INTERNATIONAL STROKE CONFERENCE 2019 POSTER ABSTRACTS
SESSION TITLE: ANEURYSM POSTERS https://doi.org/10.1161/str.50.suppl_1.WP118Stroke. 2019;50:AWP118
Tetsuro Kimura , Daisuke Kudo , Takeshi Miyamoto , Hiroki Sato , Taichi Ikedo , Michael Lawton , Tomoki Hashimoto
Most of the Vitamin D stueids are not for Hemorrhagic Stroke
- Large vessel Ischemic Stroke 13 X more likely if low vitamin D – Nov 2017
- Ischemic Stroke risk reduced by 2.5 if have good level of vitamin D – meta-analysis Feb 2018
- Overview Stroke and vitamin D has the following
Quick review of Hemorrhagic Stroke - June 2017
Vitamin D - maybe, Vitamin C - maybe, Cholesterol - maybe, Omega-3 - YES
- There has been some Hemorrhagic Stroke research: https://academic.oup.com/aje/article-lookup/doi/10.1093/aje/kwp227
There was not enough data to show that vitamin D was significant - but the trend indicated a 40% reduction
- https://www.ncbi.nlm.nih.gov/pubmed/22627988 PDF online
"We found no significant associations between dietary vitamin D and hemorrhagic stroke."
- How LOW Cholesterol Can Harm Your Health Green Medical Information, Sept 2012
Cholesterol Is Needed To Prevent Hemorrhagic Stroke:
- The Role of Omega-3 Polyunsaturated Fatty Acids in Stroke - 2016
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- Omega-3 and vitamin C both PREVENT Hemorrhagic Stroke- Life Extension 2015
- Omega-3 Good After Heart Attacks And For Hemorrhagic Stroke Prevention 2015
Introduction: Beyond its essential roles in bone and mineral homeostasis, vitamin D has been implicated in a wide range of chronic pathology. Clinical studies have shown the increased incidence of subarachnoid hemorrhage during winter to spring months when vitamins D levels are decreased because of the less sunlight exposure. Therefore, we hypothesized that vitamin D contributes to the rupture of intracranial aneurysm. Using a mouse model of intracranial aneurysm, we examined whether vitamin D deficiency promotes intracranial aneurysm rupture.
Methods and Materials: We used 15-week old C57BL/6 male and female mice. To induce aneurysm, we combined induced systemic hypertension (deoxycorticosterone acetate-salt hypertension) and a single injection of elastase (17.5 mU) into the cerebrospinal fluid at the right basal cistern. Mice were assigned to either (1) control (vitamin D 2000 IU/kg) or (2) vitamin D deficient diet (VDD) (vitamin D 0 IU/kg) group. The diet treatment was started seven weeks prior to aneurysm induction and continued until 21 days after aneurysm induction. In female mice, bilateral ovariectomy was also performed one week before aneurysm induction to avoid estrogen-dependent changes in vitamin D levels.
Results: In male mice, the vitamin D deficient diet significantly increased aneurysmal rupture compared to the control diet (control vs. VDD: 54% vs. 93%; P< 0.01). In ovariectomized female mice, there was no significant difference in the rupture rate between two diet treatment groups (control vs. VDD: 88% vs. 86%; P= 1.0). There was no significant difference in the incidence of aneurysmal formation between two groups in both sexes. Experiments using sham-ovariectomized female mice are currently ongoing.
Conclusion: Our preliminary data suggest that vitamin D deficiency promotes intracranial aneurysmal rupture in male mice, but not in ovariectomized female mice. There may be sex-dependent or sex steroids dependent effects of vitamin D on the development of intracranial aneurysm rupture. Our ongoing experiments will elucidate the underlying mechanisms for the potential sex differences in the contributions of vitamin D to the pathophysiology of intracranial aneurysm.