Zinc Deficiency: Taste Buds Stop Working, & When Severe, Food is Revolting


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Hypogeusia

A Case Report

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The diagnosis came from a non-medical book:

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Remove zinc from your diet and you will get a condition known as hypogeusia, in which your taste buds stop working, making food boring or even revolting, but until as recently as 1977 zinc was thought to have no role in diet at all.The quote leaped from the page of a book “At Home” by Bill Bryson.

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Food aversion. Revulsion toward food.

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Hypogeusia is a diminished sense of taste resulting from zinc deficiency. The patient slowly, week after week, developed a severe aversion to all food groups except cappuccino (arginine).

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Month after month it became severe before the patient was finally able to identify a descriptive term “food aversion.” Hunger was severe. Patient was desperate to find fuel for body that was not revolting.

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Not anorexia – means loss of appetite. The patient was starving.

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Not anorexia nervosa – a distorted body image in which patients severely restrict food intake and can starve to death.

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Not depression – depressed mood often associated with poor appetite or stress eating.

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Food aversion was bizarre, going to bed starving while the best foods were sitting in the fridge untouched and literally repulsive even to think about. For months, walking up and down grocery aisles, repulsed by the thought of the finest foods despite hunger, craving to find some form of fuel that was not revolting. Months and months went by as it became severe. Past favorite foods might as well have been poison. Flavor was wanting.

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Specialists and literature searches commonly view food aversion as psychosomatic or the bizarre cravings of pregnancy. Females are at particular risk of being assigned psychological diagnoses. We do our patients a disservice failing to appreciate the complexity of human physiology with our limited understanding of evolving science. The human body is complex.

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To complicate matters, it’s not easy to diagnose depression – not all patients recognize it in themselves. Further, zinc deficiency induces depressive behaviors, plays a major role in major depressive disorder and is a risk factor for treatment resistance — referenced below at end. 

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Aversion became extreme before the patient could name the correct term: food aversion, no doubt why it is barely mentioned in medical searches: a condition must have a name before it can exist, before it can be identified and understood as a symptom. Hunger at times was severe, but just the thought of driving to the grocery store was troubling and wasted hours. Complicating the picture, the coexisting autoimmune disorder also caused anorexia, i.e. loss of appetite.

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Then that sentence leaped from the page naming the cause: Zinc deficiency. What causes zinc deficiency? Malnutrition, medications. You have to string together the right words in order to search the publication leads. Thus, when you specifically search food aversion and prednisone:

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“Food aversion is found among people who take Prednisone, especially for people who are female, 60+ old , have been taking the drug for 1 – 6 months, also take medication Methotrexate, and have Osteoporosis.”

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There it was: prednisone and methotrexate, elderly female. Prednisone depletes zinc.

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The patient stopped methotrexate. Six weeks went by before a small number of foods could be added to milk and eggs. Unfortunately, the only foods tolerated were easily digestible ice cream (protein), pasta and sweets, which leads me to recall patients with autoimmune disorders whose diet consisted of processed carbs such as English Muffins, bread, pasta, who complain they cannot eat anything yet they are obese. They cannot seem to change food choices. How many cancer patients have this problem from chemotherapy?

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Vegetarians are at risk of zinc deficiency since Zinc is available primarily in oysters, meat, and poultry. Among the many causes of gustatory (taste) dysfunction in Table 6 from 2013 American Family Physician, besides malnutrition are cancer, radiation, etc, a long list of medications are listed:

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Medications

Intranasal zinc, chlorhexidine (Peridex), chemotherapy, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, dihydropyridine calcium channel blockers, diuretics, antimicrobials (macrolides, terbinafine [Lamisil], fluoroquinolones, protease inhibitors, griseofulvin, penicillins, tetracyclines, nitroimidazoles [metronidazole (Flagyl)]), antiarrhythmics, antithyroid agents, antidepressants, anticonvulsants, lipid-lowering agents

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Chemotherapy, statins, antidepressants, blood pressure medications, antibiotics – many commonly used medications can cause deficiency, yet zinc deficiency is said to be rare. Are we failing to recognize this in our patients?

