This morning I heard a snippet on the radio about a research paper which has identified an association between the amygdala in the brain and heart disease - specifically noting arterial inflammation.
This evening, seeing mention of Dr Malcolm Kendrick and his currently non-functioning website, I was reminded to look at the story. After all, inflammation is a major part of his theorising.
Brain activity 'key in stress link to heart disease'
12 January 2017
The effect of constant stress on a deep-lying region of the brain explains the increased risk of heart attack, a study in The Lancet suggests.
In a study of 300 people, those with higher activity in the amygdala were more likely to develop cardiovascular disease - and sooner than others.
Stress could be as important a risk factor as smoking and high blood pressure, the US researchers said.
This study, led by a team from Harvard Medical School, points to heightened activity in the amygdala - an area of the brain that processes emotions such as fear and anger - as helping to explain the link.
Heart experts said at-risk patients should be helped to manage stress.
Emotional stress has long been linked with an increased risk of cardiovascular disease (CVD), which affects the heart and blood vessels - but the way this happens has not been properly understood.
Rest of BBC report here:
The full paper is, as so often, behind a paywall here:
This triggered a thought about whether thyroid and amygdala have any specific connections, which led me to this paper:
PLoS One. 2011;6(10):e26582. doi: 10.1371/journal.pone.0026582. Epub 2011 Oct 24.
Adult-onset hypothyroidism enhances fear memory and upregulates mineralocorticoid and glucocorticoid receptors in the amygdala.
Montero-Pedrazuela A1, Fernández-Lamo I, Alieva M, Pereda-Pérez I, Venero C, Guadaño-Ferraz A.
1Department of Nervous System and Endocrine Pathophysiology, Instituto de Investigaciones Biomédicas Alberto Sols, Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid, Madrid, Spain.
Hypothyroidism is the most common hormonal disease in adults, which is frequently accompanied by learning and memory impairments and emotional disorders. However, the deleterious effects of thyroid hormones deficiency on emotional memory are poorly understood and often underestimated. To evaluate the consequences of hypothyroidism on emotional learning and memory, we have performed a classical Pavlovian fear conditioning paradigm in euthyroid and adult-thyroidectomized Wistar rats. In this experimental model, learning acquisition was not impaired, fear memory was enhanced, memory extinction was delayed and spontaneous recovery of fear memory was exacerbated in hypothyroid rats. The potentiation of emotional memory under hypothyroidism was associated with an increase of corticosterone release after fear conditioning and with higher expression of glucocorticoid and mineralocorticoid receptors in the lateral and basolateral nuclei of the amygdala, nuclei that are critically involved in the circuitry of fear memory. Our results demonstrate for the first time that adult-onset hypothyroidism potentiates fear memory and also increases vulnerability to develop emotional memories. Furthermore, our findings suggest that enhanced corticosterone signaling in the amygdala is involved in the pathophysiological mechanisms of fear memory potentiation. Therefore, we recommend evaluating whether inappropriate regulation of fear in patients with post-traumatic stress and other mental disorders is associated with abnormal levels of thyroid hormones, especially those patients refractory to treatment.
Full paper freely available here: