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

Why I'm a Fan of Copper

[Answering M.F.’s questions: What is the importance of taking copper? Should everyone be taking 2mg of this supplement daily, separate from a multivitamin? Or does this apply only to a specific group of individuals? Also, is there an advantage to taking either the citrate or glycinate form in terms of absorption?]

What is the importance of taking copper? Copper is an integral part of numerous enzyme systems, including amine oxidases, ferroxidase (ceruloplasmin), cytochrome-c oxidase, superoxide dismutase, and dopamine hydroxylase. Copper is also a component of ferroprotein, a transport protein involved in the basolateral transfer of iron during absorption from the intestine. As such, copper plays a role in iron metabolism (important for blood formation), melanin synthesis (important for skin color), energy production, neurotransmitter synthesis, and nervous system function; the synthesis and cross-linking of elastin and collagen; and the scavenging of superoxide radicals.[1]

From my viewpoint, the most important aspects are for the insurance of presence of sufficient quantities of copper for the cross linking of elastin and collagen and the dopamine hydroxylase.

The cross linking of elastin and collagen is of immediate importance in the health of bones, joints, tendons, skin and hair among other things. Of paramount importance though is the dopamine hydroxylase. This is because this enzyme is necessary for the hydroxylation of dopamine to noradrenalin which is the precursor to adrenalin.[2] I consider adrenalin to be of supreme importance for health when generated physiologically naturally. Of note here is that vitamin C (ascorbic acid) is a cofactor for the hydroxylation of dopamine to noradrenalin.

Don't take more than the recommended 2-3 mg daily, as at higher levels toxicity may ensue. (More isn't better). 10 mg intake can be dangerous.[1] See table:

Deficiencies and Toxicities of Metals - from Harrison's Online via AccessMedicine

It has been seen that copper did have a positive impact on HDL (the cardioprotective cholesterol) and did lower oxidized LDL values. This last is the type that tends to form the clogging cholesterol within the walls of blood vessels (specifically arteries). The study showing this was somewhat short for my taste and wasn’t consistent in its results but the logical tie-in to the heart protective factors is solid.[3] This study used the glycinate form of copper.

Another study shows that patients suffering from diabetes mellitus have lower levels of copper in their serum compared to control patients.[4] Again the tie-in here is logical.

Should everyone be taking 2mg of this supplement daily, separate from a multivitamin? Individuals whose nutrition is deficient or low in copper intake should take a separate supplement. Dietary sources of copper include shellfish, liver, nuts, legumes, bran, and organ meats. For myself I prefer not to take a chance on not getting enough of this essential mineral and hence take it anyway separate from the copper from other sources. By taking it separately as a 2 mg pill/capsule in addition to a usual 2 mg in the multivitamin tablet then we cap at 4 mg per day plus nutritional sources. We stay well below the 10 mg/day toxic level.

Is there an advantage to taking either the citrate or glycinate form in terms of absorption? It would appear that, at least in animals the glycinate form will provide superior bioavailability of the nutrient, compared to the citrate. That being said I personally take the citrate form as I also take a multivitamin tablet three times weekly, in addition to regular food intake.[5]

References:

[1] SP Russell RM (2012) Chapter 74. Vitamin and Trace Mineral Deficiency and Excess. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, eds. (ed), Harrison's Principles of Internal Medicine. 18th ed. edn., McGraw-Hill, New York, pp http://0-www.accessmedicine.com.library.ccf.org/content.aspx?aID=9099706.

[2] Molina PE. Chapter 6. Adrenal Gland. In: Molina PE, ed. Endocrine Physiology. 3rd ed. New York: McGraw-Hill; 2010. http://0-www.accessmedicine.com.library.ccf.org/content.aspx?aID=6169718. Accessed April 29, 2012.

[3] RA Disilvestro, EL Joseph, W Zhang, AE Raimo, YM Kim (2012) A randomized trial of copper supplementation effects on blood copper enzyme activities and parameters related to cardiovascular health Metabolism Doi:10.1016/j.metabol.2012.02.002.

[4] M Basaki, M Saeb, S Nazifi, HA Shamsaei (2012) Zinc, Copper, Iron, and Chromium Concentrations in Young Patients with Type 2 Diabetes Mellitus Biol Trace Elem Res Doi:10.1007/s12011-012-9360-6.