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If dysfunction occurs, stop the offending medication. Regarding chemotherapy, “These effects are usually transient and resolve within three months of treatment cessation. This adverse effect is most likely caused by toxicity to olfactory and gustatory receptor cells that have the ability to regenerate.”

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“Zinc is involved in numerous aspects of cellular metabolism. It is required for the catalytic activity of approximately 100 enzymes [1,2] and it plays a role in immune function [3,4], protein synthesis [4], wound healing [5], DNA synthesis [2,4], and cell division [4]. Zinc also supports normal growth and development during pregnancy, childhood, and adolescence [6-8] and is required for proper sense of taste and smell [9]. A daily intake of zinc is required to maintain a steady state because the body has no specialized zinc storage system [10].”

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Immune function

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“Severe zinc deficiency depresses immune function [48], and even mild to moderate degrees of zinc deficiency can impair macrophage and neutrophil functions, natural killer cell activity, and complement activity [49]. The body requires zinc to develop and activate T-lymphocytes [2,50]. Individuals with low zinc levels have shown reduced lymphocyte proliferation response to mitogens and other adverse alterations in immunity that can be corrected by zinc supplementation [49,51].”

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DIAGNOSIS

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Serum levels of zinc and copper can be tested but do not reflect levels in the body as they are stored in tissue.

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Information below is from a review in J Clinic Toxicol by Osredkar J, Sustar N (2011) Copper and Zinc, Biological Role and Significance of Copper/Zinc Imbalance. 

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“The ratio of copper to zinc is clinically more important than the concentration of either of these trace metals. Zn is the second most abundant transition metal in organisms after iron and it is the only metal which appears in all enzyme classes, while copper is present in every tissue of the body, but is stored primarily in the liver, with fewer amounts found in the brain, heart, kidney, and muscles.”

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…The optimal plasma or serum ratio between these two elements is 0.70 – 1.00 [1]….

“There are 2-4 grams of Zn distributed throughout the human body [2]. Most zinc is in the brain [primarily hippocampus, the limbic system], muscle, bones, kidney and liver, with the highest concentrations in the prostate and parts of the eye [3]. It is the second most abundant transition metal in organisms after iron and it is the only metal which appears in all enzyme classes [2,4].

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Copper is also a vital dietary nutrient, although only small amounts of the metal are needed for well-being [5]. Although copper is the third most abundant trace metal in the body [behind iron and zinc], the total amount of copper in the body is only 75-100 milligrams [6]. Copper is present in every tissue of the body, but is stored primarily in the liver, with fewer amounts found in the brain, heart, kidney, and muscles [7]….

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Diagnosing zinc deficiency is a persistent challenge. Zinc nutritional status is difficult to measure adequately using laboratory tests due to its distribution throughout the body as a component of various proteins and nucleic acids [18,136].”

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Plasma or serum zinc has poor sensitivity and specificity – these levels do not necessarily reflect cellular zinc status due to tight homeostatic control mechanisms.”

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Zinc and Vegetarian Diets is reviewed in 2012 with recommendations to minimize deficiency.

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“Since plant sources of zinc contain phytate and other inhibitors of zinc absorption, vegetarians and vegans may potentially be at risk of zinc deficiency.”

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Special cases such as those with inflammatory bowel disease, those with profuse diarrhea, or who have had bariatric surgery should consult with a nutritionist.

 

Zinc Therapy in Dermatology: A Review from 2014 is an open access PDF. Zinc is discussed in various conditions including eczema, psoriasis & psoriatic arthritis, acne, alopecia, seborrheic dermatitis, dandruff, etc.

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“It maintains macrophage and neutrophil functions, natural killer cell activity, and complement activity. It activates natural killer cells and phagocytic function of granulocytes and stabilizes the plasma subcellular membranes especially the lysosomes. It inhibits the expression of integrins by keratinocytes and modulates the production of TNF-𝛼 and IL-6 and reduces the production of inflammatory mediators like nitric oxide. It is also proposed that it is toll-like receptors mediated regulation of zinc homeostasis which influences dendritic cell function and immune processes [2]. Zinc also possesses antioxidant property and has been found useful in preventing UV- induced damage and reducing the incidence of malignancies. It has also been demonstrated to possess antiandrogenic properties as it causes modulation of 5𝛼-reductase type 1 and 2 activity [1, 3, 4].”

