Semaglutide is an agonist of the glucagon-like peptide-1 receptor (GLP-1R), and is available as an injectable (Ozempic and Wegovy) or oral tablet (Rybelsus) [1]. Off-label prescriptions for these drugs have skyrocketed of late due to endorsements by moronic celebrities and social media influencers working on behalf of Novo Nordisk, the manufacturer of semaglutide [2]. The problem is the above trio is nowhere near as safe as they are being marketed as, and healthcare providers are prescribing them like candy without informing their patients of the side effects. Following is an honest listing of these, as given in the current medical literature.
GLP-1 is a pleiotropic hormone formed by cleaving of the proglucagon protein released by the intestines and pancreas [3]. As an incretin, GLP-1 stimulates insulin secretion upon glucose intake, but it also lowers glucagon (a hormone that raises blood sugar), delays gastric emptying, and suppresses appetite [4]. Being a synthetic analog, the sequence of semaglutide is not identical to that of native GLP-1 [5]. This homology deficit brings a potential for immunogenicity, and indeed patients on semaglutide have formed antidrug antibodies which were cross-reactive toward the endogenous peptide [6]. Because native GLP-1 has a half-life of only a few minutes at best, while semaglutide has a half-life of about a week, lingering of this immunogenic analog might engender more serious reactions relating to hypersensitivity or autoimmunity [7] [8] [9]. Although rare, the autoimmune blistering disease bullous pemphigoid, anaphylaxis, and drug-induced liver injury have all been reported with semaglutide use [10] [11] [12] [13]. Add to this the fact that inconsistent manufacturing processes can create impurity profiles that contribute to immunogenicity (this has been demonstrated with follow-on versions of semaglutide), and we get a bigger drug safety problem [14] [15]. Weight regain is nothing new for obesity pharmacotherapy, and in an observational study by Wilding et al., participants going off the drug “led to most of the weight loss being regained within 1 year, and a similar change in some cardiometabolic variables back to baseline, reinforcing the need for continued treatment to maintain weight loss…” [16]. The authors also noted that “participants in the semaglutide arm with greater weight loss during the 68-week treatment period tended to have greater regain in body weight after semaglutide withdrawal,” illustrating how powerful the rebound effect is with these drugs. And of course, with rapid weight loss, not all of the weight lost is fat [17]. Ozempic face is now a popular term used to describe the gauntness of sagging skin, more prominent wrinkles, and changes to the lips, chin, and cheeks caused by the drug [18]. The loss of elastin, collagen, and nutrients for the skin barrier can accelerate the appearance of facial aging [19]. Signs of facial aging can persist when fat regained does not get distributed in the manner it did before the medication was started, and body fat redistribution is a consequence of many pharmaceuticals – visceral fat accumulation being the chief concern with this [20]. In a clinical trial published in 2021, out of 535 participants who continued to receive subcutaneous semaglutide after 20 weeks, 435 reported an adverse event, with 41 being serious [21]. In the group that switched to a placebo after 20 weeks (n = 268), 201 reported an adverse event, with 15 being serious. These are not great odds. Gastrointestinal symptoms such as nausea and vomiting are frequently experienced by semaglutide users, but concerns over induced pancreatitis have been raised, and in the SUSTAIN 5 trial, one patient developed metastatic pancreatic cancer after treatment [22] [23]. An increased risk for pancreatitis and pancreatic cancer has been observed with other GLP-1R agonists [24]. In the SUSTAIN 6 trial, rates of vitreous hemorrhage or bleeding in the eye and diabetes-related blindness were “significantly higher” in the group that received semaglutide versus a placebo [25]. Blurred vision is a listed side effect for semaglutide too [26]. The GLP-1 receptor appears to be marginally expressed in the normal human thyroid, and Bezin et al. found a heightened risk of thyroid cancer with the use of GLP-1R agonists, not including semaglutide [27] [28]. However, both semaglutide formulations come with a box warning for thyroid tumors, and in both the SUSTAIN and PIONEER trials, thyroid malignancies were more prevalent in semaglutide-treated patients versus comparator groups [29]. Worry exists over cardiovascular complications with GLP-1R agonists, as these pharmaceuticals can increase resting heart rate [30] [31]. An uptick of 5 beats per minute associates with a 17% elevation in the risk of cardiovascular mortality according to Hozawa et al., and semaglutide raises the pulse rate by roughly 3 beats per minute [32] [33]. A higher likelihood of gallbladder disease seems to be par for the course with incretin-based medications, and a meta-analysis by Nreu et al. saw the chance of cholelithiasis (gallstones) go up by 28% with GLP-1R agonist treatment [34] [35]. In the STEP and SUSTAIN programs, gallbladder events occurred more often in those given semaglutide [36] [37]. Acute kidney injury has been reported after starting semaglutide with normal kidney function prior [38]. Leukocytoclastic vasculitis (blood vessel inflammation) has also been seen with the oral form of the drug [39]. Semaglutide may bring about psychiatric symptoms in some individuals, as Li et al. recently gave two cases of semaglutide-associated depression, with one appearing in a 54-year-old man with no previous history of depression [40]. Other adverse effects such as suicidal ideation and anxiety have been linked to a GLP-1 receptor agonist previously [41]. Since semaglutide interacts with neural pathways in the brain relating to food preference and appetite regulation, one wonders what the long-term effect of GLP-1 receptor hyperactivation on eating behavior might be [42] [43]. Lastly, another potential but serious outcome of taking GLP-1RAs is intestinal obstruction, as these medications were tied to a nearly 2-fold increase in bowel obstruction risk that rose to 3.48 after 1.6 years of use, per the cohort study by Faillie et al. [44]. A hazard ratio of 3.48 means the users were 348% more likely to experience an obstruction after taking semaglutide or another drug of the same class for over a year and a half. Speaking to the same danger, Lu et al. said the following in their 2023 paper: “Because GLP-1RAs could cause continuous increases in the intestinal length and villus height, the small intestine may become as inelastic and fibrotic as a loose spring…leading to long-term upper intestinal obstruction…” [45]. Untreated bowel obstructions can be life-threatening, so this is an unsettling issue [46]. In conclusion, there are natural and safe means of helping the body lose weight healthfully, obesity medications are not the only option. With so many clinics and spas offering semaglutide right now, please do your homework and be informed before taking the advice of a practitioner who may be all too eager to write a script for Ozempic. References:
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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:
The Great Pyramid at Giza stands as the only remaining wonder of the ancient world, and it was here that the Greek hierophants Pythagoras and Plato were initiated into the Egyptian priesthood. Legend has it that Pythagoras spent 22 years under Egyptian tutelage before bringing his mathematical learnings back to Greece [1]. A few decades later, Plato arcanely divulged some of the secrets he was taught during his initiation in his dialogues, smartly using Hermetic language to do so [2]. Pharaonic Egyptians saw geometry as the hand movements of God, with mathematical relations as the mortar of creation. A map of universal mensuration was hewn into the Great Pyramid, and Plato knew it, for a dictum over the entrance to his academy shooed away students unschooled in geometry [3].
But the Pyramid was much more than a repository of measures, a compass, a geodetic marker, and even an astronomical observatory. It was a temple of initiation where neophytes were “born again” as adepts. The Egyptian Book of the Dead or Book of Going Forth by Day narrates not simply funerary rites but the stages and trials through which the neophyte would pass on their way to adeptship [4]. William Kingsland, author of The Great Pyramid in Fact and in Theory, maintained that the early Greeks personified these stages and trials in their hero and deity mythologies [5]. There are some intriguing facts that shed light on the mysteries of the Pyramid, one of them being the observation made by Antoine Bovis in the 1930s that stray animals who had wandered into and died inside the Pyramid had been curiously dehydrated and mummified simply by being placed in a trash can at the level of the King’s Chamber [6]. Antoine confirmed the preserving effect of the pyramid shape in a number of experiments he conducted using pyramidal models; later these experiments were furthered by Karel Drbal of the former Czechoslovakia who was eventually awarded a patent for a means of extending the life of razor blades using a pyramid [7]. More recently, pyramid structures have been used in a halal-compliant food preservation technique which doesn’t require any kind of physical or chemical treatment and does not reduce the nutrient quality of the food [8]. Other scientific studies have shown the pyramid shape to be capable of water-structuring, antimicrobial, anti-tumor, wound healing, cortisol-lowering, glutathione-boosting, plant growth-enhancing, and state of consciousness-altering effects [9] [10] [11] [12] [13] [14]. In one of his books, Dr. Patrick Flanagan gave a related account of two cats and a dog becoming vegetarians after sleeping within a pyramid-shaped enclosure for a few weeks [15]. Another fact that sheds light comes from Muller et al., whose brilliant paper published in a 2018 issue of Progress in Physics (peer-reviewed) revealed that pyramidal structures can effectively dampen gravity [16]. Such gravitational shielding conflicts with Einsteinian and Newtonian theory, but the authors explain the difficulties that the standard theory of gravitation has in explaining the dynamics of star systems and galaxies (also, this is not the first time that experimental gravity shielding has been reported) [17]. In answering these difficulties, the authors turn to their interscalar cosmology which involves an omnipresent ‘Fundamental Field’ and a universe that is “one giant oscillating chain system” [18]. In this model, matter like atoms and molecules are understood to be stable eigenstates of quantum oscillator systems, and there is a fractal scale of correspondence between different things, like the human body and the planets of our solar system. For instance, Dr. Hartmut Muller found metric correspondences between Jupiter and the human liver and spinal cord, between Saturn and human lungs and zygotes, and between the sun and our eyes and adult brain [19]. Pyramids made of a variety of materials (including electrical insulators) have been seen to assist with general healing in humans, with one aspect of the assistance being an amplification of conscious intent [20]. The pyramidal geometry is a technology that excellently interfaces with scalar energy, as shown by the Russian physics literature describing pyramids as torsion field generators that can distort the physical vacuum [21]. Tesla coils and other geometric objects that incorporate the golden ratio are additional examples of torsion field generators as phi acts as a waveguide inside these fields [22]. The propagation of torsion fields far exceeds the speed of light and their detection through a number of instruments over the last few decades reinforces the aetheric medium of the physical vacuum [23]. In fact, torsion wave velocity has been calculated to surpass the speed of light by more than a billion times, which allows them to travel into what we would understand as the future and past (psi phenomena such as clairvoyance, telepathy, and precognition can operate through torsion fields) [24]. Gyroscopic systems violating Newtonian mechanics via torsion fields was demonstrated by Dr. Nikolai Kozyrev in the 1950s, whose work was confirmed later by Veinik, Hayasaka and Takeuchi, and Shipov (among many others) [25] [26]. Torsion radiation from our sun and surrounding planets has been measured, and as Dr. Claude Swanson has explained, torsion fields provide the physical basis for our subtle aura as they are capable of coupling to electromagnetic fields (as shown by the experiments of Dr. Vladimir Poponin) [27] [28]. Something to note here is that torsion waves can be screened or shielded somewhat by aluminum, which is one reason why you do not want toxic aluminum inside your body [29]. Molecular chirality also plays into the filtering of torsion waves, which is one reason why you don’t want your body filled with synthetic crap that does not respect the homochirality of life [30]. Reflection of torsion fields by aluminum and synthetic toxicants hinders the body’s ability to interface with scalar waves and both organize and power the healing of tissues [31]. In conclusion, the reality of the so-called “pyramid power” has been demonstrated with “high statistical accuracy” through rigorous scientific experimentation and analysis by Takagi et al. over the course of 13 years [32]. Interestingly, the Japanese researchers found that their pyramid effect lasted for more than 10 days, and that some of it varied with the seasons, being strongest in the summertime (which corroborates the influence of solar torsion radiation) [33]. The documented benefits to immune function and tissue regeneration that pyramids can offer makes them worthy of consideration in the treatment of autoimmune diseases as well as both acute and chronic pain [34] [35]. Isn’t it neat that in going forward and creating a new Earth, we return to Sophia and her ancient wisdom as long foretold by the sages of old. “Natura est deus in rebus.” – Giordano Bruno (1548-1600) References:
Hydrogen is the most abundant element in the universe, and hydrogen gas is odorless, tasteless, and colorless [1]. Legend has it that the great Paracelsus was the first to document the observation of hydrogen gas after mixing iron with sulfuric acid [2].
Hydrogen may be said to represent levity with oxygen representing gravity, and together they of course form the stable compound water. We make hydrogen gas internally and take in oxygen gas from outside [3]. Hydrogen is the first element of the fourth octave in Russellian cosmogony and is counted as the first element perceivable by man [4]. In 1816, Dr. William Prout even went so far as to hypothesize that hydrogen was basically the primordial substance from which all other elements were fashioned (in support of the primary matter of Aristotle and other Greek philosophers) [5]. Oxygen lets us play in the terrestrial while hydrogen lifts our eyes upward. To the old luminaries hydrogen represented the water element, and water the emotional body [6]. And it is the heart, by way of feeling, that is carrying us now into the new Earth. Does the interplay between hydrogen and oxygen straddle the activities of ascension and incension then? If so, what physiological advantages can hydrogen offer the human body, at this time especially? As it turns out, a lot. Molecular hydrogen can be administered through inhalation as a gas, intravenous injection, or oral consumption of hydrogen-saturated water [7]. Molecular hydrogen is non-toxic at high concentrations and can diffuse rapidly at the cellular level, selectively scavenging hydroxyl radicals while preserving other reactive oxygen and nitrogen species for important signaling (we don’t want to blanket redox reactions and free radical signaling with antioxidants) [8]. The safety profile of hydrogen gas has been established for some time as it is often used to prevent decompression sickness in deep sea divers [9]. Reactive oxygen species are inevitably whipped up as a byproduct of breathing oxygen, and they strengthen protective mechanisms when kept below a manageable threshold [10]. But when this threshold is breached, tissue damage ensues. Hydrogen gas can protect nuclear DNA and mitochondria from oxidative stress, helping mitochondria to make more ATP [11]. Part of hydrogen’s potent antioxidative action comes from its activation of Nrf2, a transcription factor that regulates the expression of multiple detox and antioxidant enzyme genes [12]. Because hydroxyl radicals are major culprits in ionizing radiation-induced injury and hydrogen gas can neutralize hydroxy radicals, hydrogen gas administration has been proposed as a protective strategy for astronauts exposed to dangerous radiation [13]. Humans on Earth can use the same thinking to help deflect the stress of artificial EMF irradiation because electromagnetic radiation does not need to be ionizing in order for it to bear hydroxyl radicals [14]. Diatomic hydrogen combining with hydroxyl radicals in the body confers water, so there is a hydrating effect to the use of supplemental hydrogen too (non-ionizing radiation can be dehydrating to the body) [15]. Hydrogen from hydrogen-rich water can cross the blood-brain barrier (many antioxidant compounds cannot) and in an animal model of multiple sclerosis, hydrogen-rich water was able to reduce disease severity, demyelination, T cell infiltration of the CNS, and Th17 cell development, in addition to delaying disease onset and lowering maximum clinical scores when used prophylactically [16]. Hydrogen water has also prevented a stress-induced decline in learning and memory as well as the loss of neurons in a model of Parkinson’s disease [17] [18]. Hydrogen water has been shown to help avert atherosclerosis and ease allergic responses by calming the degranulation of mast cells (mast cells make histamine) [19] [20]. And hydrogen gas given through eye drops has improved a model of glaucoma through dropping apoptotic and oxidative stress markers [21]. Cool. We know that hydrogen gas produced normally by intestinal bacteria through the fermentation of carbohydrates suppresses inflammation in the colon [22]. And hydrogen water can function as a prebiotic as some intestinal bacteria eat the hydrogen that we consume or that is given off by other species in the gut [23]. Fun fact: turmeric can boost the amount of hydrogen made by gut bacteria and shorten bowel transit time [24]. Sha et al. found that drinking hydrogen water for four weeks enhanced the richness and diversity of the intestinal microbiota in a group of female athletes [25]. Moreover, water with hydrogen dissolved in it has displayed anti-aging avail to the periodontal tissues of rats [26]. Outside of the GI tract, molecular hydrogen is broadly anti-inflammatory, being a regulator of multiple genes’ expression [27] [28]. Spotlighting my favorite focus, molecular hydrogen has markedly improved glycemic control in mice with type 1 diabetes by magnifying the uptake of glucose by skeletal muscle, even under severe insulin deficiency (without causing hypoglycemia) [29]. The above study used orally administered hydrogen gas dissolved in water and the authors concluded that hydrogen gas “exerts metabolic effects similar to those of insulin and may be a novel therapeutic alternative to insulin in type 1 diabetes mellitus...” In 2006, Kim and Kim found hydrogen-containing water to have notable antidiabetic effects, and in 2007, Kim et al. amazingly witnessed the same lower blood sugar, raise serum insulin, and preserve beta cell mass in diabetic mice [30] [31]. Li et al. also looked at what hydrogen-rich water can do for T1D and reported that it increased glucose-stimulated insulin release from the pancreas by 2 – 4 times [32]. In a later paper published by some of the same researchers, feeding hydrogen water to T1D mice brought their blood sugar down and protected some of their pancreatic beta cells from apoptosis [33]. This is big folks, no pharmaceutical on the planet can safely do what I just listed for type 1 diabetics. In a sample of human type 2 diabetics, supplementation with hydrogen-rich water bettered lipid and glucose metabolism, dropping oxidized LDLs and raising adiponectin levels and insulin sensitivity (adiponectin is a hormone that improves glucose tolerance and the burning of fat) [34]. Kamimura et al. saw much the same in their study, with the addition of molecular hydrogen alleviating fatty liver and promoting fat loss in diabetic mice [35]. Hydrogen water has been shown to be great for rheumatoid arthritis as well, with a dosage of 500 milliliters per day for four weeks bringing about an effective reduction in oxidative stress and a significant improvement in disease activity [36]. When free radicals modify proteins, the proteins can become highly immunogenic and elicit the creation of autoantibodies against them [37]. This has been demonstrated with oxidatively modified glutamic acid decarboxylase in type 1 diabetes, and with other proteins in rheumatoid arthritis and systemic lupus erythematosus [38]. Good old hydrogen can assist in stopping this kind of protein modification which is why it can be of so much use for autoimmune conditions. Exercise-wise, drinking hydrogen water can attenuate the rise of blood lactate and muscle fatigue after heavy training [39]. Botek et al. also saw pre-exercise supplementation with hydrogen water allay muscle acidosis and the fatigue that comes along with it, plus a bettering of effort perception and ventilatory efficiency [40]. Some hydrogen-rich water can have an alkalizing effect on the blood too [41]. Molecular hydrogen may even elevate testosterone levels naturally by cleaning up hormonal signals in the testes [42]. Relatedly, hydrogen-rich water can help improve mood, anxiety, and activity of the parasympathetic nervous system [43]. So, the good news: molecular hydrogen can be very rewarding for a wide range of problems. The bad news: now everyone has a hydrogen water-maker to sell you. But that’s okay. Hydrogen has a spiritual role to play, and as we follow its always rising upward quality, we can partake of its physical gifts too. Have a great week! References:
In this article we will succinctly explore the interesting webwork that exists among sleep apnea, TMDs, Ehlers-Danlos syndrome, and POTS, beginning with sleep apnea.
