Bipolar disorder (formerly known as manic-depressive illness) is a mental health condition characterized by wide mood swings interspaced with euthymia and has a U.S. adult prevalence of about 2.8% [1]. It is seen in both genders almost equally, though its onset tends to occur earlier in men vs women, and rapid cycling is more common in women [2]. Bipolar disorder (BD) is spectral with three main, coarse types: bipolar I, bipolar II, and cyclothymia [3]. Bipolar I is defined by severe episodes of mania with or without major depression, bipolar II includes major depressive episodes with hypomania, and cyclothymia presents with hypomanic and depressive symptoms that fail to meet the diagnostic requirements of bipolar I or II [4].
Studies using functional brain imaging have indicated that those with bipolar disorder struggle with differentiating between irrelevant and relevant emotional stimuli and have a higher sensitivity to emotional cues, in addition to having difficulty with regulating mood [5]. There is some evidence for an aberrant neurodevelopmental trajectory being implicated in some with BD, “particularly those with an early age of illness onset and those exhibiting psychotic symptoms” [6]. Such a course could be influenced by childhood trauma, which Etain et al. argued “may alter the organization of brain development,” and “interact with genetic susceptibility factors” [7]. A mild relation between familial bipolar disorder and a heightened risk for panic attacks was given by MacKinnon et al. in 2002, but the manifestation of BD is more of epigenetic than genetic origin [8] [9]. For instance, five microRNAs were specifically altered in a group of BD participants in a study by Maffioletti et al. [10]. These miRNAs could reflect influenced pathways relevant to brain function, such as those of neuroplasticity and signal transduction. miRNAs are small, noncoding RNA molecules that help tune genetic expression by silencing genes post-transcriptionally or after the copying of a DNA sequence by messenger RNA [11]. As explained by Schloesser et al., a defect in being able to manage “neuroplastic adaptations to perturbations” from stress may invoke “compensatory adaptations that overshoot and predispose to oscillations” or the behavior swings expressed in bipolar disorder [12]. The authors go on to say that, in the above case, allostatic load (cumulative “wear and tear”) could then contribute to long-term disease progression and possibly cycle acceleration. The pathophysiologic pattern of bipolar disorder appears to involve dysfunction in the limbic system, which is regulated by the monoamine neurotransmitters dopamine, norepinephrine, and serotonin [13]. And reduced levels of 5-hydroxyindoleacetic acid (the primary metabolite of serotonin) have been seen in bipolar patients [14]. “Studies of plasma norepinephrine suggest that, on average, bipolar depressed patients appear to have reduced-to-normal resting output of norepinephrine, with a highly exaggerated noradrenergic system response to standing” [15]. This exaggerated release of norepinephrine is shared with hyperadrenergic POTS (postural orthostatic tachycardia syndrome) [16]. One analysis performed with proton NMR spectroscopy looked at postmortem brains of BD patients and found that glutamate, creatine, and myo-inositol were all elevated in the postmortem brains [17]. Comparing these measurements with changes seen in rat brains treated with lithium or valproate (both used to treat bipolar disorder), Lan et al. concluded that the balance of excitatory and inhibitory neurotransmitters may be central to the disorder. And this balance may be influenced at least somewhat by the neuroactive hormones DHEA and pregnenolone, both of which were elevated in subjects with bipolar disorder in an investigation by Marx et al. [18]. As Quiroz et al. have expressed, the proposition has been made to employ therapeutics aimed at enhancing cellular plasticity and resilience to counter maladaptive stress responses through upregulating neurotrophic pathways and bettering mitochondrial function [19]. Different quantities of neurotrophins have been discerned in bipolar patients vs healthy controls, which can mean lesser axonal arborization (treelike branching) and lesser stabilization of existing synapses [20]. Mitochondrial dysfunction has been consistently reported in BD, and some of the knowledge of the relationship between mitochondria problems and mental illness has come from the study of pharmacological impacts on these organelles [21] [22]. Per Scaini et al., these problems include irregular “mitochondrial morphology and dynamics,” and “atypical mitochondrial metabolism and oxidative stress pathways” [23]. The above paper goes on to take in aberrant calcium levels as well as “an imbalance between pro- and antiapoptotic proteins towards apoptosis, abnormal gene expression of electron transport chain complexes, and decreased ATP synthesis.” Relatedly, a 1997 examination found a mitochondrial DNA base-pair deletion to be three times higher in patients with BD compared with age-matched controls [24]. The finding may be more specific to BD than