[5] Ammerman CB, Baker DH. Bioavailability of Nutrients for Animals: Amino Acids, Minerals, Vitamins. Chapter 7. Copper Bioavailability. Pp. 127-156. Link.

Chapter 10: Depression

Opinion: It is time to relegate Freudian theories to the museum and to realize that emotions, feelings, mood and thinking are results of organic processes in the body and brain interacting with the environment. Healthy organic processes can handle bad memories.

We have repeatedly heard that depression is due to an imbalance of chemicals in the brain without specification of those chemicals and why they even became imbalanced. I will outline to you what I think is amiss and how to prevent and alleviate the condition of depression.
By not following The Pillars described in previous chapters, we run the risk of not having certain chemicals in our brains in sufficient amounts to function correctly. Specifically these chemical deficiencies are those, which are responsible for thinking, memory, feeling happy, libido, good sleeping and just overall energy. To name the main players I will mention serotonin, endorphins, TRH, GABA, adrenaline and thyroxin. Cortisol is also a player but I think that in depression it gets produced in a chaotic excess pattern more than that it is in a deficient state. So depression can ensue by not having good nutrition (vitamins included), not having enough physical activity, not sleeping regularly and not avoiding harmful substances, or a combination in varying degrees of some or all of the above.
Stress is another player that I would like to talk a little about. If a person is healthy and gets exposed to severe acute emotional stress then their reserves of the chemicals mentioned above will be drawn upon and they will be able to withstand the onslaught and not develop depression. But, if the stress is long enough, the reserves will be depleted and the depression syndrome will develop. On the other hand an unhealthy person can develop depression even without emotional stresses.
Another factor is that people who have abused their bodies with harmful substances which shut down the body’s own “machinery” for producing the chemicals above, will be much more likely to develop depression. An example of this is people who have been addicted to narcotics will have deconditioned endorphin-producing tissue. This will of course predispose them to depression but the degree of predisposition will vary with how much and how long they were addicted. Alcohol will hurt the body in a similar way. In general my advice for curing the common form of depression is to apply The Pillars Of Health judiciously and use antidepressant medicines temporarily as a helping tool. Once reasonable improvement has occurred then the antidepressants may be weaned off.
Supplements of 5-HTP, and tyrosine are beneficial in this context and will assist above curing process and assist the onboard antidepressant by supplying the building blocks for serotonin in the instance of 5-HTP, and adrenaline and noradrenaline in the instance of tyrosine. This must be done under your doctor’s supervision.

Does light or sunlight play a role in depression?

Light, especially sunlight definitely plays a role and this becomes most evident in the condition of seasonal affective disorder (SAD). The importance of light as a corrective treatment in SAD, with results superior to placebo has been established.[1]

What appears to happen in SAD, is production of the neurotransmitter serotonin is disrupted. It has been seen that the turnover (production and metabolism) of serotonin by the brain was lowest in winter, and more significantly the rate of production of serotonin by the brain was directly related to the prevailing duration of bright sunlight. The production rose rapidly with increased light intensity.[2] In a situation of lower production of brain serotonin then we can anticipate the presence of depressive symptoms of tiredness, dejectedness, appetite changes (possibly anorexia or maybe increased desire for carbohydrates) and so on.

I don't believe vitamin D plays a major role in SAD, although I would anticipate it may have a minor one, by virtue of its importance in calcium and phosphate absorption. It has been seen to have a positive impact on depression.[3] This stance should not be interpreted as belittling the role of vitamin D in health as I am a big proponent of its supplementation into our diets.

[Rev.1/2/2012]

References:

[1] B Byrne, GC Brainard (2008) Seasonal Affective Disorder and Light Therapy Sleep Medicine Clinics 3: 307 - 315. Doi:10.1016/j.jsmc.2008.01.012.

[2] G Lambert, C Reid, D Kaye, G Jennings, M Esler (2002) Effect of sunlight and season on serotonin turnover in the brain The Lancet 360: 1840 - 1842. Doi:10.1016/S0140-6736(02)11737-5.

[3] Women's mental health: depression and anxiety. Nursing Clinics of North America - Volume 44, Issue 3 (September 2009)