Sleep apnea is a condition in which airflow repeatedly ceases or is markedly reduced during sleep (resulting in intermittent hypoxia and sleep fragmentation) [1]. Mechanical occlusion of the upper airway characterizes obstructive sleep apnea, while central sleep apnea involves faulty respiratory signaling from the brain. The term ‘complex sleep apnea’ is typically used to describe the emergence of central sleep apnea following the initiation of CPAP therapy (these occurrences usually resolve on their own with time) [2]. With a pause in breathing comes a buildup of carbon dioxide in the blood which triggers the brain to wake the individual so that oxygen levels can be restored [3]. These recurring interruptions rob the apnea sufferer of restorative sleep because there is not a normal progression through the sleep cycle. With obstructive sleep apnea, some degree of soft tissue collapsing or narrowing, usually within the oropharynx, obstructs the airway (nasal congestion or a deviated septum can block things as well) [4] [5]. This narrowing comes from a reduction in the activity of upper airway dilator muscles which is more pronounced in those with OSA [6]. Significant diminishing of upper airway dilator muscle activity can lead to pharyngeal collapse [7]. So problems in pharyngeal anatomy, pharyngeal dilator muscle activation, and ventilatory control can all contribute to the experiencing of apneas (these can include damage to or dysfunction in upper airway dilator motoneurons) [8] [9]. Lung volume, upper airway surface tension, and rostral fluid shift can all play a part too [10]. In central sleep apnea, there is a lack of neurological drive to breathe during sleep, which results in repetitive periods of poor and aberrant ventilation and gas exchange [11]. But there can be overlap between central and obstructive sleep apnea, which can make the elucidation of individual etiologies more complicated [12]. Diagnosis of sleep apnea can be based on a physical exam and the results of a sleep study (the individual’s medical history may also be consulted) [13]. Polysomnography is the gold standard for evaluating sleep [14]. Some surgical options for the treatment of sleep apnea include the removal of tissues in the throat (using a scalpel, laser, or radiofrequency radiation) to open the airway, repositioning of the jawbones (maxillomandibular advancement), and hypoglossal nerve stimulation to move the tongue forward [15]. Non-surgical options involve the use of an airway pressure device (APAP, CPAP, or BiPAP) or oral appliance, as well as exercises from orofacial myofunctional therapy to restore proper oral rest posture [16]. Oral pressure therapy and nasal EPAP are newer modalities that have demonstrated some efficacy [17] [18]. A continuous positive airway pressure (CPAP) device is the most commonly prescribed, yet side effects such as dry mouth and tooth movement can arise in some users [19]. Oral appliance therapy has been shown to be safe and effective in general, though oral appliances can vary greatly and undesirable tooth position and occlusion changes are possible with extended use [20]. Tongue-stabilizing devices are simpler and can be quite effective while carrying less potential for side effects [21]. Combining modalities is also an option and doing so may give better success [22]. In the neuropsychological domain, depression and anxiety are commonly seen with obstructive sleep apnea, as well as executive dysfunction and impaired vigilance (translates to difficulty with concentration, planning, organizing, time management, regulating emotions, sustaining motivation, and remaining alert) [23]. Obstructive sleep apnea has been linked to insulin resistance and hyperlipidemia (both of which can contribute to non-alcoholic fatty liver disease), and hypoxia is considered an aggravating factor for non-alcoholic fatty liver disease (NAFLD) [24] [25]. The increase in lipogenesis and inhibition of fatty acid oxidation by hypoxia play into the development of NAFLD [26]. And hypoxia seems to decrease adiponectin and increase leptin concentrations (adiponectin is a hormone that heightens insulin sensitivity and fatty acid oxidation while leptin signals satiety) [27] [28]. Insulin resistance and glucose intolerance are probably the main factors linking OSA with PCOS, but high testosterone and low progesterone can have notable influences too [29] [30]. There is some evidence that impaired leptin signaling in the brain may contribute to respiratory depression or hypoventilation in humans [31]. And it seems to at least be possible for proinflammatory cytokines released from adipose tissue to directly or indirectly impact respiratory control [32]. Thus it is wise to view OSA as more of a systemic condition rather than a simple local one [33]. Levels of nitric oxide have been found to be decreased in OSA patients but they normalize with CPAP therapy [34]. OSA patients present with a heightened production of superoxide by neutrophils and increased lipid peroxidation, and cyclical episodes of hypoxia-reoxygenation may deplete ATP and boost the making of free radicals [35]. In remediation, airway pressure devices can ameliorate oxidative stress, improve sleep, lower blood pressure, and reduce plasma renin and angiotensin 2 [36] [37]. Hypothyroidism and sleep apnea (both obstructive and central) have clinical presentations that overlap and it has been suggested that upper airway obstruction, neuropathy, and respiratory center depression are the variables that relate the two conditions to each other [38]. In fact, thyroid hormone replacement therapy has been shown to “diminish or completely eliminate apneic episodes and arterial oxygen desaturation, as well as to effect many improvements in sleep patterns and overall sleep efficiency,” per Kittle and Chaudhary and corroborated by Jha et al. [39] [40]. Moving on to POTS, postural orthostatic tachycardia syndrome is a form of autonomic dysregulation highlighted by excessive tachycardia upon standing with a kind of intolerance to the upright position (orthostasis) [41]. Typical symptoms consist of lightheadedness, fatigue, headache, weakness, palpitations, exercise intolerance, and presyncope or syncope [42]. And most individuals with POTS report sleep disturbances or non-restorative sleep and daytime sleepiness [43]. Technically, POTS is classified as a group of disorders that present as a common clinical picture, with primary POTS being considered idiopathic and secondary POTS occurring in tandem with another disease state [44]. The pathophysiology of POTS can consist of excessive sympathetic drive, volume dysregulation, impaired sympathetic vasoconstriction, and deconditioning [45]. Neuropathic POTS is the predominant form, and its onset usually abruptly follows viral illness, vaccination, pregnancy, sepsis, concussion, surgery, or traumatic stress [46]. Neuropathic POTS has been tied to partial autonomic neuropathy or damage to autonomic nerves [47]. POTS is mostly seen in women, and women with POTS have a much higher incidence of such gynecological ailments as uterine fibroids, ovarian cysts, endometriosis, and galactorrhea [48]. The greater prevalence of POTS in females may be partly due to differences in sympathetic nerve discharge characteristics between men and women [49]. At least some with POTS have been found to have a higher prevalence of autoimmune markers and comorbid autoimmune disorders than the general population [50]. In many POTS patients, autoantibodies against alpha 1-adrenergic receptors, angiotensin 2 type 1 receptors, or muscarinic receptors can be detected, and all of these receptors participate in the functionality of the autonomic nervous system [51] [52] [53]. Antibodies against these receptors may explain some of the features of POTS in that they could promote postural tachycardia and lower standing blood pressure, as well as trigger the maturation and degranulation of mast cells [54] [55]. Regular exercise, acupuncture, meditation, and omega-3 fatty acids can all improve vagal tone and thus could be useful in treating POTS [56]. Osteopathy may also be of aid [57]. Tying sleep apnea to POTS, intermittent hypoxia and carbon dioxide retention stimulate sympathetic nervous system activity, which stresses the cardiovascular system [58]. We know there is a strong relationship between OSA and high blood pressure, we know that hypoxia can drive sympathetic activation of the renin-angiotensin-aldosterone system (which could help explain the hyperadrenergic state of many POTS patients), and impairment to the vasodilation response has been seen in humans exposed to prolonged hypoxia [59] [60] [61]. Furthermore, prolonged hypoxia is capable of reducing the mass and respiration of mitochondria [62]. Because of the fragmenting of sleep and the greater hypoxemia during REM sleep, those with sleep apnea achieve less time spent in REM sleep [63]. Changes in heart rate variability (HRV) partly differentiate REM sleep from non-REM sleep, and in persons with POTS we see a pattern different from normal in the HRV changes between REM and non-REM sleep, which points to autonomic imbalance [64]. And manifestations as seemingly unrelated as achiness, eczema, thyroid troubles, sexual dysfunction, nocturia, and brain fog can all be correlated with abnormal sleep [65]. Accordingly, we must place sleep at the axis mundi of our consideration because if the body is not sleeping, it is not healing. Stepping to the next stone, a 2003 study by Gazit et al. suggests that dysautonomia (of which POTS is a type) may occur in roughly 80% of persons with Ehlers-Danlos syndrome [66]. Ehlers-Danlos syndrome is a group of connective tissue disorders characterized by joint hypermobility and can include weakness in the tissues that support organs and blood vessels for problems with collagen are typical with the syndrome [67]. Poor sleep, fatigue, and psychologic distress are common in those with Ehlers-Danlos syndrome (EDS), and adult populations with EDS are more likely to have sleep-disordered breathing or obstructive sleep apnea because of the oral and maxillofacial manifestations of the malady [68]. Exercise therapy can be very beneficial for EDS and supplementation with such nutrients as vitamin C, magnesium, glucosamine, MSM (methylsulfonylmethane), coenzyme Q10, carnitine, and pycnogenol has been proposed to treat the expressions of EDS [69] [70]. Hydrocephalus, CCSVI (chronic cerebrospinal venous insufficiency), and mastocytosis have been labeled potential culprits in the pathogenesis of POTS (especially in Ehlers-Danlos syndrome subjects), which makes sense as problems with the flow or drainage of cerebrospinal fluid and blood in the central nervous system could cause autonomic dysfunction [71] [72]. A faulty capacity to drain cerebrospinal fluid or a weak blood-brain barrier (which can be seen in Ehlers-Danlos) could make the brain more susceptible to the sudden onset of POTS symptoms after trauma to or viral infection of the brain (which is frequently seen) [73]. Now let’s look at the final node in our web: TMDs. Temporomandibular disorders (TMDs) frequently stem from abnormal muscular tension around the temporomandibular joint or anatomical derangements affecting the joint [74]. Hypermobility and arthritis can have a role too [75]. TMDs can certainly have a multifactorial etiology, with dental occlusion often being a misunderstood piece of the puzzle [76]. Multiple criteria can be referenced for the diagnosis of a TMD, which is often done clinically but can be aided by medical imaging [77]. Temporomandibular disorders are more common in POTS patients [78]. Manual therapy and therapeutic exercise can be used effectively for treating TMDs [79]. Acupuncture and low-level laser therapy may also be helpful, and while there are surgical options for the treatment of TMDs, they are usually not recommended [80] [81] [82]. On average, the modern human has smaller jawbones and a smaller airway than those of our predecessors, and this is a result of our conventional diet and means of feeding infants [83]. So it stands to reason that a firm relationship exists between TMDs and obstructive sleep apnea because TMD-related orofacial issues can compromise airway patency [84]. Oral appliances can be successfully employed for TMDs (including sleep bruxism or teeth grinding) and OSA, but there is potential for these devices to exacerbate or even promote the development of TMDs [85] [86]. However, sometimes the pain or discomfort that can come with the initiation of oral appliance therapy subsides on its own [87]. Long-term use tends to bring about a higher risk of dental changes and issues with the temporomandibular complex [88]. Extensive literature indicates that TMDs are around one and a half to two times more prevalent in women than in men [89]. And TMDs have been associated with multiple comorbidities, as Hoffmann et al. have uncovered: “The most frequent comorbid conditions included fibromyalgia, chronic fatigue syndrome, irritable bowel syndrome, rheumatoid arthritis, chronic headache, depression, and sleep disturbances. Commonly associated comorbidities will surely provide clues about pathophysiology. For example, a relevant finding was the high prevalence of allergies that preceded the TMJD diagnosis suggesting an autoimmune etiology for a subset of TMJD patients” [90]. So temporomandibular disorders (including sleep bruxism), sleep-disordered breathing, and POTS can all be connected to each other [91] [92]. The pathway to correcting one or more of these hardships can vary and therefore must be individualized. But we understand the webwork, and with natural medicine we can put the necessary pieces together and place the person in the best position to heal. The body is capable of amazing turnarounds when we remove its restraints, and when we permit the life force to flow freely, we can be gifted with a displaying of true medicine. References:
The 2019 novel coronavirus (2019-nCoV) has been formally named ‘severe acute respiratory syndrome coronavirus 2’ (SARS-CoV-2) with its associated illness being labeled ‘coronavirus disease 2019’ (COVID-19) [1]. The SARS-CoV-2 outbreak marks the third coronavirus outbreak in two decades [2]. Coronaviruses derive their name from the characteristic covering of their surface by peplomers that resembles a solar or stellar corona [3].
