This could be a topic in-and-of-itself. Although and importantly, I don't want to hijack or derail this gentleman's thread. For the last several years I've intentionally kept my LDL-C at or slightly >120mg/dL. I've had two CT calcium scans done over the last 5 years, both scan scores showed zero coronary calcium. At 51 years old, I'd say that's reasons enough not to fall prey to the cholesterol hypothesis
I've also had several NMR and VAP tests done looking at several different lipoprotein subfractions. I know many others here can attest to the same with their LDL >100mg/dL.
Nonetheless, addressing raising/lowering strategies on the different lipoprotein subfractions is of value. Though it's not the leading cause of CVD.
With that, some of the suggestions outlined prior is relevant to be discussed that may hinder a beneficial outcome for the individual (OP).
I personally don't favor the use of Statins. Unless, one's predisposed to familial hypercholesterolemia. Nonetheless, by the standards set forth by the American College of Cardiology (ACC)/American Heart Association (AHA), this individual doesn't fit into the criteria for Statin therapy.
Amongst other criterias' for the lowering of LDL-C, one would be as :
Adults ≥ 21 years of age with a primary LDL-C ≥ 190 mg/dL should be treated with high-intensity statin therapy unless contraindicated. This is also subject of the treating clinician if the patient falls within other criterias'.
Nonetheless, I'd like to point out a few things that would hinder boosting this individual 25-hydroxyvitamin D levels by suggesting a Statin. Statins induce activation of the pregnane X receptor, in which by doing so, can disrupt his vitamin D metabolism/function. As well, Statins induce mitochondria dysfunction. It's known that Statins interfere with the production of mevalonic acid, in which is a precursor to the synthesis of CoQ10, which this can lead to insufficient CoQ10 levels. Aside from depletion of CoQ10, two vital enzymes are responsible for activation or inactivation of 25-hydroxyvitamin D. These two enzymes are CYP27B1 (1a-hydroxylase) and CYP24A1 (24-hydroxylase). Both enzymes are located within the mitochondria, this could potentially lead to vitamin D insufficiency on the metabolism and function of from Statin therapy. This would be a one-two punch on this individuals attempts to regain his vitamin D status.
Not to mention Statins can pose the detriments of neurological and myopathic syndromes, as well, a compromised immune system from taking ones LDL-C too low from Statin therapy. Also, Sex hormones are synthesized via cholesterol. So why would we want to drive it low? Take away sufficient amounts of the raw material (cholesterol) would equate to insufficient hormones synthesis.
CVD is more-so related to endothelial dysfunction/chronic inflammation/hyperglycemia/hyperinsulinism than that independently of lipoproteins. Given that, oxidation of both LDL and HDL is a contributor to arteriosclerosis. Dysfunctional HDL via elevated copper levels induced by supraphysiological estradiol levels and the use of progestin based hormones can lead to arteriosclerotic plaques. Many here use several aromatizing compounds, without controlling their E2 levels. Bad, bad idea.
As a final note, LDL acts on repairing damaged (inflammation, scaring) of the endothelial that leads to plaques. Not the over-abundance of or greater than 100mg/dL of LDL-C.
Back to the OP. Are you still taking Lexapro? Have you had your prolactin levels checked. SSRI's are not Sex hormones best friend, at all.
On a side note, there's an interrelationship of upping your magnesium intake, should help raise your Vitamin D levels. Try to get some natural sunlight