i can't answer that question adam but i've been having a think about all this:
i looked into DVT, and associated antithrombin (AT) deficiency (AT is not only anticoagulant but also anti-inflammatory and antiproliferative).
where AT is synthesized? in hepatocytes, the main tissue cells of the liver.
how does the body build liver tissue, so that it can make AT? here's what i found:
from Essentials of Stem Cell Biology:
The liver is known to have a very high capacity for regeneration. In fact, mammals (including humans) can survive surgical removal of up to 75% of the total liver mass. The original number of cells is restored within 1 week and the original tissue mass within 2 to 3 weeks.
HNF4 (Hepatocyte Nuclear Factor 4) is a nuclear receptor protein ... that is critical for liver development
from J Molecular Endocrinology:
...HNF41 positively regulates genes involved in the transport of lipids and vitamins as well as genes involved in lipid, amino acid, and glucose metabolism. It also regulates genes involved in the regulation of several serum proteins such as blood coagulation factors, erythropoietin, and antithrombin III.
can anything affect the amount of HNF4 available?
from Am J Pathology - an article on alcoholic mice:
Zinc-enhanced liver regeneration was associated with an increase in hepatocyte nuclear factor-4 (HNF-4), a liver-enriched, zinc-finger transcription factor.
so, possibly zinc repletion could optimize antithrombin synthesis and maybe prevent DVT???
Summary: Antithrombin 3 deficiency... an autosomal dominant disorder causing hypercoagulability and recurrent thrombosis.
so, if DVT in may thurner syndrome is from antithrombin deficiency... and antithrombin deficiency is genetic...
could zinc deficiency affect a genetic problem...?
from J Human Nutrition: Human Zinc Deficiency
Notable examples that have been suggested but that require further research include involvement in the regulation of cellular growth and differentiation, including gene expression, and in the regulation of apoptosis(Zalewski et al. 1994 ).
The other is the central but still incompletely understood role, or complex combination of roles, that zinc has in gene expression and in cellular growth and differentiation.
Even a partial understanding ... alerts us to the special vulnerability to an inadequate supply of zinc of the rapidly growing embryo, fetus, infant and young child or of the patient mounting an immune response or requiring tissue repair. ...the extraordinary rapidity ... effects of dietary zinc restriction on growth and differentiation ... correctly alerts us to the special vulnerability to zinc deficiency of cells that are rapidly turning over, notably those of the immune system...
. or, the liver.
and lastly, recalling '(HNF-4), a liver-enriched, zinc-finger transcription factor' (same article Human Zinc Deficiency)
Other zinc atoms have specific structural roles in enzyme molecules as well as in many other proteins and in biomembranes. ... One outstanding example that has generated a great deal of recent interest is the zinc finger motif (Berg and Shi 1996 , Rhodes and Klug 1993 ), the most common recurring motif in transcription proteins. The configuration of these "fingers," which determines their binding to DNA, is determined by the single zinc atom at their base. The linking of these zinc fingers to corresponding sites on DNA initiates the transcription process and gene expression.
so it looks like yes, zinc deficiency could affect a genetic problem, especially in high cell turnover areas of the body like the liver.
we know that zinc tends to be in the lower end of the 'normal range' in MS patients, compared to healthy controls. could low zinc be linked to comorbities such as DVT in patients with more serious manifestations of may thurner syndrome?