SARS-CoV-2 has an average incubation period of about 5 days, and is mainly transmitted through respiratory droplets, with direct contact and aerosol transmission being lesser routes [4] [5]. Common symptoms include cough, fever, shortness of breath, and fatigue, but sore throat, headache, dizziness, nausea, and diarrhea may also be seen [6]. Evidently, coronaviruses can persist on inanimate surfaces for up to nine days, but they can be inactivated with disinfectants containing ethanol or hydrogen peroxide [7]. SARS-CoV-2 is a positive-sense, single-stranded RNA virus that falls under the Betacoronavirus genus and is closely related to two SARS-related coronaviruses found in Chinese rufous horseshoe bats [8]. The genetic information of positive-sense RNA viruses can be quickly translated in the nuclei of host cells by ribosomes, and coronaviruses house the largest known RNA genomes [9]. Genomic investigations suggest that SARS-CoV-2 could have originated in a seafood market in Wuhan or the nearby Wuhan Institute of Virology [10]. Yu et al. have proposed that the virus was imported from outside the market, with the market only having catalyzed its spread [11]. Pradhan et al. discovered four insertion sequences in the SARS-CoV-2 genome that are not present in any other coronavirus yet match what can be found in two key proteins of HIV-1 (human immunodeficiency virus type 1) [12]. This finding has generated suspicion of genetic engineering as the researchers concluded that the natural acquisition of these insertions is highly unlikely. A combination of the two antiretroviral drugs lopinavir and ritonavir (normally used to combat HIV-1) being efficacious against SARS-CoV-2 lends support to the genetic engineering origin of SARS-CoV-2 [13]. Relatedly, chloroquine and hydroxychloroquine (both antimalarial drugs) have also been used successfully in the treatment of COVID-19 [14]. According to the work of Xu et al., SARS-CoV-2 has a strong binding affinity to the angiotensin-converting enzyme 2 (ACE2) receptor in humans, which drives entry of the virus into host cells so that replication can take place [15]. ACE2 is highly expressed in the alveolar cells of the lungs and the enterocytes of the small intestine, which is why SARS-CoV-2 gains access to the body most easily through the respiratory and gastrointestinal routes [16]. Just a few days ago, Hoffmann et al. reported that SARS-CoV-2 also relies on spike protein priming by TMPRSS2 (transmembrane protease serine 2) for entry into cells [17]. The coexpression of ACE2 and TMPRSS2 in pneumocytes (cells that line the alveoli in the lungs) apparently allows for a cleaving of the SARS-CoV-2 spike protein which then diminishes viral recognition by neutralizing antibodies as SARS-CoV spike protein fragments can serve as antibody decoys [18]. SARS-CoV-2 can also hide from the immune system by downregulating gene expression related to antigen presentation [19]. Inflammation and damage to the lungs may also be worsened by the induction of ACE2 ectodomain shedding by SARS-CoV-2, which has been associated with acute lung injury and hindered lung function [20]. Interestingly, evidence exists for a higher level of ACE2 expression in the bodies of East Asian populations compared with non-Asian populations [21] [22]. Once the viral RNA is released into the cytoplasm, host cell machinery is used to replicate the genome, after which virion-housing vesicles fuse with the plasma membrane to release and spread the virus [23]. In the cohort study of Yang et al., lymphocytopenia (low white blood cell count), possibly caused by pyroptosis, occurred in over 80% of the critically ill patients [24]. Because lymphocytopenia is prominent in critically ill subjects with SARS-CoV infection, the severity of lymphocytopenia may reflect the severity of SARS-CoV-2 infection [25]. Antigen presentation in response to SARS-CoV-2 exposure should stimulate the crafting of virus-specific antibodies, but if T cell hyperactivation takes place, a cytokine storm can be triggered and inadvertent injury to lung tissue can result, potentially leading to ARDS and ultimately death (ARDS is the main cause of death in COVID-19) [26] [27]. Older patients are statistically more likely to develop ARDS (acute respiratory distress syndrome) from viral pneumonia than those of a younger age [28]. Is there a connection between the incidence of pneumonia and air quality in Wuhan? Absolutely there is. As Qian et al. have expressed in their 2007 examination, “There are approximately 4.5 million residents in Wuhan who live in the city core area…where air pollution levels are higher and pollution ranges are wider than the majority of cities in the published literature” [29]. In 2012, Liu et al. found a significant association between ambient air pollution in Wuhan and daily respiratory disease mortality (this includes pneumonia) [30]. In 2017, Ren et al. found “Strong evidence of an association between [nitrogen dioxide] and daily respiratory disease mortality among men or people older than 65 years,” and concluded “There was a positive association between air pollutants and respiratory disease mortality in Wuhan, China. Both time-series and case-crossover analyses consistently reveal the association between three air pollutants and respiratory disease mortality” [31]. In 2013, Chen et al. studied the seasonal variation between ambient particulate matter and daily mortality in Wuhan and discovered that particulate matter pollution was greatest in the winter seasons, which matched the peaks in total mortality over a three-year period [32]. Qian et al. also discerned that the effects of three air pollutants on respiratory mortality was greatest during the winter seasons in Wuhan [33]. The outbreak of SARS-CoV-2 in Wuhan began in December of last year did it not? Next, the link between COVID-19 and 5G demands examination. China has made the deployment of 5G technology a national priority, and Wuhan has been chosen as a primary 5G hub with thousands of base stations already in place, making Wuhan one of the most electropolluted cities on the planet [34]. And a score of 5G antennas have been installed in the new hospitals built to treat patients with COVID-19 [35]. Behind China, South Korea and Italy have two of the highest number of SARS-CoV-2 cases in the world, and both have been heavily implementing 5G [36]. And let’s note that almost every single Italian COVID-19 fatality has been tied to a previous medical condition, and the average age among these fatalities is greater than the average life expectancy in the United States [37]. Additionally, Iran is an epicenter for the rollout of 5G and has had more reported deaths from COVID-19 than any other country in the world outside of China as of the writing of this article [38]. Digging deeper, mountains of research show the detrimental effects of man-made electromagnetic field irradiation on immune function, but specifically we know that millimeter waves or radiation from the extremely high frequency band (this band is used by 5G systems) can significantly disturb the activity of peripheral blood neutrophils [39]. We also know that neutrophils are important for controlling viral infections, and that their improper or prolonged activation can “lead to detrimental effects to the host and can even cause severe disease, including pneumonia and acute respiratory distress syndrome,” as explained by Galani and Andreakos in 2015 [40] [41] [42]. Drescher and Bai corroborate the above in their 2013 paper, stating that the unbalanced recruitment of neutrophils “may cause severe damage to the targeting tissues or organs during influenza and other viral infections” [43]. More specifically, it is known that oxidative stress can increase the infectivity of coronaviruses, as can abnormal calcium influx from the activation of voltage-dependent calcium channels by EMFs [44] [45] [46]. What this tells us is that exposure to very discordant EMFs can greatly weaken the immune system and make the body much more vulnerable to opportunistic infections [47]. Furthermore, pneumonia can be exacerbated by aberrant calcium influx (which 5G radiation can trigger), and because calcium channel blockers can reduce the severity of pneumonia, we can say that 5G radiation can both promote the development and worsen the severity of pneumonia [48]. And there is no denying that the eruption of COVID-19 paralleled the rapid construction of Wuhan’s 5G network. I’ve discussed the evil of 5G in another article, but let’s just mention here that many experiments do not account for pulsing and carrier signal modulation and therefore do not accurately reflect the very adverse and systemic effects of wireless radiation [49]. Let me also mention that millimeter waves activate voltage-dependent calcium channels in the body and excessive activation of these channels can promote fear conditioning, which is being clearly evinced around much of the world right now [50]. Now, most individuals who have contracted SARS-CoV-2 have presented with mild symptoms that resolved without problem, and many exhibited no symptoms at all [51]. And the toll of COVID-19 stands weakly compared to influenza, for in 2018, Iuliano et al. reported an estimate of between 291,243 and 645,832 for the number of annual influenza-associated deaths globally [52]. As of March 14, just under 5,400 deaths from COVID-19 have been tallied, the majority of which are from China. Turning to pneumonia, in 2011, Ruuskanen, Lahti, Jennings, and Murdoch reported that roughly 200 million cases (this bears repeating, 200 million cases!) of community-acquired viral pneumonia occur every year [53]. I feel it is safe to say that few folks were panicking over pneumonia before it began being associated with