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Study linking POTS/Fibromyalgia/EDS to UARS. Any suggestions to offset nightly electron loss?

Discussion in 'Beginners Area' started by MattD1995, Oct 21, 2019.

  1. MattD1995

    MattD1995 Gold

    I posted this in the Ask Jack section as well. However, I know he's a busy man, and I'm hoping to get as much input as possible from all forum members. I've pored over @Sean Waters journal and noticed that he and I experience a plethora of similar symptoms, specifically the apnea like symptoms. I also noticed he's a leaner guy like myself, and wonder if any of this information may apply to him as well.

    There is a variant of sleep disordered breathing known as UARS (Upper Airway Resistance Syndrome) that is becoming more commonly recognized in the sleep medicine world. Most patients with UARS tend to be thin, young women. Although the men it affects tend to be thin and young as well. Also, UARS is commonly associated with hypotension, poor circulation, POTS, IBS, CFS, EDS. UARS differs from sleep apnea in a few ways:

    1) UARS patients tend to have structural issues, specifically, narrow nasal passageways and narrow throats. Some dentists and ENTs are attributing this to braces and wisdom teeth removal procedures (both of which can cause the mouth to shrink). Many of these patients experienced tongue thrust, bed wetting, and excessive night time urination.

    2) During sleep, UARS/structural airway issues cause the patient to gasp for air creating excessive intrathoraic pressure which forces the heart to pump out massive levels of Atrial Natriuretic Petide. ANP directly lowers aldosterone, catecholamines, and cortisol. ANP also causes magnesium and sodium wasting.

    3) The resulting chronic dehydration due to nocturia and electrolyte wasting leads to a plethora of issues, primarily POTS/IBS/EDS/Fibromyalgia.


    "Abstract. This hypothesis paper discusses the “ANP hypothesis” and the scientific evidence which suggests the following: Atrial Natriuretic Peptide (ANP) levels are markedly elevated in upper airway resistance syndrome (UARS), more so than in obstructive sleep apnea syndrome (OSAS), and are responsible for much of the symptomatology in UARS outside of sleep deprivation. In OSAS ANP resistance develops, as a result of hypoxia as well as obesity, and this will decrease the somatic and other symptoms that are caused by ANP. The ANP resistance caused by hypoxia implicates OSAS as a cause of obesity, due to ANP effect on lipolysis. The effects of ANP on the hypothalamic‐pituitary‐adrenal axis implicate UARS as the cause of “adrenal fatigue” and chronic fatigue syndrome (CFS). These effects may be able to be used to develop a biomarker panel to aid diagnosis and follow up in UARS. ANP effect on magnesium excretion may explain magnesium deficiency mediated illnesses which are associated with sleep disordered breathing. Gender differences in ANP secretion may explain gender differences seen between UARS and OSAS, as well as within the somatic syndromes. The actions of ANP on Nitric Oxide (NO) suggest the “ANP/NO/ONOO hypothesis” via upregulation of the NO/ONOO (nitric oxide/peroxynitrite) cycle which has been implicated in the somatic syndromes. The extreme ANP elevations seen in UARS would act as a perpetuating factor to maintain the NO/ONOO vicious cycle mechanism and perpetuate these chronic illnesses once triggered; therefore it is suggested that UARS underlies all of these chronic somatic syndromes."

    I have been diagnosed with UARS, and even more recently with POTS. Obviously, the laws of light, water, and magnetism still apply to me. However, I'm losing more water and electrons during the night time than I am able to replenish during the day via DHA, sunlight, and cold thermogenesis.

    Short of getting palate expansion, turbinate reduction, or any other type of invasive procedure, what would you recommend I do to offset the severe loss of fluid and electrons I am experiencing at night?

    I have begun sleeping upright/inclined and this has somewhat improved my nocturia and morning nausea. I am desperate for suggestions as APAP and mandibular advancement devices have failed me thus far.

    I must find a way to offset the electron/water loss I'm experiencing at night. I still believe, as Dr Kruse commonly states, that environment is a big issue. Based on this study, however, it would seem to indicate that people like myself with structural airway issues may be fighting an uphill battle even when changing my environment and getting DHA, cold, and sun.

