Barbara slowly developed disturbance of mood and mind [mood became labile and distressed, nonspecific problem seeing [to be able to read] and reduced cognition.

It turned out that Ferric Iron was very very low even though she did not yet have and anemia. She had had very heavy blood loss during menstruation, for years], which resulted in near depletion of iron stores and most likely depleted her thiamine as well This explained her distress and the swelling in her ankles [mild heart or kidney failure?]

One year supplementation with oral iron and 6 months heavy supplementation with oral thiamine resulted in complete recovery of normal mood and normal mind.

Iron deficiency, it seems, from blood loss [injury, giving birth, and heavy menstruation can cause disturbances in mind and mood that can be devastating and need to be correctly diagnosed and treated.

Vital signs were never got, but I am sure there was a pattern that would suggest this problem.

It seems that iron deficiency [and thiamine deficiency] will disturb the chemical balance of the blood and cause reversible [if treated] disturbance of mood and mind.

J Clin Invest. 2016 Jun 1; 126(6): 2139–2150. Published online 2016 May 3. doi: 10.1172/JCI85715PMCID: PMC4887172PMID: 27140401

Clinical iron deficiency disturbs normal human responses to hypoxia

Matthew C. Frise,¹Hung-Yuan Cheng,¹Annabel H. Nickol,²M. Kate Curtis,¹Karen A. Pollard,¹David J. Roberts,³Peter J. Ratcliffe,⁴Keith L. Dorrington,¹ and  Peter A. Robbins¹

Abstract

BACKGROUND. Iron bioavailability has been identified as a factor that influences cellular hypoxia sensing, putatively via an action on the hypoxia-inducible factor (HIF) pathway. We therefore hypothesized that clinical iron deficiency would disturb integrated human responses to hypoxia.

METHODS. We performed a prospective, controlled, observational study of the effects of iron status on hypoxic pulmonary hypertension. Individuals with absolute iron deficiency (ID) and an iron-replete (IR) control group were exposed to two 6-hour periods of isocapnic hypoxia. The second hypoxic exposure was preceded by i.v. infusion of iron. Pulmonary artery systolic pressure (PASP) was serially assessed with Doppler echocardiography.

RESULTS. Thirteen ID individuals completed the study and were age- and sex-matched with controls. PASP did not differ by group or study day before each hypoxic exposure. During the first 6-hour hypoxic exposure, the rise in PASP was 6.2 mmHg greater in the ID group (absolute rises 16.1 and 10.7 mmHg, respectively; 95% CI for difference, 2.7–9.7 mmHg, P = 0.001). Intravenous iron attenuated the PASP rise in both groups; however, the effect was greater in ID participants than in controls (absolute reductions 11.1 and 6.8 mmHg, respectively; 95% CI for difference in change, –8.3 to –0.3 mmHg, P = 0.035). Serum erythropoietin responses to hypoxia also differed between groups.

CONCLUSION. Clinical iron deficiency disturbs normal responses to hypoxia, as evidenced by exaggerated hypoxic pulmonary hypertension that is reversed by subsequent iron administration. Disturbed hypoxia sensing and signaling provides a mechanism through which iron deficiency may be detrimental to human health.