a coronavirus by every media outlet. We must also keep in mind that much of the data and testing for SARS-CoV-2 infection is unreliable, knowledge of which is making its way through the grapevine [54]. In corroboration, Zhuang et al. reported that approximately half of the results from nucleic acid testing currently being used in China might be false positives [55]. So what can we do to naturally oppose COVID-19? Firstly, the SARS-CoV-2 3a protein can trigger apoptosis via the mitochondrial death pathway where cytochrome c is released into the cytosol [56]. This disruption of mitochondrial dynamics by SARS-CoVs can cripple signaling within the innate immune system which helps SARS-CoVs evade immune responses and increases their infectivity [57]. Thankfully, vitamin C can do a great job of deflecting the apoptotic cascade and thus the virus-induced death of cells [58]. And this is why vitamin C has been and is continuing to be heavily used in China to successfully treat COVID-19 patients [59] [60] [61]. Of course, this information is being suppressed to instill fear and promote the false belief that nothing can be done for COVID-19 outside of vaccination. In fact, so much stigma and panic has been generated that many innocent Wuhan citizens have been the targets of violent attacks by vigilantes in the region [62]. And the CDC knows better than anyone that fear sells vaccines. Continuing, in 2017, To et al. found that many RNA viruses can block the signaling for type 1 interferon production, which is important because type 1 interferons help defend the body against viral infection [63]. In response, alpha-lipoic acid, sulforaphane, and spirulina may counter this blocking and boost the making of type 1 interferons, enhancing the antiviral response [64] [65] [66]. Zinc and selenium may help quell inflammation in the lungs induced by viral infection and slow the rate at which an infecting virus mutates, respectively [67] [68]. These nutrients could then aid in thwarting acute respiratory distress syndrome (ARDS). Furthermore, beta-glucan and elderberry have demonstrated effectiveness in protecting against RNA viruses [69] [70]. Cinnamomum cassia has demonstrated effectiveness against HIV-1, and curcumin has exhibited notable anti-SARS-CoV activity [71] [72]. And it seems that quercetin can help block the entry of SARS-CoV into host cells [73]. From the Chinese pharmacopeia, Stephania tetrandra, Salvia miltiorrhiza, Lycoris radiata, and Ganoderma lucidum have all shown strong antiviral abilities against coronaviruses [74] [75] [76] [77]. Houttuynia cordata has demonstrated significant inhibitory effects on SARS-CoV, while astragalus and resveratrol have done the same with other coronaviruses [78] [79] [80]. Essential oil-wise, the diffusing of peppermint and thyme could be helpful in preventing the spread of SARS-CoV-2 [81]. To conclude this article I would like to quickly bring us back to looking at things from a higher perspective, and ask that we please all do each other a favor and stop obsessing over propaganda from CNN and elsewhere. Instead, go for a walk, read a good book, and maybe eat an orange or two. We’re gonna be fine. Solar coronas illustrate that light always prevails over darkness – all we have to do is let love in. References:
The TurboSonic is a whole-body vibration (WBV) apparatus whose platform uniquely vibrates vertically in a sinusoidal pattern generated by sound waves that harmoniously oppose the direction of force exerted by gravity. A voice coil actuator and audio amplifier power the precise, vertical movement of the platform. Although a mountain of research exists on the potential benefits of whole-body vibration therapy in general, this article will only include references that specifically involve the use of a TurboSonic or Sonix device (Sonix devices being the next iteration of the TurboSonic) as these apparatuses are unique in the sonic therapy they offer.
Use of the TurboSonic has been shown to inhibit the proliferation of preadipocytes (fat cell precursors) and enhance the expression of two adipogenic genes, which may help with glucose and lipid homeostasis as a drop in the expression of adipogenic genes has been associated with obesity by way of an accumulation of larger fat cells in subcutaneous tissue coupled with insulin resistance [1] [2] [3]. Sonic vibration has also been seen to decrease lipid droplet size in mature adipocytes and boost the making of hormone-sensitive lipase, an enzyme that mobilizes stored fats so they can be used as fuel [4]. Sonic whole-body vibration (SWBV) therapy could be a significant aid to regenerative medicine as it has been demonstrated to induce the differentiation of adipose tissue-derived mesenchymal stem cells into cells of the central nervous system like neurons, oligodendrocytes, and astrocytes after only four days [5]. Another paper by Kim et al. confirmed the ability of sonic vibration to promote the neural differentiation of mesenchymal stem cells [6]. Continuing along the lines of neurological rehabilitation, whole-body vibration training using a TurboSonic bettered static sitting balance and postural sway in a group of spinal cord injury patients, as well as improved spasticity, balance, and walking ability in another group with a cervical spinal cord injury [7] [8]. In subacute stroke patients, sonic vibration therapy was just as effective as conventional physical therapy for the recovery of balance [9]. And in a collection of elderly women, whole-body vibration exercise yielded gains in muscle strength, balance, and fall efficacy [10]. In 2008, sonic whole-body vibration training was tested in a pilot study with a geriatric population from two assisted living facilities and successfully increased “activity and participation levels” as well as improved “mental health and quality of life” [11]. Health-related quality of life is a more specific measure that the TurboSonic has benefited in older adults, as are scores for both osteoporosis and osteoarthritis [12] [13] [14]. In the above osteoarthritis study, the TurboSonic reduced the pain of chronic knee osteoarthritis and heightened both dynamic balance and strength of the quadriceps muscle group. By suppressing the upregulation of proinflammatory cytokines triggered by lipopolysaccharide (a bacterial endotoxin), a TurboSonic has also attenuated bone loss and facilitated the recovery of bone volume and bone mineral density [15]. Utilizing the TurboSonic as an exercise tool, different activation patterns in muscles throughout the body can be achieved by altering the machine’s frequency and amplitude settings [16]. Whole-body vibration training has empirically demonstrated an ability to improve both rate of force development and electromechanical delay (these measures refer to how quickly a muscle responds after receiving neural input), which translates to better sports performance and injury prevention [17]. After a four-week training protocol, the TurboSonic has boosted postural stability and leg strength with only nine minutes of exposure per week [18]. Interestingly, sonic vibration has been employed in the detection and characterization of primo vessels and subcomponents of the primo vascular system [19]. Existence of the primo vascular system was confirmed just a few years ago, and this system evidently functions as a chemical and biophoton highway, in addition to serving as an adjunct immune and endocrine network [20]. Because the primo vascular system can be signaled acoustically, using a TurboSonic may have effects akin to those of traditional acupuncture [21]. Importantly, whole-body vibration is an excellent modality for lowering cortisol while upping growth hormone and testosterone [22]. And much like other vibration devices, the TurboSonic can augment blood circulation and lymph drainage, including the correction of rouleaux or stacked red blood cells, which are associated with a weak negative charge and an acidic pH [23] [24]. The separating of rouleaux allows for cells to receive nutrition more effectively and to discard their waste more easily. Lastly, for those who sing, use of the TurboSonic has even effectively treated vocal fatigue [25]. Subjecting the body to vertical movement produced by sound waves of discrete frequencies and amplitudes can be greatly health-promoting and can introduce highly matchless stimuli for growth, repair, conditioning, and remedying. The TurboSonic is a surprisingly wonderful instrument and I highly recommend you give one a try. References:
Glyphosate is a non-selective herbicide patented and brought to the consumer market by Monsanto in the 1970s [1]. It is a synthetic analogue of the amino acid glycine (N-phosphonomethylglycine). Glyphosate-based formulations vary in their constitution but generally consist of a surfactant like polyoxyethyleneamine (POEA) and the isopropylamine (IPA) salt of glyphosate [2]. Surfactants like POEA and TN-20 (found in Roundup®) as well as toxic metals like arsenic and lead enhance the toxicity of glyphosate-based herbicides [3] [4]. As excellently reviewed by Mesnage et al., adjuvants in pesticide formulations are falsely labeled “inerts” by the manufacturer despite the fact that they enhance up to 1000 times the toxicity of the so-called “active principle” (glyphosate is the active principle in Roundup®) [5]. To quote Mesnage et al.: “Roundup was found in this experiment to be 125 times more toxic than glyphosate. Moreover, despite its reputation, Roundup was by far the most toxic among the herbicides and insecticides tested. This inconsistency between scientific fact and industrial claim may be attributed to huge economic interests, which have been found to falsify health risk assessments and delay health policy decisions” [6].