affective disorders in general, as the deletion was not seen in the autopsied brains of nine suicide victims, nor was it detected in another study of autopsied schizophrenics [25]. Such a deletion could be inherited or acquired from free radical damage or pharmaceutical use, for it is well documented that all classes of psychotropic drugs (including antidepressants, antipsychotics, anticonvulsants, and mood stabilizers) can injure mitochondria, as can statins and analgesics like acetaminophen (Tylenol®) [26] [27]. Antibiotic medications can be even worse, as many can induce psychosis outright [28]. One version of this side effect is common enough for it to have its own name, antibiomania or antimicrobial-induced mania [29]. Not surprisingly, mitochondrial toxicity testing is not required by the worthless FDA for drug approvals [30]. Supporting mitochondria can be done with L-carnitine or acetyl-L-carnitine, as this amino acid can enhance energy production and the elimination of ammonia [31]. In fact, L-carnitine is often used to treat hyperammonemia caused by the mood-stabilizing drug valproate, which happens frequently [32]. Lithium has its own side effects, having been associated with a decline in thyroid and parathyroid function, in addition to a “three-fold increased risk of renal impairment” and a “two and a half-fold increased risk” of renal failure [33] [34]. Einat et al. presented some animal data in 2003 in an attempt to make a connection between ERK signaling and BD in humans, but it was a stretch in my opinion [35]. The extracellular signal-regulated kinase (ERK) pathway is an intracellular enzyme chain that relays signals pertaining to cell growth, cell metabolism, and cell survival, and the above researchers were investigating activation of the ERK signaling cascade by the antimanic drugs valproate and lithium [36]. Epidemiological studies have linked BD with high rates of inflammatory comorbidities such as autoimmune conditions, cardiovascular disease, and metabolic dysfunction, and elevated “proinflammatory cytokines in BD has been repeatedly demonstrated” [37]. Peripherally circulating cytokines can cross the blood-brain barrier (especially where it is disrupted or leaky) and alter monoamine neurotransmitter levels, overactivate microglial cells, and further oxidative stress in the brain [38] [39]. This includes inflammation-induced increases in brain glutamate and excitotoxicity [40]. In turn, triggered microglia can release inflammatory mediators that break down the blood-brain barrier, allowing for the infiltration of peripheral immune cells and the pouring of gas on the brain fire [41]. In a study by do Prado et al., patients with bipolar I had fewer regulatory T cells than their healthy controls (Tregs help to check misguided or exaggerated immune responses) [42]. A higher prevalence of asthma has been found in BD patients, though medications could be a confounding variable here [43]. And a pathophysiological overlap between bipolar disorder and fibromyalgia was looked at by Bortolato et al. in 2016, with the team noting that both BD and FM can display circadian rhythm and cognitive issues, fatigue, and an altered stress response [44]. Their paper also mentioned that overactivation of the kynurenine pathway could drive tryptophan away from the making of serotonin and melatonin, resulting in some of the shared symptoms. The kynurenine pathway is the main route for the catabolism of tryptophan, and trouble with this pathway can contribute to neurodegeneration [45]. In their 2010 review on oxidative stress and bipolar disorder, Steckert et al. stated that “It has been widely demonstrated that the generation of reactive oxygen species (ROS) plays a critical role in the pathophysiology of several neuropsychiatric disorders, such [sic] BD” [46]. So chronic inflammation can lead to affective and cognitive dysfunction by changing neurotransmitter levels, and neuroinflammation in the form of microglia activation can cause “pathologic synaptic pruning and impaired neuroplasticity in key brain regions sub-serving mood and cognition” [47]. Synaptic pruning is the process of removing weak or unnecessary connections between neurons, and we now know that this continues at least into early adulthood [48]. Neuroprogression is the term used for the trajectory leading to “cognitive, functional, and clinical deterioration in the course of BD” stemming from immune pathway encumbrance [49]. In other words, the progression of BD is characterized by an expansion of both structural abnormalities in the brain and cognitive impairment, and it has been argued by Kapczinski et al. that repeated mood episodes invite a rewiring of the brain that makes the patient more vulnerable to not only follow-up episodes, but environmental stressors and drugs of abuse [50] [51]. Indeed, Mahon, Burdick, and Szeszko wrote an extensive review on the indications for brain white matter abnormalities in the etiology of BD, with changes in the tracts connecting the amygdala, hypothalamus, striatum, and frontal cortex [52]. However, we should be careful to not wholeheartedly accept the kindling hypothesis, as this