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2. H. Kitamura, H. Morikawa, H. Kamon et al.,“Toll-like receptor-mediated regulation of zinc homeostasis influences dendritic cell function,” Nature Immunology, vol. 7, no. 9, pp. 971–977, 2006.

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TREATMENT

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Based on limited reading, for zinc deficiency – NOT routine use – consider 20 to 50 mg zinc with 2 mg copper for a limited time. Follow cautiously for toxicity. HIGH AMOUNTS OF ZINC ARE UNSAFE.

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From Penn State Hershey Medical Center

 

Available Forms

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Zinc is available in several forms….

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More easily absorbed forms of zinc are zinc picolinate, zinc citrate, zinc acetate, zinc glycerate, and zinc monomethionine. If zinc sulfate causes stomach irritation, you can try another form, such as zinc citrate.

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The amount of elemental zinc is listed on the product label (usually 30 – 50 mg). To determine the amount to take in supplement form, remember that you get about 10 – 15 mg from food. [if you eat oysters, meat, poultry]

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Zinc lozenges, used for treating colds, are available in most drug stores. There are also nasal sprays developed to reduce nasal and sinus congestion, although they may have some safety issues (see “Precautions”). [Avoid nasal sprays as it destroys the olfactory nerve, the sense of smell.]

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How to Take It

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You should take zinc with water or juice. If zinc causes stomach upset, it can be taken with meals. Don’t take zinc at the same time as iron or calcium supplements.

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A strong relationship exists between zinc and copper. Too much of one can cause a deficiency in the other. If you take zinc, including zinc in a multivitamin, you should also take copper..

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Take copper on an empty stomach. The tablets I have seen are so tiny they stick in the throat. Copper is water soluble but dissolves better in hot water.

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Memorial Sloan Kettering Cancer Center [MSKCC] has important Cautions not to take, and also Warnings on taking zinc if you have certain medical conditions or take certain medications. Bear in mind, the highest concentration of zinc is the prostate. I strongly recommend reading all zinc sections from MSKCC.

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“Consumption of zinc >100 mg/day may increase the risk of prostate cancer (31).

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Although human studies have been equivocal, patients should take zinc 2 hours before or after foods that are high in calcium, phosphorus, bran fiber, or phytate to avoid nonabsorbable complexes (45) (67).

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When taken orally at large doses (100-300 mg/day), zinc can cause chronic toxicity including copper deficiency, depressed immune function, headache, chills, fever, and fatigue (58) (59).”

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“Intake recommendations for Zn are provided in the Dietary Reference Intakes developed by the Food and Nutrition Board (FNB) at the Institute of Medicine of the National Academies…. U.S. National Research Council set a Tolerable Upper Intake for adults of 40 mg/day[82,83].

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Zinc Fact Sheet for Health Professionals, NIH Office of Dietary Supplements  

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Recommended daily allowance for Zn

RDAs 8 mg/day for female, 11 mg/day for male

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Recommended intake for copper

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The 10th edition of Recommended Dietary Allowances (RDA) did not include an RDA for copper; rather a safe and adequate daily intake was suggested…. The following Table 2 provide the Recommended daily dietary intake (RDI) of copper for children and adults and Tolerable upper intake levels for copper [83,85].

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Recommended daily intake RDI’s

90 mcg

Tolerable upper intake levels TUL
10,000 mcg”

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Of interest, a 2005 publication, Re-establishment of olfactory and taste functions describes results of treatment. Very small numbers were tested limiting interpretation. Were large doses complicating the results, causing toxicity and/or copper deficiency?

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In an open study (n=119; idiopathic taste disturbance, n=45; drug-induced taste disturbance, n=38; zinc deficiency, n=36), taste improvement by 50% was achieved after 4 weeks and by 80% after 8 weeks of treatment with zinc sulfate (100 mg, three times daily) [201]. In a double-blind, placebo-controlled study (n=73; idiopathic taste disturbance, n=48; lowered zinc levels, n=25), treatment with zinc picolinate (30 mg, three times daily) for 3 months did not improve subjective taste assessment or taste performance in the entire mouth, although the group receiving zinc picolinate performed significantly better than the placebo group in the filter paper test [202]. However, both the double-blind study by Henkin et al. [171] and the double-blind study in 65 patients by Yoshida et al. [203] failed to confirm this difference. Nevertheless, if the patients with drug-induced taste disturbances were excluded and only the patients with idiopathic taste disturbances and zinc deficiency were analyzed, the result was significant [203]. A double-blind study in hemolized patients (n=22) with low zinc levels demonstrated a significant improvement in response to zinc (50 mg/day) given for 12 weeks [204]. Similarly, preliminary findings from a double-blind study with zinc gluconate by Heckmann et al. seemed promising in idiopathic dysgeusia [205], [206].