What must also be realized is that pesticides bioaccumulate or build up in animal organisms, and in an experiment conducted by Seralini et al., it was discovered that a Roundup® concentration of only 0.1 parts per billion (!!) was needed to provoke pathologies in rats after two years (illustrating that the harmful effect of pesticide exposure is cumulative) [7]. Of course, as toxins accumulate in the body, compounded and negatively synergistic effects can be seen [8]. In 2015, the International Agency for Research on Cancer labeled glyphosate a probable carcinogen [9]. In humans, a positive relationship has been demonstrated between exposure to glyphosate and the onset of lymphoma [10] [11]. Internal documents from Monsanto consisting of unpublished studies acquired via the Freedom of Information Act clearly illustrate how strongly glyphosate can damage the kidneys and how readily glyphosate can induce tumors in the pituitary gland, thyroid gland, thymus gland, mammary glands, testes, kidneys, pancreas, lungs, and liver [12]. Monsanto colluded with the Environmental Protection Agency in obtaining approval for the registration of glyphosate and there was even blatant and open dissention among the members of the review committee [13] [14]. There is also evidence of ingested glyphosate reacting with nitrites in the colon and skin, forming N-nitrosoglyphosate metabolites that are carcinogenic [15]. Indeed, an age-adjusted analysis conducted in 2004 revealed “an 80% increased risk of melanoma associated with glyphosate use” in pesticide applicators from Iowa and North Carolina [16]. Furthermore, glyphosate can impair the intestinal microbiota’s production of folate (not folic acid, a synthetic mimicker), a deficiency of which has been linked to cancer of the colon, brain, pancreas, ovaries, cervix, lungs, and breasts [17]. Lastly, Roundup® can promote the onset of cancer by constraining the tumor suppressing enzymes succinate dehydrogenase and fumarate hydratase [18]. There is no refuting the dramatic rise in chronic disease prevalence in the United States paralleling the exponential increase in the use of glyphosate (and other pesticides) and the consumption of genetically modified foods [19]. Even though the following fact is outside of this article’s focus, it must be understood that genetic modification is not identical to the natural interbreeding that can take place between species of the same genus or even different genera [20]. GM crops cannot be considered even remotely equal to non-GM crops. Animals like cows, chickens, and pigs that are housed in confined animal feeding operations (or CAFOs) are commonly fed genetically modified food crops and thus animal products such as eggs, milk, cheese, butter, and meat can be strikingly contaminated with herbicide residues [21]. Undeniably, glyphosate in some form is present in the foods comprising the typical Western diet [22]. Glyphosate exerts its herbicidal effect by disrupting the shikimate pathway, seven steps utilized by plants and microorganisms in the making of the amino acids phenylalanine, tryptophan, and tyrosine [23]. Because the human GI tract is obviously filled with bacteria, glyphosate ingestion can poison the intestinal microbiota and engender significant dysbiosis [24]. In 2013, Samsel and Seneff argued that glyphosate can impair the crafting of sulfate by endothelial nitric oxide synthase (eNOS) and its transport in the bloodstream, as well as contribute to the development of intestinal hyperpermeability or leaky-gut syndrome [25]. Senapati et al. found that glyphosate-treated fish experienced a reduction in digestive enzyme counts and injury to the intestinal wall [26]. Samsel and Seneff have also proposed that glyphosate can reduce bile acid production by the liver, hurting the health of the gallbladder and small bowel and encouraging the development of small intestinal bacterial overgrowth (SIBO) in addition to hampering the assimilation of nutrients [27]. Continuing, glyphosate has been shown to damage DNA in human cells and function as a potent endocrine disruptor [28] [29]. Roundup® can disrupt the hypothalamic-pituitary-adrenal axis and bring about a condition very similar to adrenal insufficiency [30]. Roundup® has also been shown to disrupt oxidative phosphorylation in mitochondria and thus the making of ATP [31]. And in rat testes, a low dose of Roundup® injured fertility by opening voltage-dependent calcium channels leading to severe oxidative stress and cell death [32]. Glyphosate can markedly inhibit the cytochrome P450 (CYP) family of enzymes, which are primarily located in the liver to power detoxification, but also exist in the endoplasmic reticula and mitochondria of cells outside the liver [33]. CYP enzymes are involved in the metabolism of cholesterol, vitamin D3, estrogen, and testosterone too [34]. It has been contented that glyphosate is partly responsible for the vitamin D deficiency epidemic in the U.S. [35]. Moreover, glyphosate depletes glutathione through its generation of oxidative stress (glutathione being a critical antioxidant and detoxificant) [36]. Most Americans are bombarded with xenobiotics from food preservatives (such as BHA and BHT), toxic metals (such as aluminum, mercury, and cadmium), water contaminants (such as fluoride, chlorine, and pharmaceuticals), and food additives (such as monosodium glutamate and aspartame). By hindering the body’s ability to deal with encountered xenobiotics, ubiquitous glyphosate exposure amplifies the harm of environmental toxins [37]. And by ubiquitous I mean glyphosate can be found in soil, sediment, surface water, groundwater, and rainwater, in addition to the plants and animals within the GM food chain [38]. It is also very plain that glyphosate significantly hurts the health of honey bees and their effectiveness as pollinators [39] [40]. By negatively altering the gut microbiota of honey bees, glyphosate increases susceptibility to infection by opportunistic pathogens and is no doubt playing a part in the scourge of colony collapse disorder that has swept across North America and Europe [41]. Glyphosate is clearly uptaken by plants, animals, and humans, and as concluded by a study conducted by Kruger et al., “Chronically ill humans had significantly higher glyphosate residues in urine than healthy humans” [42]. Because glyphosate is a chelator of ionized metals like calcium, iron, zinc, magnesium, and manganese, it can obstruct plant uptake from the soil and rob the human body of these necessary minerals [43]. Next, glyphosate is fully capable of penetrating the placenta and a huge increase in the rate of birth defects has been seen in Argentina and Paraguay where glyphosate has been heavily applied to core crops [44] [45]. Beecham and Seneff have proposed that in utero subjection to glyphosate can cause neurodevelopmental defects characteristic of autism as well [46]. Because of glyphosate’s molecular similarity to the amino acid glycine, glyphosate can operate as a glycine mimetic and undesirably bind to receptors for glycine [47]. In the brain, undesirable binding by glyphosate to NMDA receptors can cause a haphazard influx of calcium into neurons that leads to the death of these cells [48]. A carefully choreographed entry of calcium into immature neurons is necessary for proper neurodevelopment and the deflection of autistic or ASD-like presentations [49]. Partly because of its ability to induce a deficiency in manganese, Samsel and Seneff have suggested that glyphosate could contribute to the manifestation of other related conditions such as Alzheimer’s disease, Parkinson’s disease, depression, and anxiety, as well as osteoporosis, osteomalacia, and chronic fatigue syndrome [50]. In addition to glyphosate’s ability to bind to receptors for glycine, glyphosate may also substitute for glycine during protein synthesis, creating misfolded or dysfunctional proteins that are toxic and capable of causing cell death [51]. Notably, because insulin receptors normally contain glycine, glyphosate substitution for glycine could create dysfunctional insulin receptors that engender insulin resistance and chronic inflammation [52]. In the same vein, it seems glyphosate can make it more difficult for the liver to metabolize fructose, potentially contributing to fructose-induced fatty liver disease [53]. And the replacing of glycine by glyphosate could weaken the immune system by neutralizing the antimicrobial action of alpha defensin peptides [54]. Finally, glyphosate could be playing a marked part in the etiology of multiple autoimmune conditions by way of molecular mimicry [55]. As discussed by Shoenfeld and Aron-Maor in their 2000 paper, autoimmunity can be conjured through molecular mimicry in subsequence to microbial infection or vaccination [56]. And sure enough, the presence of glyphosate in numerous vaccines has been verified (the MMR vaccine contained the highest level) [57]. Glyphosate uptake from vaccine-derived gelatin excipients into various proteins seems to be the common pathway through which glyphosate in glyphosate-contaminated vaccines fosters autoimmunity (note that glyphosate exerts more of a toxic effect when injected directly into the bloodstream versus administered orally) [58] [59]. For corroboration, an excellent example of vaccine-induced autoimmunity can be seen in the narcolepsy epidemic that followed the mass vaccination campaign against H1N1 influenza (swine flu) across the European Union beginning in 2009 [60]. Here the Pandemrix vaccine contained a peptide from the influenza virus that invoked cross-reactivity with hypocretin receptor 2, a protein expressed in the brain that can drive the appearance of sleep disorders like narcolepsy when altered or damaged [61]. In conclusion, there is no argument against the fact that the widespread and indiscriminate use of glyphosate-based herbicides is unacceptable. Monsanto’s Roundup® is devastating the microbial diversity of our soils and compromising the health of the biosphere as a result [62]. By consuming organic foods and supporting both sustainable farmers and natural beekeepers, we can help to restore the richness and well-being of our planet while undermining the profitability of genetic engineering in agriculture. We only have one Earth, and right now she desperately needs our aid. References:
5G refers to the fifth-generation wireless network currently being deployed by the telecommunications conglomerate. The fifth-generation network will utilize millimeter waves that range from a frequency of 30 GHz to 300 GHz between the microwave and infrared bands of the electromagnetic spectrum (other frequencies will also be used). The extremely high frequency region of the EM spectrum will provide for a broader bandwidth and thus the transfer of more data faster. However, the necessity of this article and others like it is due to the fact that adding a colossal amount of high frequency, millimeter wave radiation to the already chaotic sea of radiation from man-made sources is asinine. There is absolutely no argument to the contrary that the installment of millions of small cell antennas around the world which will irradiate the planet to an astronomical degree represents an unprecedented crime against humanity.
