I have no clue what the systemic effects of something like kaempferol or anything that affects d2-d3 would be, and while I've been called a pig before I may not be a guinea pig on this one yet.
A curious idea on D3 (and on thyroid hormone being bad):
The Thyroid Hormone-Inactivating Type III Deiodinase Is Expressed in Mouse and Human β-Cells and Its Targeted Inactivation Impairs Insulin Secretion
"
In conclusion, the present findings provide evidence that reduced thyroid hormone signaling in pancreatic β-cells during development (and potentially adulthood) is important for normal islet function and glucose homeostasis. The leading defect caused by the untimely exposure to thyroid hormone in the D3KO is impaired insulin secretion in response to glucose stimulation. D3 is also expressed in human fetal pancreas and adult pancreatic islet, suggesting that an analogous role is likely in human β-cells. Because D3 expression remains throughout adulthood in human and mouse β-cells, it would be interesting to explore the possibility that dysregulation of Dio3 could play a role in states of impaired insulin secretion. Moreover, suppression of thyroid hormone signaling could potentially be used as a strategy to improve β-cell function ( ). These data therefore suggest that D3 could be a novel target for therapeutic intervention in insulin related pathologies, especially diabetes."
A curious idea on D3 (and on thyroid hormone being bad):
The Thyroid Hormone-Inactivating Type III Deiodinase Is Expressed in Mouse and Human β-Cells and Its Targeted Inactivation Impairs Insulin Secretion
"
In conclusion, the present findings provide evidence that reduced thyroid hormone signaling in pancreatic β-cells during development (and potentially adulthood) is important for normal islet function and glucose homeostasis. The leading defect caused by the untimely exposure to thyroid hormone in the D3KO is impaired insulin secretion in response to glucose stimulation. D3 is also expressed in human fetal pancreas and adult pancreatic islet, suggesting that an analogous role is likely in human β-cells. Because D3 expression remains throughout adulthood in human and mouse β-cells, it would be interesting to explore the possibility that dysregulation of Dio3 could play a role in states of impaired insulin secretion. Moreover, suppression of thyroid hormone signaling could potentially be used as a strategy to improve β-cell function ( ). These data therefore suggest that D3 could be a novel target for therapeutic intervention in insulin related pathologies, especially diabetes."