 

 

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Zinc: an Antidepressant by a psychiatrist writing in Psychology Today in 2013,  zinc is anti-inflammatory and antidepressant. “Inflammation is the primary driving mechanism behind the whole shebang and may decrease brain zinc levels all on its own.”

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“300 or more enzymes in our bodies use zinc as a buddy to help them do their thing, making DNA, protein synthesis, cell division, all hugely important stuff. Zinc is also critical to cell signaling (a major receptor motif, the “zinc finger” is as famous as the G protein in cell biology circles). The highest amount of zinc in the body is found in our brains, particularly in a part of our brains called the hippocampus [limbic system]. Zinc deficiency can lead to symptoms of depression, ADHD, difficulties with learning and memory, seizures (2), aggression, and violence (3).”

 

“…As always, there is a sweet spot of zinc consumption, and more is not always better. More than 50 mg a day can lead to improper copper metabolism, altered iron function, and reduced immune function. We need enough zinc in the right place at the right time…a typical zinc supplement pill of 25-50mg is probably best taken only every few days, unless you are an oyster connoisseur, in which case no supplementation is necessary.” [oysters are highest in zinc]

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That author reviews this 2013 publication: Potential roles of zinc in the pathophysiology and treatment of major depressive disorder.

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Abstract

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Incomplete response to monoaminergic antidepressants in major depressive disorder (MDD), and the phenomenon of neuroprogression, suggests a need for additional pathophysiological markers and pharmacological targets. Neuronal zinc is concentrated exclusively within glutamatergic neurons, acting as an allosteric modulator of the N-methyl D-aspartate and other receptors that regulate excitatory neurotransmission and neuroplasticity. Zinc-containing neurons form extensive associational circuitry throughout the cortex, amygdala and hippocampus, which subserve mood regulation and cognitive functions. In animal models of depression, zinc is reduced in these circuits, zinc treatment has antidepressant-like effects and dietary zinc insufficiency induces depressive behaviors. Clinically, serum zinc is lower in MDD, which may constitute a state-marker of illness and a risk factor for treatment-resistance. Marginal zinc deficiency in MDD may relate to multiple putative mechanisms underlying core symptomatology and neuroprogression (e.g. immune dysfunction, monoamine metabolism, stress response dysregulation, oxidative/nitrosative stress, neurotrophic deficits, transcriptional/epigenetic regulation of neural networks). Initial randomized trials suggest a benefit of zinc supplementation. In summary, molecular and animal behavioral data support the clinical significance of zinc in the setting of MDD.

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The material on this site is for informational purposes only.

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It is not legal for me to provide medical advice without an examination.

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It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

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Comments are welcome.

This site is not for email, not for medical questions, and not for appointments.

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For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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Please IGNORE THE ADS BELOW. They are not from me.

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After Ketamine for pain, complaints of depression dropped in half & pain reports were lower


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KPBS Radio highlighted a new study today by UCSD School of Pharmacy

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San Diego Scientists Find Further Evidence A Club Drug Could Treat Depression

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In a new analysis published Wednesday in the journal Scientific Reports, UC San Diego researchers said millions of FDA side effect records reveal that people who took ketamine for pain relief reported lower rates of depression.

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“The occurrence of complaints about depression dropped in half after ketamine administration,” said UC San Diego Skaggs School of Pharmacy professor Ruben Abagyan, who led the study.

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The researchers focussed on the FDA’s Adverse Effect Reporting System, a database that tracks negative side effects among people who take various drugs. But the researchers were not primarily interested in bad outcomes.

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Instead, they looked for a positive outcome: declining rates of depression among people taking drugs not typically thought of as antidepressants.