Millimeter waves are capable of transmitting a large amount of data but only for a short distance (due to atmospheric attenuation), hence the need to place a massive number of small antennas throughout the 5G network [1]. 5G technology will blanket the Earth with highly damaging electromagnetic radiation with consequences to every ecosystem around the globe. The full deployment of 5G will also include the use of thousands of satellites emitting powerful beams of millimeter wave radiation orbiting within the Earth’s magnetosphere. An enormous upsurge in EMF generation will negatively impact both our magnetosphere and ionosphere – disturbances that can lead to “cancer, reproductive, cardiac and neurological disease and death,” as Dr. Neil Cherry has explained [2]. Severe pollution of the global electric circuit will be detrimental to all life on this planet [3]. Thousands of peer-reviewed studies have exhibited the harmful effects that radiofrequency EM radiation can have on the human body at levels far less than what 5G base stations will employ. And the flora and fauna of our planet are no more safe from the toxicity of EMFs than we are [4] [5]. Also know that the impact of radiofrequency EMFs extends all the way to microorganisms, and it has been clearly demonstrated that exposure to RF-EMFs can make pathogenic bacteria resistant to antibiotics [6]. And let’s not forget that radiofrequency radiation (millimeter waves fall into this category) has irrefutably been shown to be carcinogenic (cancer promoting) [7]. MMW (millimeter wave) irradiation can foster cancer development by causing chromosomal lesions and pathological mitosis or cell division [8] [9]. The notion that non-ionizing radiation can only have a thermal effect upon the human body is not only completely false but absurd, for non-thermal biological injury occurs at levels far below established exposure guidelines [10] [11]. And the conventionally propagated falsity that non-ionizing radiation does not have the power to damage DNA is despicably defended by organizations like the National Cancer Institute despite the fact that mobile-phone radiation has clearly induced single- and double-strand breaks in human DNA via a non-thermal mechanism [12]. As Pakhomov et al. have explained, aside from the direct effect of MMW radiation subjection, organism-level responses can be mediated by neuroendocrine pathways via signaling from the skin [13]. Electric fields impressed upon the body can also be amplified or reradiated after they make initial contact, allowing for the equivalence of deep penetration (see Brillouin precursors) [14] [15]. Thus, the idea that MMWs are harmlessly absorbed and dissipated in the epidermal and dermal layers of the skin is erroneous [16]. As Dr. Martin Pall has described, MMWs can elicit a wide array of bodily injury through activation of voltage-dependent calcium channels and the generation of highly destructive peroxynitrite (a potent oxidant) [17]. In 2002, Kolomytseva et al. showed the phagocytic activity of peripheral blood neutrophils (in mice) being suppressed by roughly 50% after a single exposure to MMW radiation [18]. And in a Russian study declassified by the CIA in 2012, Zalyubovskaya revealed the following consequences of subjecting rats and mice to radio waves of the millimeter range (again, 5G will use millimeter waves): disruption of vesicular membrane permeability; generation of micronecroses and tissue dystrophy (degeneration); suppression of hematopoiesis (the making of blood cells); demyelination of nerve fibers; adrenal gland stress and elevation of adrenaline; mitochondrial injury in the liver, heart, kidneys, and brain; nucleic acid destruction in the liver, spleen, kidneys, heart, and lungs; weakening of the immune system; and disturbance to central nervous system activity [19]. Undeniably, organisms are negatively affected by man-made EMFs, despite abominable lies to the contrary. As discussed in a paper compiled by the European Academy for Environmental Medicine, the prevalence of electromagnetic hypersensitivity has skyrocketed over the last few years with the massive increase in EMF exposure rates [20]. Reducing EMF exposure is necessary for the restoration of health in those with electromagnetic hypersensitivity, yet the rollout of 5G will make doing so incredibly difficult. Indeed, extrapolating the current trend of rising electrosensitivity, Hallberg and Oberfeld have expressed the concern that electrosensitivity will soon become universal [21]. The mountain of research papers illustrating adverse effects from EMFs continues to expand at an approximate rate of 350 papers per year, yet numerous governmental and corporate entities continue to falsely assert that there exists no convincing evidence of harm from artificially-generated electromagnetic fields. Numerous declarations and treaties are being criminally violated by the forced implementation of 5G technology, and national governments are removing barriers to entry for telecommunications services and prohibiting local governments from enforcing laws relating to the protection and health of environments in order to steamroll opposition to the erection of the 5G network. The EPA and FCC have indictably failed to perform their purported duty to protect American citizens. By no means do we require an enormous and worldwide upscaling of our wireless network, and the true agenda behind 5G lies not in the enhancement of mobile communication and entertainment, but in the establishment of an electronic ecosystem that will feed an overseer-like nervous system of artificial intelligence [22]. Plans for the Internet of Things barely relate to what’s advertised, and the digital matrix to be spawned from the IoT will strongly disconnect humans from the natural world and reality to the extent of literally dehumanizing mankind [23]. The savant Dr. Rudolf Steiner (in the early 1900s) forewarned of the creation of a shadowlike, automaton intelligence which would corrode the spiritual essence of the human and attempt to conquer its intellect via the fixation and digitization of thought [24]. And this is exactly what the artificially intelligent brain of the Internet of Things will seek to achieve – ensnarement of human consciousness and the averting of spiritual deliverance. We as a species have a decision to make right now, either we stand up for our divine rights to life, liberty, and the pursuit of happiness, or we stand idly by and allow our health, freedom, and consciousness to be surrendered to totalitarian rule. References:
Hypertension or high blood pressure is one of the most common chronic conditions and can be classified as either primary (or essential) hypertension or secondary hypertension [1]. The etiology of primary hypertension is considered indeterminate but multifactorial, while secondary hypertension results from an overt cause such as some form of kidney or adrenal gland disease, or the use of oral contraceptives [2]. High blood pressure is conventionally defined as a systolic measure of greater than or equal to 140 mmHg or a diastolic measure of greater than or equal to 90 mmHg [3]. A systolic measure ranging between 120 and 139 mmHg or a diastolic measure ranging between 80 and 89 mmHg is considered prehypertensive. Compensatory mechanisms exist for the homeostatic regulation of blood pressure, so in order for blood pressure to remain elevated, the compensatory mechanisms in place must be persistently overburdened or dysfunctional [4].
Arterial blood pressure is normally a variable powerfully controlled by baroreceptors (such as those found in the carotid arteries and aortic arch) and the renin-angiotensin-aldosterone system (RAAS). The RAAS is powered by the kidneys, liver, and adrenal glands, and involves the protein renin, the peptide hormone angiotensin 2, and the steroid hormone aldosterone. The kidneys convert prorenin into renin and secrete renin into circulation. The liver supplies angiotensinogen which renin converts into angiotensin 1. Angiotensin 1 is largely inert and thus must be transformed into angiotensin 2 by angiotensin-converting enzyme (ACE), found predominantly in the lungs. Angiotensin 2 is a potent vasoconstrictor, but it also triggers the adrenal glands’ release of aldosterone, which raises blood pressure by upping sodium and water reabsorption (as well as the excretion of potassium). Problems in any of the steps or components of the RAAS can disrupt electrolyte and fluid balance or blood pressure modulation [5]. The most commonly identified factor in the onset of hypertension is an excessive intake of dietary sodium, wherein the kidneys become unable to excrete the ingested sodium unless the blood pressure is increased [6]. Evidence suggests that our ancient ancestors consumed a diet that provided around 1,000 milligrams of sodium per day, whereas the average intake in the United States is greater than 3,000 milligrams [7]. Investigations into populations with a low daily intake of salt have found little or no hypertension with little or no rise in blood pressure with age [8]. On the other hand, a 30-year study of 144 Italian nuns demonstrated that the hypertensive effect of dietary salt can be blunted by a low-stress lifestyle [9]. An uptick in the sympathetic nervous system’s stimulation of the kidneys can boost renin secretion and renal sodium reabsorption, and heightened sympathetic nervous system activity is a frequent finding in those with primary hypertension [10]. Mental and emotional stress then, can activate the sympathetic branch and prevent urinary sodium loss through sparking the RAAS [11]. Relatedly, inflammation and oxidative stress in the kidneys can easily promote renal dysfunction and the onset of renal artery stenosis (stenosis meaning abnormal narrowing), also resulting in a boost in renin secretion and activation of the RAAS [12]. Also note that caffeine strongly stimulates the HPA axis and can stiffen the aorta and elevate blood pressure [13]. The hypothalamus is a key element in central blood pressure control and serves as an interface between the nervous and endocrine systems [14]. It has been proposed that more than half of primary hypertension cases can be categorized as neurogenic, and lessening inflammatory signaling within the hypothalamus has attenuated angiotensin 2-induced hypertension [15]. Accordingly, ongoing inflammation and free radical marauding in the brain can be a major factor in the sustainment of high blood pressure. Furthermore, angiotensin 2 can impair the integrity of the blood-brain barrier and drive hypertensive signal transduction in the hypothalamus [16]. So the more permeable the blood-brain barrier from whatever cause (e.g., gluten, toxins, EMFs, and heavy metals), the more blood pressure will be pushed upward. A high concentration of leptin in the blood can rouse the sympathetic nervous system and excite the RAAS in much the same way as mental or emotional stress, and hyperleptinemia can be triggered by proinflammatory cytokines as well as high insulin and fasting glucose [17] [18]. Leptin is a hormone crafted mainly by adipose or fat tissue that signals satiety. Generally speaking, greater fat mass equals greater leptin production which equals greater RAAS stimulation [19]. Elevated leptin can also directly exert oxidative stress upon the endothelial cells of arteries, contributing to vascular pathology and hypertension [20]. Note that renin, angiotensinogen, angiotensin 1, and angiotensin 2 can all be manufactured by fat tissue too, so through multiple means reducing excess adiposity can better blood pressure values [21]. Angiotensin 2 can instigate the generation of reactive oxygen species in vascular cells