is used to favor early drug treatment [53] [54]. Substance abuse is quite common during the course of bipolar disorder, with drugs and alcohol relating to worsened treatment responses and both symptomatic and functional recovery [55]. Comorbidity of BD and alcoholism, as well as other psychoactive substance use disorders, is highly prevalent, as they are risk factors for each other [56] [57]. Cannabis use disorder is particularly likely in BD, and has been linked with an earlier age of onset, worsened affective episodes, rapid cycling, psychotic symptoms, decreased long-term remission, poorer global functioning, suicide attempts, and increased disability [58] [59] [60] [61]. Naturally, with ongoing inflammation comes prolonged activation of the HPA axis, which drives hypercortisolemia or high circulating cortisol and desensitization of glucocorticoid receptors (these receptors mediate the effect of cortisol) [62]. A stressed HPA axis impairs neurocognitive function, and abnormal glucocorticoid receptors have been seen in postmortem BD brains [63]. A 2016 meta-analysis of 41 studies observed that “BD was associated with significantly increased levels of cortisol…and ACTH” [64]. ACTH is the abbreviation for adrenocorticotropic hormone, the tropic hormone made by the anterior pituitary which prompts the adrenals to secrete cortisol [65]. Psychological stress can certainly be accompanied by the release of counterregulatory hormones that raise blood sugar, and allostatic load promoting insulin resistance is one reason why “The prevalence of DM [diabetes mellitus] in BD may be three times greater than in the general population” [66]. The role of the microbiota-gut-brain axis in neuropsychiatric disorders is an obvious large one, as the gut and brain communicate bidirectionally via the nervous and immune systems [67]. Specific to bipolar disorder, in 2015 Hamdani et al. gave a case report describing the safe and successful treatment of a manic episode in a 46-year-old woman using nothing but activated charcoal [68]. The authors suspected that the manic episode occurred as a result of disruption to her gut microbiota and intestinal wall, and therefore prescribed activated charcoal because of its potent ability to adsorb inflammatory cytokines [69]. Fifteen days later the patient was asymptomatic and all of the inflammatory markers tested had normalized. Strong substantiation for the above suspicion comes from a recent study by Kilic et al. which found significantly higher levels of zonulin and claudin-5 (biomarkers for excessive permeability of the small intestine and blood-brain barrier, respectively) in patients with BD [70]. The association between BD and chronic infections has been examined as well, and it seems the strongest evidence points to Toxoplasma gondii infection as a possible culprit [71] [72]. Toxoplasma gondii is a protozoal parasite usually contracted through ingesting contaminated food or water, or by contacting cat feces, and it “encysts and persists in the brain and in cardiac and skeletal muscle,” with the brain being the major organ for encystment [73]. Sleep disturbance and circadian dysregulation are commonly reported in BD, even during interepisode or euthymic periods [74]. Sleep disturbance has been associated with markers of inflammation in general, and with proinflammatory cytokines in BD [75] [76]. An abnormal sleep-wake cycle is frequently observed in BD as well as other neuropsychiatric conditions, and “Bipolar patients have been demonstrated to have significantly lower nocturnal melatonin peaks compared to healthy controls” [77]. Moreover, hypersensitivity to the suppression of melatonin production by ambient light has been seen in those with BD, suggesting a greater vulnerability to external sleep disruptors [78]. Since melatonin exerts a controlling hand over insulin, leptin, and lipid metabolism, it makes sense that melatonin supplementation in humans prescribed antipsychotics was able to safely diminish the adverse metabolic effects of these drugs in a clinical trial by Romo-Nava et al. [79]. Standard treatments for bipolar disorder have “poor long term outcomes with high rates of treatment resistance and relapse,” and antipsychotic drugs are notorious for having “serious metabolic side effects such as substantial weight gain, intra-abdominal obesity, and type 2 diabetes mellitus” [80] [81]. On top of that we have the carcinogenicity of psychotropics, as a 2015 systematic review revealed that roughly 71% of all the drugs examined displayed “evidence of carcinogenicity in…experimental studies” [82]. Quoting from the paper, “US Food and Drug Administration-based analyses demonstrate that almost all atypical antipsychotics and anticonvulsants are carcinogenic in animals, as are the majority of antidepressants and benzodiazepines and methylphenidate.” And then we have the common difficulty experienced with the withdrawal of pharmaceutical treatment, which often involves a rebounding of the systems opposed by the drug(s) [83]. Kupka et al. found a higher prevalence of thyroid autoimmunity in their sample of bipolar patients, and a follow-up study reported a