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They found signs that other common drugs — including Botox, a pain reliever called diclofenac and the antibiotic minocycline — also reduced depression among patients in the FDA database.

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[minocycline is a glial modulator and it can prevent CRPS from spreading.]

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University of Miami psychiatry professor Charles Nemeroff wrote that the study was, “very interesting.”

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“The findings are of considerable interest. However the interpretation of the findings are key,” he wrote, saying it will be important to understand whether ketamine is directly treating depression or simply relieving pain, which can indirectly help people experience less depression.

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The UC San Diego researchers said they controlled for this variable by comparing people who took ketamine with those who took other pain medications. They said they still found a larger drop in depression among those who took ketamine.

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This is the open source (free) article in Nature with brief excerpts below:

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Population scale data reveals the antidepressant effects of ketamine and other therapeutics approved for non-psychiatric indications

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.Isaac V. Cohen, Tigran Makints, Rabia Atayee, Ruben Abagyan

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We found that patients listed in the FAERS database who received ketamine in addition to other therapeutics had significantly lower frequency of reports of depression than patients who took any other combination of drugs for pain (LogOR −0.67 ± 0.034) (Fig. 1c). This reduction in depression is specific to ketamine and is known to be much more rapid than current antidepressants, making this observed effect very promising for treatment of patients with acute depressive or suicidal episodes. These patients cannot afford to wait up to six weeks for reductions in their depressive symptoms. Pain reports were also significantly lower for ketamine patients (LogOR −0.41 ± 0.019) (Fig. 1c).

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The analysis of the whole FAERS database revealed several other unintentional depression reducing drugs among antibiotics, cosmeceuticals and NSAIDS (Fig. 2). Our data supported previous studies that observed the psychiatric polypharmacology of minocycline [my emphasis], a tetracycline antibiotic14 (Fig. 2). The NSAID, diclofenac [that has highest incidence of heart attack and cardiac arrhythmia of any NSAID], was also observed to have some antidepressant properties (Fig. 2). It is theorized that both of these drugs may accomplish antidepressant effects through an anti-inflammatory mechanism. Because of the antidepressant activity of several NSAIDs, we further separated the non-ketamine pain cohort. Ketamine patients were then compared to patients who received any other combination of drugs for pain excluding NSAIDs. It was observed that depression event rates remained low (LogOR −0.56 ± 0.035) (Fig. 2)..The reduction of depression rates in ketamine patient records makes a case for study of ketamine as a psychiatric drug. These results imply that ketamine may be further explored as a monotherapy or adjunct therapy for depression. It should also be noted that FAERS data revealed that ketamine use [may] lead to renal side effects and awareness and caution in patients with renal or hepatic impairment may be warranted (Fig. 1a and b). [my emphasis].

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As an important side note, we also evaluated efficacy and side effects with the use of ketamine for pain management. We found that patients who were on ketamine had reduced opioid induced side effects including constipation (LogOR −0.17 ± 0.023), vomiting (LogOR −0.16 ± 0.025), and nausea (LogOR −0.45 ± 0.034) than patients who received any other combination of drugs for pain indications (Fig. 1d). Our data supports ketamine’s opioid-sparing properties and alludes to the fact that patients may receive benefits of improved pain, reduced requirement of opioids, and ultimately less opioid reduced side effects.

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The results of this study support previous small scale studies’ conclusions that ketamine is a good monotherapy or adjunct therapy for depression. In clinical practice ketamine would be especially useful for depression because of the quick onset of its action compared to existing first line therapies. Regardless of the causative mechanism ketamine appears to have therapeutic potential for TRD. Further, the potential to reduce many of the most complained side effects of opioid treatment makes ketamine adjunct therapy for pain seem desirable.

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Overall, this study demonstrates that the therapeutic potential of ketamine can be derived from appropriate statistical analysis of existing population scale data. This study also outlines a methodology for discovering off label pharmacology of existing approved drugs. This method can be applied to other indications and may reveal new important uses of already approved drugs, providing reliable justification for new indications without large investments in additional clinical trials.

