Thiamine is known to be reduced in the body in response to various conditions or drugs, most notably diabetes (where it may be reduced by 75-76% in both type I and type II diabetes) and alcoholism. These two conditions have different ways of reducing thiamine levels with alcoholism impairing the way low amounts of thiamine are absorbed (active transport) whereas high blood glucose increase the rate of thiamine elimination through urine.
Thiamine deficiency has also been noted in subjects with obesity with one study referencing a 15.5-29% rate of frequency based on evidence from studies on subjects seeking bariatric surgery; it was speculated that, beyond increase rate of thiamine elimination from high blood glucose, that a diet predominant in processed food and oils may be contributive since they lack thiamine.
It has been noted, in part due to a lack of long term stores of thiamine in the body and reliance on dietary intake, that thiamine replenishment in these instances may take as short as 2-3 weeks. However, as alcohol inhibits the mechanism responsible for absorption of low thiamine concentrations and not high concentrations replenishment involves taking doses significantly above the RDA of 1.1-1.2mg.
Both alcoholism and high blood glucose can increase the risk of thiamine deficiency, and as they do so in two different manners their risks may compound. Obesity is also seen as a risk factor
Benfotiamine and Sulbutiamine are two stand-alone supplements related to the thiamine molecule, with the former being a fat-soluble derivative and the latter two thiamine molecules bound together. While sulbutamine has drastically different properties, benfotiamine is claimed to be a pro-drug for thiamine (converting into thiamine after ingestion) with at least one study suggesting a 2.7-fold greater bioavailability when compared to thiamine HCl and another claiming that only 40% of the oral dose is needed if aiming for the same circulating levels of thiamine after supplementation.
Thiamine is investigated for interactions with blood pressure due to evidence in the spontaneously-hypertensive rat (SHR) line where thiamine administration reduced blood pressure associated with down-regulating (normalizing) abnormalities of a few genes in the renin-angiotensin system such as PAI-1, TGFβ-1, the AT-1 receptor and angiotensinogen. There is also thought to be an additional link to hyperglycemia (high blood sugar) since high blood glucose an increase thiamine elimination in the urine and one human study in subjects with liver cirrhosis found that repleting low levels of thiamine greatly helped both blood glucose and blood pressure levels.
When tested in subjects with hyperglycemia, supplementation of 300mg thiamine (HCl) for six weeks appeared to reduce mean arterial pressure and diastolic blood pressure to a minor degree (2.3% and 4.3% respectively) when compared to placebo with no effect on systolic blood pressure or pulse.&spreference;
While a modest effect, it seems supplemental thiamine could help blood pressure in subjects who have high blood glucose
Thiamine is involved in the glucose synthesis pathway