    Open to any and all input. Thanks!
  2. MattD1995

    MattD1995 Gold

    A few more interesting tidbits from the study:

    "4. Adrenal and Hypothalamic Effects of ANP: Implications for CFS

    All natriuretic peptides and their receptors are widely present in the hypothalamus, pituitary, adrenal cortex, and medulla. In the hypothalamus, they reduce norepinephrine release, inhibit oxytocin, vasopressin, corticotropin releasing hormone (CRH), and luteinizing hormone releasing hormone release. In the hypophysis, natriuretic peptides inhibit basal and induced ACTH release. They are also well known to inhibit basal and stimulated aldosterone secretion. The effect on growth hormone is not yet clear. Natriuretic peptides inhibit catecholamine release in the adrenal medulla [18]. Multiple publications refer to the well documented inhibitory effect of ANP on aldosterone [18‐20]. ANP has been shown to inhibit basal aldosterone production and also antagonizes aldosterone stimulation by the agonists angiotensin II, ACTH, dibutryl cyclic AMP, and potassium [20]. What this suggests, is that it may be possible to use an aldosterone level as a biomarker in UARS, not just for an aid in diagnosis, but also to follow response to treatment, given that UARS is so difficult to detect on PSG."

    "With so many adrenal related hormones being suppressed by ANP, it suggests that in UARS there may be an adrenal dysfunction that because of the episodic nature of the ANP secretion would look like a partial adrenal insufficiency, something that endocrinologists do not acknowledge as a possibility. In endocrinology it seems that the adrenals must be either “on” or “off”, with no acceptance of the concept of “adrenal fatigue”. Over 50 years ago, Tintera proposed adrenal exhaustion as a cause of chronic fatigue syndrome (CFS). There are several studies which point to a disruption of the hypothalamic‐pituitary‐adrenal (HPA) axis in CFS. Symptoms seen in CFS and in adrenal insufficiency are myalgias, postexertional fatigue, as well as disturbances of mood and sleep [21]. Demitrack et al. demonstrated a pattern of HPA suppression in CFS which suggested a CRH deficiency. They showed blunted ACTH responses to CRH but enhanced adrenocortical sensitivity to exogenous ACTH. They also noted that evening basal plasma ACTH levels were elevated in the CFS patients, something they could not fully explain [22], however a rebound by the evening after suppression the prior night by ANP could certainly explain this finding. Here it is also of interest to note that the evening basal plasma ACTH levels were positively correlated with levels of fatigue and depression [22]. Demiralay et al. showed that exogenous intravenous ANP produced a pattern of HPA suppression which is consistent with it behaving as a CRH inhibitor. The researchers noted that ACTH was suppressed during the ANP infusion and then rebounded after the infusion stopped [23]. Another study, using an intranasal form of ANP, showed that it has a direct action on the central nervous system to inhibit stimulated HPA activity at the hypothalamic level (via suppressing CRH) [24]. Taken together, this information suggests that: 1) ANP clearly suppresses HPA function at the level of CRH; 2) this is the same pattern seen in CFS; 3) therefore, elevated ANP as we assume is present in UARS probably causes an adrenal suppression which may explain some of the hypotension and the orthostasis seen in these patients, as well as the excessive fatigue as compared to OSAS patients. Because the adrenals are presumably not damaged and the ANP secretion in UARS by definition must be episodic, this would appear as a partial adrenal suppression."

    "There is more suggestive evidence for the CFS/UARS connection as it relates to the adrenal and hypothalamic effect of ANP: Boneva et al. found that aldosterone levels are low in CFS patients. The authors commented that the mechanism for this remains unexplained [25], however we can see that this is consistent with an elevation of ANP as would be seen in UARS. Anderberg et al. found that a subgroup of Fibromyalgia patients with perception of severe pain, depression and stress had low levels of oxytocin, with oxytocin levels being higher in patients with less pain, depression and stress [26]. A recent study found that adolescents with CFS had significantly lower antidiuretic hormone (vasopressin) levels than controls. The authors concluded this was likely due to a primary decrease in pituitary secretion, because it was associated with an increase in serum osmolality [27]. These preliminary results suggest that both oxytocin and vasopressin might also be used for the UARS biomarker panel."
  3. MattD1995

    MattD1995 Gold

    I am a member of a POTS group on Facebook. Interestingly, 90% of the POTS patients have frequent urination (especially at night), bad insomnia, dehydration, and are young and quite thin. A large portion have also had braces and wisdom teeth removal.

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