants are dangerous as a group.
DA

Mucuna Pruriens in Anxiety/Depression

Question: AnonymousNovember 13, 2015 at 2:45 PM
What are your thoughts on the herbal supplement, mucuna pruriens, for anxiety/depression? 

Answer: I have personally not been aware of this herb, Mucuna pruriens, till your question. After a quick research I found the following:

The major phenolic constituent of M. pruriens beans was found to be L-dopa (5%), along with 5-indole compounds, two of which were identified as tryptamine and 5-hydroxytryptamine.

The thought is that L-dopa being a precursor of dopamine, thence the different pharmacological effects. (Anti-diabetic, anti-inflammatory, neuroprotective, and anti-oxidant properties). 

I would think that the benefit of this herb would be via 1- the increased production of adrenaline (from the precursor L-dopa), outside the brain, 2- the provision of a significant amount of precursors (tryptamine and 5-hydroxytryptamine), for serotonin peripherally and centrally, and 3- provision of L-dopa to the brain (as it crosses the blood brain barrier), which is a precursor for dopamine centrally. The increased production of adrenalin physiologically, in addition to increased production of serotonin and dopamine centrally should have a positive impact on depression.

In India, the seeds of M. pruriens have traditionally been used as a nervine tonic, and as an aphrodisiac for male virility.

It looks promising logically for anxiety but more so for depression, but I'm afraid I can't endorse its use at this time as I am not familiar with its dosing, its safety profile, purity of preparation, and studies where it has been used for anxiety or depression.

[Ref.- Lampariello LR, Cortelazzo A, Guerranti R, Sticozzi C, Valacchi G. The Magic Velvet Bean of Mucuna pruriens. Journal of Traditional and Complementary Medicine. 2012;2(4):331-339.] 

How to Decide On How Much 5-HTP (5-Hydroxytryptophan) and L-Tyrosine to Take In Mild Depression? (Edited: 1/15/17)

The question posed: “I am taking 5-HTP and L-Tyrosine supplements for mild depression and have been doing some research. I have read that a 10:1 ration (L-tyrosine to 5-HTP) is recommended so that no neurotransmitter is depleted. What are your thoughts? How about a 5:1 ratio? I know everyone is different but how would you recommend starting out and adjusting dosage?”

My answer: (run the following by your doctor first before applying) 

I don’t agree with tying these two building blocks together in a ratio as posed because of the following: each one is involved in the production of different neurotransmitters, and everyone has a different magnitude of symptoms of depression which is commensurate with the neurotransmitter that is deficient. Therefore the symptoms and the response thereby to ingesting these precursors can be your guide on how much to take in the beginning and thereafter tailor accordingly.

If the exhibited symptoms include headache, poor sleep, inexplicable body pains, and/or memory issues then the anticipated deficiency is more in line with serotonin deficiency. Hence I would think 5-HTP is going to be needed for sure. I would start with a dose of 50 mg nightly after the evening meal and escalate a week later to 100 mg nightly and hold there for at least one month to see if the symptoms described here improve. It takes time to build up the amino acid pools in the body. This is assuming the 5-HTP is good quality and pure. If nausea arises, or if you become jittery, sweaty or get a rapid heart rate 30-60 minutes after (Edited: 1/15/17) intake of the 5-HTP in spite of taking it after a regular sized meal then you may be taking too much.

If the exhibited symptoms include sugar and starch craving, fatigue, preponderance of gloom, poor stamina, feeling cold more than normal people around you then the anticipated deficiency would be more in the adrenaline, and noradrenaline (neurotransmitter) arena. In this setting the tyrosine will be essential to production of the forementioned, as it is the precursor to both. As such I would go with a starting dose of 100 mg daily with a meal. This may be upped 100 mg every three days to a maximum of 1000 mg daily depending on side effects and therapeutic response. Once you get improvement then I would hold at that dose for 6 to 9 months then start weaning off over the following 3 months. I started low on the tyrosine as some patients may be deficient in this amino acid and on taking it in a large dose may result in hypotension, and or dizziness secondary to a higher production of adrenaline in a more than used to fashion. The body should be able to adjust to this over the following weeks, and if not I would do the escalation even more slowly.