and enhance the oxidation of low-density lipoproteins (LDLs) by macrophages [22] [23]. Such LDL oxidation engenders foam cell accumulation and the onset of atherosclerosis [24]. As free radical numbers build in the endothelium, nitric oxide counts fall, encouraging endothelial dysfunction and atherogenesis [25]. As atheromas grow, blood vessels become blocked, blood flow becomes impeded, and blood pressure rises [26]. Though vitamin A, vitamin C, and vitamin E can scavenge free radicals in blood vessels and help thwart vascular injury from oxidant stress (vitamin E also helps dilate blood vessels and block platelet aggregation via the making of prostacyclin) [27] [28]. Similarly, vitamin D deficiency can induce hypertension by upping the crafting of renin and enhancing the progress of atherosclerosis [29]. Heightened free radical concentrations along with lessened nitric oxide and antioxidant concentrations in the cardiovascular system is a popular feature in the pathology of hypertension [30]. Again, escalated reactive oxygen species or free radical formation in arterial walls fosters endothelial dysfunction, vascular inflammation, and negative remodeling of the heart [31]. The tripeptide glutathione (made from glycine, cysteine, and glutamic acid) stands as one of the major gatekeepers between oxidative stress and hypertension, and in addition to its antioxidant roles, helps to maintain nitric oxide availability via the making of S-nitrosothiols which dilate blood vessels [32]. Nitric oxide normally exerts an anti-inflammatory effect in blood vessels by inhibiting the adhesion of leukocytes or white blood cells too [33]. So a draining of glutathione by toxins and free radicals can sap nitric oxide availability and weaken the body’s ability to manage blood pressure [34]. Indeed, glutathione depletion has been clearly observed in hypertensive subjects [35]. In remediation, augmenting the body’s supply of glutathione by supplementing with N-acetylcysteine or alpha-lipoic acid can notably slash blood pressure (vitamin C administration can help in much the same way) [36] [37] [38] [39]. In the same vein, mitochondrial dysfunction can lead to abnormal upregulation of the RAAS and foster insulin resistance, which in turn can further damage mitochondria and perpetuate a vicious cycle of mitochondrial injury, insulin resistance, hyperleptinemia, and hypertension [40]. A resistance to insulin can decrease the making of nitric oxide in endothelial cells and amplify its destruction [41]. In countering insulin resistance, supplementation with L-carnitine can be used to improve fatty acid oxidation by mitochondria and glucose utilization in skeletal muscle tissue [42]. Bettering insulin resistance with L-carnitine can improve nitric oxide availability, vascular cell function, and blood pressure [43]. The presence of chronic inflammation can be described as the prime facet of most hypertension cases. And inarguably hypertensive patients tend to exhibit a high plasma measurement of C-reactive protein (an inflammatory marker) [44]. Persistent inflammation can overstimulate the RAAS, and it is important to understand how immune cells have been implicated in the development of hypertension. As insightfully explained by Dinh et al.: “Hypertensive stimuli, including salt, overactivity of the RAAS, oxidative stress, and inflammation lead to an initial elevation in blood pressure (mainly because of central actions but also due to endogenous hormones such as Ang II and aldosterone), which results in protein modifications. These altered proteins are no longer recognized as self (i.e., they serve as neoantigens), and T cells are activated. T cell-derived signals promote entry of macrophages (and other inflammatory cells) into the vasculature and kidney which results in cytokine release. In the vasculature, activated T cells promote vasoconstriction and remodeling. Together with the promotion of sodium and water retention in the kidney, more severe hypertension can result” [45]. The conjuring of inflammation represents the body’s chief approach to the elimination of pathogens and the repair of damaged tissue, and inflammatory processes normally continue until the targeted pathogens are destroyed or the wounded tissue is healed. Ergo, if inflammation is ongoing, then pathogen subsistence and/or continual tissue injury is fanning its flame and must be resolved if hypertension is to be reversed. Appropriately, let us now turn our attention to the gastrointestinal tract, the most frequent source of inflammation in the human body. Compared with healthy controls, hypertensive patients have been seen to exhibit decreased microbial diversity in the GI tract and a Prevotella-dominated gut enterotype [46]. An overgrowth of gram-negative Prevotella and Klebsiella bacteria characterizes the gut dysbiosis associated with high blood pressure, and it has been found that hypertension can be transferred via fecal transplant (meaning the transfer of stool from a human with high blood pressure to a mouse, begetting high blood pressure in the mouse). Importantly, lipopolysaccharide or endotoxin from gram-negative bacteria in the gut can elicit a strong immune response and increase blood pressure by stoking the fire of systemic inflammation [47]. Indeed, lipopolysaccharide-triggered inflammation is the cardinal expression of pathogenicity from Prevotella and Klebsiella bacteria, and has been identified as a significant contributor to the manifestation of high blood pressure [48]. Fortunately, dysbiosis can be treated with probiotics, and probiotic supplementation with multiple strains has been shown to lower blood pressure in humans through multiple means [49]. Lastly, thyroidopathies can markedly alter blood pressure regulation and it is common to see hypothyroidism accompanying hypertension. The thyroid hormone triiodothyronine (T3) relaxes smooth muscle in blood vessels so a lack of functional T3 can drive blood pressure up by worsening arterial compliance and thus increasing systemic vascular resistance [50]. T3 is also needed for the proper development of a population of parvalbuminergic neurons in the hypothalamus that play a role in blood pressure management [51]. Now that we understand that inflammation, prooxidation, nervous system stress, and immune system strain are the chief ingredients in hypertension’s etiology, we can list some natural treatment options and agents. - In those who are overweight, weight loss can effectively lower blood pressure by calming the sympathetic nervous system and bringing down renin, aldosterone, and angiotensinogen release [52]. - A diet low in potassium induces sodium retention and a rise in blood pressure while potassium supplementation promotes natriuresis (the excretion of sodium in the urine via the kidneys) and a fall in blood pressure [53]. Therefore, consuming more potassium-rich foods like winter squash, radishes, broccoli, kale, bananas, cantaloupe, nectarines, lima beans, blackstrap molasses, salmon, tomatoes, and avocados can be helpful for those with hypertension [54]. - Consuming additional garlic and omega-3 fatty acids can also aid blood pressure values [55] [56]. Anti-inflammation and vasodilation appear to be the main effects exerted by fish oil and garlic [57]. - Meditation and appropriate exercise can lower blood pressure and the activity of renal sympathetic nerves [58] [59]. - Coenzyme Q10 can be a wonderful aid for hypertension as it not only supports mitochondria and ATP production, but also inhibits LDL oxidation, dilates blood vessels, reduces proinflammatory cytokines, and lessens blood viscosity [60]. - Overgrowth of the fungal species Candida albicans can exacerbate inflammation in the gut, worsen intestinal permeability, and fan inflammation outside the gut [61]. Many natural agents can be used to treat this popular aggravator of systemic inflammation, the beneficial yeast Saccharomyces boulardii being one of them [62]. - Aberrant methylation status or a deficiency of methyl donors (from methyl consumers like pesticides, toxic metals, food additives, and pharmaceuticals) can encourage high blood pressure via the generation of reactive oxygen species and vascular injury [63]. Eating more foods containing choline, betaine, or methionine (think eggs, chicken, spinach, carrots, cauliflower, Brussels sprouts, beets, mustard seeds, and shrimp) as well as supplementing with methylated folate (vitamin B9) or methylated cobalamin (vitamin B12) can augment your supply of methyl donors [64]. Fun fact: the simple act of sweating can help curb oxidative stress and methyl depletion by assisting the excretion of xenobiotics. - The enzyme nattokinase can function as an excellent tonic for the cardiovascular system and is capable of potent fibrinolytic, antihypertensive, antiatherosclerotic, and neuroprotective effects [65]. Nattokinase is available in isolated supplement form. - The amino acid taurine is capable of effectively lowering blood pressure and improving insulin resistance, while the shrub hawthorn is a time-tested hypotensive [66] [67]. - Calcium amplifies sodium excretion (preventing sodium retention) while sodium amplifies calcium excretion (pushing calcium deficiency). Hence, too much sodium or too little calcium can give rise to high blood pressure via the parathyroid hormone-incited outflow of calcium from bone into soft tissue (like blood vessels which harden as a result), the lack of sympathetic nervous system modulation by calcium, and the loss of arterial relaxation betterment by calcium [68] [69] [70]. - Magnesium can increase insulin sensitivity and bring down blood pressure by modulating vascular tone and prompting the release of both nitric oxide and prostacyclin [71]. Undeniably many Americans are deficient in magnesium. - The herb Indian snakeroot has a long history of use and can be beneficial for treating hypertension because of its ability to systemically lower sympathetic tone [72]. Reishi mushroom has demonstrated similar efficacy [73]. - Bark from the Terminalia arjuna tree is widely employed in Ayurveda for cardiovascular ailments and has documented antioxidant, hypolipidemic, antiatherogenic, and antihypertensive properties [74]. Ayurveda has also utilized the herb Coleus forskohlii for some time, which has the ability to combat inflammation, bring down blood pressure, block the aggregation of platelets, and relax smooth muscle in blood vessels [75]. - Olive leaf extract is another safe and effective antihypertensive that possesses antioxidant, antiatherogenic, anti-inflammatory, hypoglycemic, and hypocholesterolemic qualities [76]. The herb yarrow can notably lower blood pressure and blood lipids too [77]. - Lastly, black cumin seed oil has significantly decreased blood pressure without any adverse effects [78]. In conclusion, with natural medicine we can treat the causes of hypertension and restore health to the body long-term. As stated by Woolf and Bisognano, “For many patients, maximal medical therapy [meaning pharmaceutical prescription] is insufficient to adequately treat refractory hypertension” [79]. Conventional medicine struggles with treating high blood pressure because hypertension is usually multifactorial and pharmaceuticals ignore its root causes. But by taking a sensical approach and improving the diet, cleaning up the gut and liver, exercising more, reducing stress, detoxifying, and healing the circulatory system with natural tools, high blood pressure can be made a thing of the past. References:
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AuthorDenton Coleman is an Exercise Physiologist and Medical Researcher. Archives
October 2023
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