higher prevalence of brain-, stomach-, and pancreas-specific autoantibodies [84] [85]. An increased risk of comorbid multiple sclerosis and rheumatoid arthritis has also been seen [86] [87]. There is some evidence for a role of autoimmunity against the N-methyl-D-aspartate (NMDA) receptor in BD, as manic individuals have been shown to have increased levels of anti-NMDA receptor antibodies, and the expression and function of these receptors are often atypical in mood disorders [88] [89]. Further support of a part to play for NMDA receptor dysregulation comes from randomized, placebo-controlled studies testing the antidepressant effect of ketamine infusions, with one trial reporting a significant improvement in depression within 40 minutes, and another within 2 hours that remained significant for a week [90] [91]. Ketamine is an NMDA receptor antagonist, and NMDA receptors are key to learning and memory processes via their modulation of synaptic plasticity [92]. Synaptic plasticity refers to the strengthening or weaking of synapses that occurs as the brain adapts to new stimuli [93]. High anti-NMDAR antibody titers cause a decrease in the density of NMDA receptors which leads to a swelling of extracellular glutamate and a toxic influx of calcium into nerve cells [94]. Ketamine, as an excitotoxicity attenuator, can counter this glutamate release and calcium influx, and thus help save injured neurons [95]. Ketamine can additionally act as a neuroprotectant by inhibiting proinflammatory cytokine activity both in the periphery and in the central nervous system [96] [97]. If immune irregularity is so central to the pathophysiology of BD, why is it ignored by the symptomatic drug targeting of conventional medicine [98]? Rhetorical. Interestingly, glutathione, besides its well-known antioxidant work, doubles as a neuromodulator in the CNS, being able to protect neurons against glutamate-induced excitotoxicity by displacing glutamate from NMDAR binding sites and therefore intercepting excitatory input [99]. In 2014, Rosa et al. found that “bipolar patients had significantly lower levels of total glutathione and it was more oxidized,” and that “Age of illness onset…correlated with total glutathione levels and its oxidation status” [100]. How many Freud-trained psychiatrists prescribe glutathione for their bipolar patients? Zero is the answer to that. What has undeniably been coming out of the psychopharmacology woodwork against the best efforts of Big Pharma to keep the lid on, is how fully capable of disabling the brain psychiatric drugs are [101]. In a superb article published in a 2012 issue of Nursing Ethics, Barker and Buchanan-Barker relayed some powerful statements from a 1996 paper by the then Director of the National Institute of Mental Health, Dr. Steve Hyman: “…the actual effect of psychiatric drugs was to throw the brain into chemical chaos, creating ‘perturbations in neurotransmitter functions’…Hyman and Nestler added that prolonged use of such drugs resulted in ‘substantial and long-lasting alterations in neural function’…confirming that any ‘chemical imbalance’ that might exist in the brains of people with ‘mental illness’, was produced by long-term usage of psychotropic drugs not by some putative ‘mental illness’” [102] [103]. According to Breggin and Gotzsche, Young, and Crace, antidepressants, antipsychotics, psychostimulants, and mood stabilizers have all been shown to induce damage to brain tissue in humans, potentially leading to premature death, dementia, and other brain disorders [104] [105]. As expressed by Healy, “…the best available evidence shows that unmedicated patients with bipolar disorder do not have a higher risk of suicide” [106]. Using data from an analysis of placebo-controlled trials comparing active medications to placebos in BD conducted by Storosum et al., Healy calculated that “…active agents are most likely to be associated with a 2.22 times greater risk of suicidal acts than placebo” [107]. And data from a meta-analysis performed by Baethge tell us that early treatment with medication does not change the subsequent severity or frequency of mood episodes [108]. It is also interesting to note that in the pre-drug era (per a 1942 study by Rennie on manic-depressive illness), 21% of patients did not relapse after an initial manic attack, and 32.2% of those that did remained in remission for at least 10 years [109]. Contrast that with the results of a natural history study from 2002, where 146 bipolar I patients were symptomatic for nearly half of a 12.8-year follow-up [110]. Juvenile bipolar disorder was pretty well absent in prepubescent children before the common prescribing of antidepressants and stimulants like Ritalin® in this age group, especially outside the United States where these medications are given less routinely [111] [112] [113] [114]. On top of the references just given backing up that claim, a retrospective case review by Faedda et al. from 2004 looked at 82 children who met the diagnostic criteria for pediatric bipolar disorder and learned that almost 70% of them had been given a mood-elevating agent at least once within 30 days of