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FDA Adverse Event Reporting System. The FAERS database was created to support FDA’s post marketing surveillance on drugs and biologic therapeutics. It contains adverse reaction and medication error reports sent to the FDA through MedWatch, the FDA Safety Information and Adverse Event Reporting Program. Reporting is voluntary and is done by patients, family members, legal representatives, doctors, pharmacists and other health- care providers. If any party reports an adverse effect to the manufacturer, the manufacturer is legally obligated to forward the report to the FDA. Data is available online in quarterly format for AERS from the first quarter of 2004 to the third quarter of 2012 and for FAERS from the fourth quarter of 2012 to the first quarter of 2016.

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The study used over 8 million adverse event reports from first quarter of 2004 to the first quarter of 2016. All the quarterly files from 2004 to 2016 were combined into a master file which was used as the primary source for analysis. . . .

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Out of 8 million reports, 279,853 reports were used for analysis of ketamine in Fig. 1. Two cohorts for ketamine (K) patients and pain (P) patients with 41,337 and 238,516 patients respectively....

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The material on this site is for informational purposes only.

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It is not legal for me to provide medical advice without an examination.

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It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

~~

This site is not for email and not for appointments.

If you wish an appointment, please telephone the office to schedule.

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For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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Ketamine & Opioids Stop Working – TOLERANCE – the body no longer responds no matter how high the dose


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The comments below on ketamine tolerance apply to its use either for intractable pain or major depressive disorder. I have written about ketamine several times since April 2009. Tolerance means the medication no longer has an effect. If ketamine is to be needed for decades to come, we don’t have more than 10 years experience with repeated use to understand if and when it will stop working for our patients.

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Tolerance to ketamine is a growing potential as more infusion centers open each year.

Infusions are being used at fixed dosages

that are often too high or toxic

and predispose to tolerance and loss of efficacy.

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I’ve seen two cases of ketamine tolerance since about 2009 among persons with Complex Regional Pain Syndrome (CRPS). And the neuropathic pain of CRPS responds differently than other pain syndromes. We are all snowflakes, not one of us is alike another. But CRPS is unpredictable in many ways, and very predictable in others. It is also more dynamic and capable of being reversed in many who have it.

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Ketamine is given usually IV in a few centers in the country for CRPS and for Major Depressive Disorder. I prescribe it either via nasal spray or under tongue. I may, later this year, offer IV infusions to a small number of my patients who need both.

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If tolerance develops, would drug holidays work?

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Some people develop tolerance to their medication. In the old days, when I was training in the 1970’s, Parkinsons medication over time would stop working. Our only recourse was to do an inpatient drug holiday for weeks. We had to stop the drug. The resting tremor, the constant flailing, was exhausting and life threatening, especially if you had a heart condition. Newer Parkinson’s drugs completely circumvent this.

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Would drug holidays work if tolerance develops for ketamine or is it a goner forever?

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Opioids can cause tolerance through a known mechanism. They produce inflammation that causes more pain. Higher and higher doses fail to help pain. Addicts seek the high they once felt but cannot capture. This is why addicts die, chasing the impossible. Detox. Drug holiday. In the case of addiction, many are placed on Subutex, an opioid that acts on two opioid receptors and seems to prevent craving, in part at least because it has such a long half life that the blood level never dips.

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Ketamine infusions centers springing up.

Is that all they do?

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NIH and Yale began to test IV ketamine infusions in the 1990’s for major depressive disorder, and Robert Schwartzman, MD, at Hahneman in Philadelphia was one of the early ones to infuse ketamine for CRPS and contribute a large body of research on this pain.

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But in the last 2 or 3 years I receive a growing number of mailings advertising ketamine infusion centers. Just that, nothing more. Ketamine infusion centers, not pain specialists. All these young anesthesiologists popping out of training every year have a cash pay business; insurance doesn’t cover.

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Will ketamine stop working for patients who need to use it regularly for decades and decades? We don’t know. It should be studied.

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The first patient I saw with ketamine tolerance, I referred from San Diego to Professor Schwartzman in Philadelphia. She received inpatient IV around the clock for one week, then outpatient IV boosters every month. After eight months, she stopped responding. That’s when I called him to ask what to do? He did not know. So I used glial modulators. I posted her case years ago. She is in her 70’s, pain free since 2010, and two weeks ago, as a volunteer for the Red Cross, she supervised RN’s and evacuees from the flooding at Oroville dam. Tens of thousands of people, emergency care for families and homeless.