Note: to produce neurotransmitters from precursors like you are targeting, there must be available certain vitamins which are part of certain enzymes and co-enzymes necessary for this production. Specifically I will mention vitamin C for production of serotonin and noradrenaline. Also copper and iron for production of noradrenaline. The amount I recommend is vitamin C 250 mg daily, copper 2 mg daily and iron 8-15 mg daily, or even better getting the equivalents in food (tomatoes, peanuts, red meat) (Edited: 1/15/17). The last two may be found in many multivitamin preparations. I would also recommend taking the multivitamin after the main meal of the day to enhance their absorption and decrease the possibility of nausea.

Note: do not take above supplements with anti-depressants.

A DIET FOR FIBROMYALGIA? FOODS ACCEPTABLE FOR FIBROMYALGIA AT THE RESTAURANT.

Regarding the diet for Fibromyalgia, with a couple of exceptions, it is basically the one found here:  http://thepillarsofhealth.blogspot.com/2008/04/appendix-diet.html

For Fibromyalgia I prefer that the patient not have any products containing white flour, because of its refinement and the ease with which it is absorbed into the blood stream as glucose, which will elicit an insulin response which will inhibit adrenalin output, which we don’t want.

A practical principle here is to avoid high glycemic index foods. A nice list is here: http://www.health.harvard.edu/newsweek/Glycemic_index_and_glycemic_load_for_100_foods.htm

Another point is that there should be emphasis on protein intake (fish, chicken, turkey, eggs, cheese, etc.), as there is the need to keep the amino acid pool satisfactorily stocked with the building blocks for energy hormones, and neurotransmitters.  In addition amino acids can act as a source for slow production of glucose (which shouldn’t initiate an insulin secretion response – I have not verified this factoid). This production of glucose takes place in the liver in a process called gluconeogenesis.

Acceptable restaurants foods for Fibromyalgia:

·         Chicken paprikash without the dumplings or noodles. More sour cream or yoghurt and vegetables.

·         Salads topped with chicken, or steak.

·         Steak and eggs. For breakfast. Hold on the white bread.

Basically apply: no refined sugars and no white starches.

Smoking and Depression

First, let us try and understand what cigarettes do as relates to depression.

According to the American Heart Association, nicotine addiction (I prefer calling it tobacco addiction because it is not only nicotine that is addictive in the tobacco), has historically been one of the hardest addictions to break, while the pharmacological and behavioral characteristics that determine tobacco addiction are similar to those determining addiction to heroin and cocaine.

Is there anything mystical about how cigarettes are addictive? No. It is all very organic, and physical. The tobacco contains two categories of chemicals that establish addiction in addition to the conditioned reflex aspect (Pavlovian), which also fortifies the addiction. This last part is more related to the whole process of the activity itself of the cigarette touching the lips, the action of inhalation, the smell of the cigarette, holding the cigarette, etc. As nicotine enters the body, it is distributed quickly through the bloodstream and crosses the blood–brain barrier reaching the brain within 10–20 seconds after inhalation. The elimination half-life of nicotine in the body is around two hours.^[i]

Tobacco smoke contains, in addition to nicotine (the first category I alluded to above), the monoamine oxidase inhibitors harman and norharman (the second category I alluded to above). These second category compounds significantly decrease MAO activity in smokers. This was evidenced by positron emission tomography imaging that showed smokers have a much lower activity of peripheral and brain MAO-A (30%) and -B (40%) isozymes compared to non-smokers.^[ii],^[iii] MAO enzymes break down monoaminergic neurotransmitters such as dopamine, norepinephrine, and serotonin. It is thought that the powerful interaction between the MAOIs and the nicotine is responsible for most of the addictive properties of tobacco smoking.^[iv] Therefore when the activity of MAO enzymes is impeded these neurotransmitters are higher in quantity (enhancing brain function artificially), but the flip side of this is when the tobacco is gone the MAO enzymes increase and hence decrease those neurotransmitters (at least temporarily. This translates into the withdrawal syndrome from tobacco in addition to worsening of any depression state present. The magnitude and duration of these phenomena will vary with how long and how much the person has been using tobacco, and how healthy the individual is. In other words a less healthy person will take longer to renovate their brain neurotransmitter production compared to a healthier person.

As such a treatment strategy for you: target increasing the neurotransmitters in the brain by all means possible which are safe if supervised:

1. Decrease MAO enzymes activity by taking a MAO enzyme inhibitor drug. An example of this kind of drug is phenelzine (Nardil). [As a last resort only].
2. Provide the building blocks for the neurotransmitters: i.            Protein is the major component of almost all major currently recognized neurotransmitters. ii.            Vitamin C is essential for the manufacture of certain neurotransmitters. iii.            All the B-complexes play a significant role in the production of neurotransmitters and are of paramount significance for their function. iv.            Good hydration. How this works is multifactorial and I won't go into here in biochemical/physiological detail. That being said, intake sufficient fluid to maintain urine color a very light light yellow. If you are sweating in your exercise routine then replace your losses with a fluid containing sodium chloride (salt), potassium and some magnesium. The last isn't as important as the first two, so if not present in the purchased fluid then no worries.
3. Stimulate the production of adrenaline peripherally to stimulate neurotransmission and neurotransmitters in the brain. This is done by regular exercise targeting sweating 10 minutes per session in the beginning and later increasing that according to what your body tells you. Do one day per week (minimum), per decade of your age. If you are 28 years old then minimum three days exercise per week. If you are 44 years old, then five days per week, and so on.
4. Avoid food substances that inhibit adrenaline production. Any food that leads to secretion of insulin in high quantities causes inhibition of adrenaline secretion. This would be all foods that are assimilated and absorbed rapidly into the blood stream as glucose (a simple sugar). Examples are all refined sugars and all white refined starch products. (Candy, candybars, pastries, pasta, lasagna, pizza, mashed potatoes, rice, etc.)
5. Provide an environment to your body which enhances production and conservation of these neurotransmitters. In other words, sufficient regular sleep. To the tune of 8 hours per 24 hours. Preferably in one block.
6. Stop smoking, start 7 mg patch nicotine (while awake) for two weeks, start the MAO enzyme inhibitor, all in addition to above.
7. You must be off escitalopram for 10 days prior to starting MAO enzyme inhibitor. (They interact).

Comments:

1. Overcoming the conditioned reflexes will take time. Think months to a year. So the craving triggered by memory will take a while to go away.
2. The physical organic aspect of the addiction goes away quicker.
3. Taking MAO enzyme inhibitors as an antidepressant medication is serious business and must be supervised closely by the prescribing physician. Avoid over the counter medications unless cleared by physician who is aware you are on a MAO enzyme inhibitor.
4. Tobacco smoke will enhance the activity of the escitalopram in an ongoing fashion. (answering your question above.
5. The nicotine content of popular American-brand cigarettes has slowly increased over the years, and one study found that there was an average increase of 1.6% per year between the years of 1998 and 2005. This was found for all major market categories of cigarettes.^[v] So the sooner you quit the better.

References:

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[i] http://en.wikipedia.org/wiki/Nicotine

[ii] Herraiz T, Chaparro C (2005). "Human monoamine oxidase is inhibited by tobacco smoke: beta-carboline alkaloids act as potent and reversible inhibitors". Biochem. Biophys. Res. Commun. 326 (2): 378–86.

[iii] Fowler JS, Volkow ND, Wang GJ, et al. (1998). "Neuropharmacological actions of cigarette smoke: brain monoamine oxidase B (MAO B) inhibition". J Addict Dis 17 (1): 23–34.

