Jessica M. Gannon, J Ayurveda Integr Med. 2014 Oct-Dec;5(4):241-5
Dysfunction of the Hypothalamic‐Pituitary‐Thyroid neuroendocrine axis has been implicated in the pathogenesis of major depressive and bipolar disorders.[1,2] Moreover, symptoms such as fatigue, tiredness, mental slowing, concentration and memory impairments, weight gain and depression are common to both overt hypothyroidism and to unipolar depressive and bipolar disorders. Taking this into account, and as the relationship between lithium and hypothyroidism is well known, thyroid status is often assessed and monitored in mood disorders. Furthermore,there is some support for adjunctive treatment with thyroxine in treatment‐resistant depression and in rapid‐cycling bipolar disorder.[1,2] Extracts of the medicinal herb, Withania somnifera (called Ashwagandha in Sanskrit, ASW) have been used for centuries in Ayurvedic medical practice in India as an “adaptogen”,i.e. to diminish and alleviate mental and physical stress. Modern data point to its immunomodulation, brain antioxidant, neuroprotective, anti‐inflammatory, and memory enhancing properties. We tested a standardize ASW extract (Sensoril®) for its procognitive properties in patients with bipolar disorder.
However, in view of a case report of thyrotoxicosis associated with ASW, and animal data suggesting that ASW induces increases in thyroid hormones,[7,8] wemonitored serum levels of thyroid stimulating hormone (TSH), tri‐iodothyronine (T3), and Laboratory indices of thyroid function (TSH, Free T4, and T3) were measured in a randomized clinical trial in which Ashwagandha (ASW) was used to improve cognitive function in patients with bipolar disorder. This was done in light of a case‐report of ASW‐associated thyrotoxicosis, and data from mice administered ASW that showed significant increases in thyroxine levels. Ten (of the original 60) patients showed abnormal results in one of the thyroid measures either at the beginning or end of the 8‐week study. One ASW‐.treated patient had subclinical hypothyroidism (TSH ‐.5.7 mIU/L)at baseline that normalized, and all three ASW treated patients experienced T4 increases from baseline (7%, 12%, and 24%). Six of 7 placebo assigned patients showed decreases in T4 from baseline (4% to 23%), and one patient’s TSH moved from the normal to subclinical hypothyroid range (6.96 mIU/L). As thyroid indices were done for safety, and not the primary goal of the original study, only 16.7% had abnormal thyroid indices, and as there was no sub‐stratification for treatment assignment by thyroid status, unequal numbers of subjects received ASW (n = 3) or placebo (n = 7).
In spite of these limitations, the subtle laboratory changes noted in thyroid indices in an 8‐week study suggest that ASW may increase thyroxine levels, and therefore vigilance regarding hyperthyroidism may be warranted. Nonetheless, the thyroid enhancing properties of ASW may also represent a clinical opportunity for the treatment of subclinical hypothyroidism, and these results suggest the need for further study of the effects of ASW on thyroid indices, especially in those with bipolar and unipolar mood disorders.