their symptomatology manifesting [115]. The researchers stated that “Treatment with mood-elevating agents in children diagnosed with BPD led to new manic, and often psychotic or aggressive, behavioral changes in half of cases exposed and almost half of those given an antidepressant.” Another retrospective review by Cicero et al. recognized an earlier diagnosis of bipolar disorder in children who had previously received an antidepressant or stimulant [116]. They also noticed that few children had any family history of manic-depression, which points blame at the drugs. A few years back, Dr. Joseph Biederman of Massachusetts General Hospital, a prominent advocate for diagnosing bipolar disorder in young children and treating them with antipsychotics, was involved in several lawsuits concerning the defrauding of state Medicaid programs and the duplicitous pushing of drugs made by Johnson & Johnson [117]. Because of his criminal activity, childhood bipolar disorder diagnoses shot up 40-fold (!!!) between 1994 and 2003, per Moreno et al. [118]. And nearly all (90.6%) of these kids were prescribed one medication or another for their diagnosis. As no surprise, Biederman continues to teach at Harvard Medical School and still has his position of Chief of the Clinical and Research Programs in Pediatric Psychopharmacology and Adult ADHD at Mass General. The late Dr. Fredrick K. Goodwin and Dr. Charles Nemeroff of the University of Texas engaged in similar prostitution, both having received hundreds of thousands of dollars from GlaxoSmithKline for promoting their drugs for children [119]. How damaging is this agenda you might ask? For one telling example, we have the death of Rebecca Riley in 2006 which made national news [120]. This poor 4-year-old girl was on three psychiatric medications at the time of her death, all three prescribed to her by a quack psychiatrist who diagnosed her with bipolar disorder and ADHD before her third birthday. And then we have the story of Destiny Hager, a 3-year-old girl from Kansas who died shortly after a concomitant prescription of quetiapine and ziprasidone (both antipsychotics) [121]. The mother and father of Destiny were advised to get an attorney by one of the air ambulance crew members that cared for her and obviously realized the wrongdoing at play. Big shocker: quetiapine is made by AstraZeneca and ziprasidone is made by Pfizer. Good job Pfizer, everything you make is so very safe and effective, everyone knows that. Remember that Pfizer is the company that was convicted of violating the Organized Crime Control Act of 1970 via engagement in racketeering over a 10-year period [122]. In 2003, the United Kingdom banned almost all SSRIs for use in children and adolescents, why have we not done the same [123]? Our children do not have broken brains that are going to be fixed by pharmaceuticals that falsely claim to do so. Challenging the prevailing standard of care for schizophrenics and their prolonged (even lifelong) treatment with antipsychotic medications, a 20-year longitudinal study found that “SZ [schizophrenic] patients not on antipsychotics for prolonged periods were significantly less likely to be psychotic and experienced more periods of recovery; they also had more favorable risk and protective factors. SZ patients off antipsychotics for prolonged periods did not relapse more frequently” [124]. Another paper published by the same team looking at whether or not antipsychotics actually help schizophrenics came to the following conclusion: “More than 70% of SZ continuously prescribed antipsychotics experienced psychotic activity at four or more of six follow-up assessments over 20 years. Longitudinally, SZ not prescribed antipsychotics showed significantly less psychotic activity than those prescribed antipsychotics…The 20-year data indicate that, longitudinally, after the first few years, antipsychotic medications do not eliminate or reduce the frequency of psychosis in schizophrenia, or reduce the severity of post-acute psychosis…” [125]. The same is corroborated in a summary by Robert Whitaker from his 2004 paper published in Medical Hypotheses: “Although the standard of care in developed countries is to maintain schizophrenia patients on neuroleptics, this practice is not supported by the 50-year research record for the drugs. A critical review reveals that this paradigm of care worsens long-term outcomes, at least in the aggregate, and that 40% or more of all schizophrenia patients would fare better if they were not so medicated” [126]. Turning to antidepressants, in an excellent response to the National Institute for Health and Clinical Excellence review, Moncrieff and Kirsch wrapped up with the following points: “Recent meta-analyses show selective serotonin reuptake inhibitors have no clinically meaningful advantage over placebo,” “Methodological artefacts may account for the small degree of superiority shown over placebo,” and “Antidepressants have not been convincingly shown to affect the long term outcome of depression or suicide rates” [127]. A year later, Moncrieff and Cohen published an essay in PLoS Medicine which suggested that “…psychotropic drugs create abnormal [brain] states that may coincidentally relieve symptoms…No evidence shows that antidepressants or any other drugs produce long-term elevation of mood or other effects that are particularly useful in treating depression” [128]. So if antidepressants do not offer a remediation that warrants their short-term or long-term use, why are they prescribed like candy? N-acetylcysteine, an orally bioavailable precursor to glutathione, has shown great effectiveness in the treatment of BD, with one double-blind, randomized, placebo-controlled trial seeing “a substantial decrease in symptoms during the eight-week open-label NAC treatment phase,” and another randomized clinical trial witnessed 80% of the participants achieving at least a 50% reduction in depression severity [129] [130]. NAC has benefited manic symptoms too [131]. Omega-3 fatty acids can also help bipolar depression, partly through boosting BDNF (brain-derived neurotrophic factor) production [132] [133]. EPA and DHA, both omega-3s, have a role in the making of serotonin and its action [134]. A meta-analysis by McNamara and Welge found a robust deficit of DHA in bipolar subjects [135]. Focusing on curcumin for the inhibition of NF-kappa B (a transcription factor involved in immune responses) and the calming of proinflammatory cytokines, Gazal et al. saw its administration to rats reduce episode relapse and oxidative damage from mania [136]. In their review on the use of curcumin for bipolar disorder, Brietzke et al. laid out the benefits of curcumin as being able to lower microglia activation, ease oxidative and nitrosative stress, raise BDNF, suppress NF-kappa B, prevent apoptosis of brain neurons, and enhance brain serotonin and dopamine [137]. That is a home run for BD, the only thing is that curcumin is poorly absorbed through the oral route [138]. But this can be overcome with liposomes (liposomal curcumin) and other delivery systems [139]. There is an implication of vitamin D in affective and cognitive states for this hormone apparently has a hand in melatonin synthesis, neurotrophin release, and glucocorticoid signaling, and one study saw vitamin D deficiency to be 4.7 times more common in a group of outpatients with bipolar disorder, schizophrenia, or schizoaffective disorder [140] [141]. In one case report, a 15-year-old boy was effectively cured of his BD symptoms with vitamin D supplementation [142]. Magnesium and L-tryptophan have exhibited helpfulness for mania, while folate can be great for both mania and depression [143]. Folate is essential for brain health across the lifespan, and a 2019 meta-analysis evinced a significantly lower serum folate level in BD patients [144] [145]. Folate is used for DNA methylation, neurotransmitter synthesis and degradation, and stabilizing the genome, and a weakening of the blood-brain barrier can cause brain-specific folate deficiency [146]. A lack of usable folate drives up homocysteine, which may stimulate autoimmunity through the homocysteinylation of proteins [147]. There is talk in the orthomolecular sphere on manipulating DNA methylation and histone acetylation patterns for affective struggles with nutrients like SAMe and vitamin B3, but the problem is that these patterns are inconsistent in bipolar individuals and they do not really lend themselves to simple tinkering [148] [149]. With that said, ensuring nutrient adequacy and methylating power is definitely valid, it is just that way more of one thing or another may not be appropriate for these folks. Relatedly, heightened urine pyrroles can be detected in bipolar patients and those with other mental health challenges, and this may be due to physical or emotional trauma, intestinal dysbiosis, or toxicity [150]. Mikirova has also presented data correlating excessive pyrrole excretion with improper digestion and raised histamine [151]. Urine pyrroles can be brought down by supplementing with vitamin B6 and zinc [152]. Pyrroles are pyrrole-containing compounds, one of which has to do with the crafting of heme (a building block for hemoglobin as well as antioxidant and detox enzymes) [153]. Urinary pyrrole excretion can be measured via the metabolite hydroxyhemopyrrolin-2-one [154]. Pyrroles can bind to and sequester vitamin B6 and zinc, encouraging their depletion and consequently, imbalance in the activity of serotonin, GABA, glutamate, and norepinephrine [155] [156] [157]. This can spell trouble for depression, anxiety, and overall behavior. In closing, everyone is free to make their own decisions, but these truths need to be known. I recommend considering natural medicine for safe and effective medicants, for ill-health is rectified through building health, not by swallowing carcinogens that pretend to be evidence-based. “Never doubt that a small group of thoughtful, committed citizens can change the world. Indeed, it is the only thing that ever has.” – attributed to Dr. Margaret Mead References:
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AuthorDenton Coleman is an Exercise Physiologist and Medical Researcher. Archives
October 2023
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