[iv] Villégier AS, Blanc G, Glowinski J, Tassin JP (September 2003). "Transient behavioral sensitization to nicotine becomes long-lasting with monoamine oxidases inhibitors". Pharmacol. Biochem. Behav. 76 (2): 267–74.

[v] Connolly, G. N; Alpert, H. R; Wayne, G. F; Koh, H (2007). "Trends in nicotine yield in smoke and its relationship with design characteristics among popular US cigarette brands, 1997–2005". Tobacco Control 16 (5): e5. doi:10.1136/tc.2006.019695. PMC 2598548. PMID 17897974.

Is it safe to take 200-300mg of 5-HTP a day for Depression? Is Rhodiola Rosea useful for depression?

Depending on the actual bioavailability provided by different 5-HTP preparations I would say a good pure preparation of 100 mg daily should be a sufficient amount in this situation. Taking too much could end up in a serotonergic reaction (agitation, consciousness impairment, tachycardia, hallucinations, etc.)[1]. Therefore with a reliable preparation, as seen with ‘PureEncapsulations’ I would stick to 100 mg daily only.

Rhodiola Rosea: In Russia and Scandinavia, it has been used for centuries to cope with the cold Siberian climate and stressful life.[2] The theory is that is has a positive impact on serotonin, dopamine and acts as a monoamine oxidase inhibitor. This would affect depression in a positive way.[3] In light of what it can do and the lack of studies, and lack of standardization I would only use it with a high degree of caution and under direct supervision of your physician lest you trigger a sertonergic reaction as described above. I have never used this substance before but after reading about it, it does look interesting.

For depression: Are there any other herbs, amino acids, or vitamins you would recommend? I also like Copper 2-3 mg once daily with a meal (which can be in a multivitamin). Be cautious with other amino acids though as they can have some pretty significant effects and side effects. Sometimes I will also use St. Johns Wort at 300 to 900 mg daily in divided doses. This last is a weak serotonin reuptake inhibitor.  

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[1] http://www.nlm.nih.gov/medlineplus/ency/article/007272.htm

[2] http://en.wikipedia.org/wiki/Rhodiola_rosea

[3] Monoamine oxidase inhibition by Rhodiola rosea L. roots. [J Ethnopharmacol. 2009] - PubMed - NCBI . http://www.ncbi.nlm.nih.gov/pubmed/19168123. Accessed 10/7/2012 2012.

How to Raise GABA (Gamma-amino-butyric acid) in the Brain by Natural Means

[Answering M.F.’s questions: You recently stressed that I need to increase the levels of GABA in my body to help with my persistent anxiety. Are there natural ways to do this through specific foods or even drinks, such as loose leaf tea (due to its precursor l-theanine)?]

Background: As a general rule, in promoting health I like to stay as close as possible to letting and assisting the body in building its own enzymes, hormones, different substances via its own machinery because of my fear of disrupting the body’s magnificent equilibrium. This fear encompasses different issues of feedback mechanisms, rate limiting steps, dependency issues, etc.

Without further ado: GABA (Gamma-amino-butyric acid) functions in brain tissue as an inhibitory neurotransmitter by altering transmembrane potential differences. Throughout the adult brain, where scientists have mostly studied the roles of glutamate and GABA, it has been established that both amino acids function primarily as signals transmitted between cells. Most of the cells transmitting either glutamate or GABA signals are neurons. After release, GABA diffuses a very short distance and binds to receptor proteins on the surface of the target neuron, which are specialized for sensing either GABA or glutamate via either glutamatergic or GABA receptors. GABA subsequently will be taken up, or transported out by carrier proteins. The uptake process requires energy and involves co-transport of GABA, which is neutral at physiological pH, together with two sodium ions and one chloride ion.[3],[5] The result of GABA stimulation of GABA receptors specifically serves to retard the stimulatory effects of glutamate throughout the brain.

Why is it important for anxiety? All anxiogenic agents act on the GABA-A receptor/chloride ion channel complex, implicating this neurotransmitter system in the pathogenesis of anxiety and panic attacks.[7] As such increasing GABA availability, and or increasing the efficiency/effect of, or sensitivity of GABA receptors should help alleviate the feelings of anxiety.

How to promote its availability: GABA (Gamma-amino-butyric acid) can be formed from glutamic acid in the presence of pyridoxal phosphate[1]  (as a cofactor for glutamic acid decarboxylase – GAD).[2] The pyridoxal phosphate arises from vitamin B6 (pyridoxine). Therefore availability of B6 is necessary. Don't overdo. Too much B6 has neurotoxic effects. 10 mg per day is easily sufficient. Other factors that may promote healthy GABA metabolism would be physiological levels of sodium and chloride (salt), in an ample fluid medium. Practical translation: sufficient salt and water intake. Lyte-Hydrate well.

Valerian raises GAD (glutamic acid decarboxylase) activity[4] which may raise GABA (Gamma-amino-butyric acid) in the neuronal tissues which should have a calming effect. The extract also contains GABA[8] which may have a direct impact on GABA receptors.

Make sure the building block of GABA is available (glutamic acid): All meats, poultry, fish, eggs, dairy products, and kombu are excellent sources of glutamic acid. Some protein-rich plant foods also serve as sources.[1]

To my knowledge only certain pharmaceuticals (such as phenobarbitone) function as a GABA receptor modulator which enhances the target function of said receptors.

Theanine: is an amino acid present in green tea which appears to have stimulatory effects and inhibitory effects on glutamic acid. For calming one would desire the inhibitory effect. How it works seems unclear to date (5-28-12). As such I would think it would be okay to use although in this case it is functioning more as a pharmaceutical agent and not as a building block. Theanine is similar in molecular structure to glutamic acid and hence could be ‘pressuring’ glutamic acid and causing it to be more available for transforming into GABA. Here I am theorizing. Then again it could be occupying glutamatergic receptors without causing the usual excitatory activity which glutamic acid usually results in. Here I am theorizing again.

References:

[1] Rodwell VW. Chapter 30. Conversion of Amino Acids to Specialized Products. In: Bender DA, Botham KM, Weil PA, Kennelly PJ, Murray RK, Rodwell VW, eds. Harper's Illustrated Biochemistry. 29th ed. New York: McGraw-Hill; 2011. http://0-www.accessmedicine.com.library.ccf.org

[2] http://en.wikipedia.org/wiki/Glutamate_decarboxylase

[3] GABA as a Neurotransmitter and Neurogenic Signal - eLS - Barker - Wiley Online Library . http://0-onlinelibrary.wiley.com.library.ccf.org/doi/10.1038/npg.els.0000121/full. Accessed 5/13/2012 2012.

[4] R Awad, D Levac, P Cybulska, Z Merali, VL Trudeau, JT Arnason (2007) Effects of traditionally used anxiolytic botanicals on enzymes of the gamma-aminobutyric acid (GABA) system Can J Physiol Pharmacol 85: 933-942. Doi:10.1139/Y07-083.

[5] Nicotinic Acetylcholine Receptors - eLS - Lindstrom - Wiley Online Library . http://0-onlinelibrary.wiley.com.library.ccf.org/doi/10.1002/9780470015902.a0000245.pub2/full. Accessed 5/20/2012 2012.

[6] Russek, S. J. 2006. γ-Aminobutyric Acid (GABA) Receptors. eLS.

[7] Reus VI. Chapter 391. Mental Disorders. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, eds. Harrison's Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012. http://0-www.accessmedicine.com.library.ccf.org/content.aspx?aID=9112222. Accessed May 27, 2012.

[8] http://en.wikipedia.org/wiki/Valerian_%28herb%29#Biochemical_composition