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A recent patient has had more than 20 surgeries in her hand that has CRPS. She has failed  IV ketamine, opioids, propofol given together in ICU for weeks and weeks. Surgery triggers the glia to produce neuro-inflammation.

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Another case though unusual, also posted years ago, a young male athlete, bedridden with CRPS affecting almost entire body. Flew to Professor Schwartzman 9 times and each time, the relief was gone by the time they reached the airport. He was taking opioid medication that may have been impossible to offset.

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This is what I advise when I prescribe ketamine for my patients to use at home as a nasal spray or sublingual:

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  1. Do not use it with opioids.Opioids cause inflammation, ketamine does the opposite. It modulates (reduces) inflammation.

  2. Never use it alone. It is a glial modulator, it is not only an NMDA receptor inhibitor.

  3. For intractable, treatment resistant cases, use as many glial modulators as you can.

  4. Ultra low dose naltrexone (20 micrograms TID) can profoundly reduce tolerance in patients on opioids: they may now need 1/2 to 1/8th the dose of opioid that simply had never quite done enough. Naltrexone not only relieves pain, it may profoundly improve function.

  5. Opioids stimulate glia to produce pro-inflammatory cytokines -> pain. Stop opioids if you can. You are likely to get far better results with glial modulators, especially if you have CRPS.

  6. Pain specialists should be offering a trial of glial modulators before they choose opioids for life.

  7. Use glial modulators as needed: ketamine, oxytocin (a hormone), tricyclic antidepressants (weaker than the others but can be profound for some), metformin.

  8. Metformin, a glial modulator!  for pain! in people who do not have diabetes. I will be posting on it this coming week — inshallah

  9.  Use it sparingly. Whether ketamine or opioids, use sparingly because of tolerance.

  10. If it is a good day, use less and use sparingly. If pain spikes, use higher dose, use sparingly.

  11.  When tolerance develops to ketamine, what then?

  12. Is it possible that a drug holiday would work? Should that be in months or years? we may never find out.

  13. Use ketamine and/or opioids sparingly. Prevent tolerance. You may not always need the same dose on a good day or when pain spikes.

  14. Make sure you are doing other things to relieve pain, not just ketamine or opioids.

  15.  Dextromethorphan helps, a sigma I receptor antagonist that reduces the excitotoxic glutamate

  16. Try as much as you can to exercise.

  17. Lift the mind to positive things. Learn to block thoughts of pain, dissociate from that. Choose life and doing and being.

  18. Develop momentum. Try never to judge; that includes being hard on yourself and others.

  19. Expand your spiritual life. Find your path if you don’t already have one. It may begin for all sorts of reasons, but figure it out. It’s real. Spiritual giants from all paths have had direct perception of the infinite in many ways and forms. Direct perception.

  20. S-ketamine clinical trials are now ongoing in the US. I was very disturbed to hear the side effects of S-ketamine infusion related last week. S-ketamine deeply disturbing. It is wrong to give everyone the same dose of ketamine. Not once have I ever heard anyone recount similar side effects from ketamine infusions. I got the impression from her they were not inclined to attribute it to S-ketamine, but it would be disturbing if they did not. Ketamine’s dose no matter how you give it is idiosyncratic, meaning some respond to 2 mg, some to 400 mg. It is wrong and should be unethical to subject someone to doses 200 times the dose they may need. It is dangerous and promotes tolerance.

  21.  If you’ve been stuck in bed, branch out and vary the things you do. Find music and poetry and literature. Maya Angelou suffered yet her words make you soar. Check out James Baldwin in the Oscar-nominated documentary “I Am Not Your Negro.” Baldwin’s immensely powerful analysis deconstructs movies, not as a mirror, but as a window into the imaginary; and how movies shape our thinking. As a movie critic, his writing is about poverty, class and “not everything that is faced can be changed, but nothing can be changed if it is not faced.” …  “There are days — this is one of them — when I wonder, how precisely are you going to reconcile yourself to your situation here…” So many writers fail to teach us how to analyze and think with such clarity. Something we don’t always do. We need to train ourselves to become critical thinkers. Baldwin brilliant mind demonstrates critical thinking at its best.

    Critical thinking is not a partisan issue. Tens of millions will lose jobs as robots rapidly take over in the next 3 years. Industry will reap more than ever in history. We all need to rethink our lives at some point.

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    Dylan’s song is about “the possibility that the most important (and least articulated) political issue of our times is that we are all being fed a false picture of reality, and it’s coming at us from every direction.”[10]

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    “Propaganda, all is phoney,” Dylan says in “It’s Alright, Ma (I’m Only Bleeding).”

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    Advertising signs that con you
    Into thinking you’re the one
    That can do what’s never been done
    That can win what’s never been won
    Meantime life outside goes on
    All around you.

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    Public Warning:

    Ketamine is a controlled substance.

    Administered improperly, or without the guidance of a qualified doctor,

    Ketamine may cause injury or death.

    No attempt should be made to use Ketamine

    in the absence of counsel from a qualified doctor.

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    “Off label” means ketamine is FDA approved for another purpose, decades ago it was approved for anesthesia. In qualified hands, ketamine is one of the safest medications we have in our formulary.

     

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    The material on this site is for informational purposes only.

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    It is not legal for me to provide medical advice without an examination.

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    It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

    ~~

    This site is not for email and not for appointments.

    If you wish an appointment, please telephone the office to schedule.

    ~~~~~

    For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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    Please IGNORE THE ADS BELOW. They are not from me.

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Ketamine Consensus Statement for Mood Disorders Needed


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I just had a call from a student writing a paper on ketamine. Question #1: What % respond to ketamine.

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Why are we still asking this rather than treating with ketamine?

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3.7% of Americans are disabled with Major Depression, many for decades, or entire lives. Antidepressants may work on only 30%. It’s time we had a consensus statement on use and training of ketamine.

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Read Cornel West: Pity the sad legacy of Obama, before you read on.

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Pity the sad legacy of psychiatry. Even neoliberals fail to speak up, stuck in the dictates of the few. We’ve known for decades that ketamine is effective treatment. It can work in hours. IV ketamine clinics are popping up like Jack in the Boxes and will continue to increase in number.

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It is time to ask: Is IV the only way to administer? Is it cost effective? Do these doctors have the right training?

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We need a consensus statement from psychiatrists and from the American Academy of Psychiatry and Neurology on training in inflammation, the innate immune system and treatment with ketamine.

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Every psychiatrist and mental health specialist should be instructed in rationale, the innate immune system, glia, inflammation, addiction medicine, glial modulators (ketamine is only one), and how to look at the whole system, holistically, not just one more drug. Inflammation, diet, exercise, among these.

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A focus on Ketamine alone in treating a complex organ like the brain is incomplete. Think inflammation, brain, spinal cord, glial modulators, not just drugs, not just ketamine. Ketamine is potentially addicting, a schedule III drug. Evaluate a patient just as you do when prescribing opioids.

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Then we need consensus on its use for intractable chronic pain including RSD/CRPS.

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Why don’t schools teach anything on the human body and the immune systems rather than biology and cutting up frogs?

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 Data below is from National Institute of Mental Health:

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Major Depression Among Adults.

  • Major depression is one of the most common mental disorders in the United States.

  • The 12-month prevalence data for major depressive episode presented here are from the National Survey on Drug Use and Health  (NSDUH). Based mainly on the 4th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), in the NSDUH study a major depressive episode is defined as:

    • A period of two weeks or longer during which there is either depressed mood or loss of interest or pleasure, and at least four other symptoms that reflect a change in functioning, such as problems with sleep, eating, energy, concentration, and self-image.

    • Unlike the definition in the DSM-IV, no exclusions were made for a major depressive episode caused by medical illness, bereavement, or substance use disorders.

  • In 2015, an estimated 16.1 million adults aged 18 or older in the United States had at least one major depressive episode in the past year. This number represented 6.7% of all U.S. adults.

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The material on this site is for informational purposes only.
.
It is not legal for me to provide medical advice without an examination.

.
It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

~~
This site is not for email and not for appointments.

If you wish an appointment, please telephone the office to schedule.

~~~~~

For My Home Page, click here:  Welcome to my Weblog on Pain Management!

.

Please IGNORE THE ADS BELOW. They are not from me.

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