In accordance with clinical usage, the correct dose is the "lowest dose required to produce the desired effects (soft-formed and comfortable stool)". This is either 1-2g of the powdered extract or fruit usually standardized to 10-30mg active Sennosides.
Higher doses are used only if the aforementioned lower dose is not effective (it should be noted that senna alexandria is a delayed laxative unlike the immediate effects of Caffeine and it may take a few hours to assess whether a dose is effective or not).
Senna alexandria tends to be taken prior to bed in order to time its laxative effect with a morning bowel movement.
The Human Effect Matrix looks at human studies (it excludes animal and in vitro studies) to tell you what effects senna alexandrina has on your body, and how strong these effects are.
|Grade||Level of Evidence|
|A||Robust research conducted with repeated double-blind clinical trials|
|B||Multiple studies where at least two are double-blind and placebo controlled|
|C||Single double-blind study or multiple cohort studies|
|D||Uncontrolled or observational studies only|
Level of Evidence
||Magnitude of Effect Size
See all 6 studies
Due to the strong laxative effect, constipation is greatly reduced with supplemental Senna Alexandria. Has been noted effective against regular, postpartum, and opioid-induced ... show
See all 10 studies
Senna Alexandria is a reference drug for its laxative effects, with comparable efficacy to oral polyethylene glycol (PEG; used before colonoscopies) and lactulose, but ... show
It is sometimes traditionally referred to as . It has traditionally been used as a laxative which is clinically supported, and has further been claimed to be an expectorant, a wound dressing, an antidysenteric, and a carminative agent; and for the treatment of gonorrhoea, skin diseases, dyspepsia, fever, and haemorrhoids. None of these latter claims are scientifically validated yet.
The active ingredients can also be derived from the fruits of Cassia angustifolia or acutifolia (considered synonymous), the fruits of which are sometimes referred to as Fructus Sennae. Rhubarb also has a small sennoside content, at around 0.5%.
As a herbal supplement, Senna contains a variety of molecules and bioactives such as:
The sennosides are seen as the active ingredients, and are pictured below. They are glycosides of a rhein anthrone molecule, which then bind to each other in pairs. For the drug to be bioactive, the glycoside must first be broken off (by intestinal bacteria metabolism) and then the dirheinanthrone molecule (also known as Sennidin) passively separates.
Sennosides may passively degrade into glycosides of rhein anthrones, called 8-glucosyl rhein anthrones, but usually passively reform before being metabolized by bacteria and moving rightwards in the diagram below.
Sennosides are insoluble in water, and barely soluble in methanol; however, an aqueous mixture of 30% water and 70% methanol can dissolve Sennosides. Sennosides are also soluble in sodium bicarbonate as it neutralizes their acidity.
It is possible that Sennosides can be degraded into rhein anthrone molecules during shelf-life, and it is recommended to avoid all moisture and heat in storage of Senna plants, extract, or pills/capsules.
The anthranoid class of molecules are resistant to acid digestion in the stomach as well as enzymatic digestion by the small intestine due to possessing a beta-glycosidic bond, typical of dietary fibers. Due to an inability to be metabolized and absorbed, they are then sent to the large intestines (colon) where colonic bacteria (of the Bifidobacterium class) can hydrolyze the bond and release free rhein anthrone, which is bioactive in the colon. In this sense, the rhein anthrone is seen as the active component whereas the Sennosides are seen as pro-drugs.
Although Senna should not reach systemic circulation by the above mechanisms, a small amount of rhein has been reported in the breast milk of mothers after oral Senna usage (although insufficient to cause laxative effects in the infant fed).
There are two mechanisms by which Senna products (and the anthranoid class of laxatives) exerts pro-motility effects. Altering intestinal contractions to favor peristalsis while inhibiting location contractions (in and of itself a pro-motility effect) and inducing secretion of electrolytes into the colon and limiting liquid absorption to increase colonic water content and exert stool softening effects.
In studies on rats, senna appears to exert little toxicity. The LD50 has been implicated at around 5,000mg/kg bodyweight in both rats and mice, and is possibly secondary to electrolytic imbalance from the colon.
When looking at the causative molecules, it appears that the main laxative components Sennoside A and B exert minimal toxicity while lesser molecules (such as rhein-8-glucoside) exert more toxicity relative to the Sennosides.
A rat study using 1% dietary anthranoid (hidroxyanthraquinones) intake for 480 days, a large intake coupled with prolonged dietary period, induction of bowel tumors was noted. Lower doses (50-300mg/kg bodyweight whole extract) over 2 years does not cause carcinogenic effects, but may cause some reversible abnormalities such as benign colonic hyperplasia in rats which is not seen in clinically relevant doses of 5-25mg/kg bodyweight over 2 years in rats.
In humans, an association was found in the past between laxatives of this class (the anthranoid laxatives) but is contested. No causation has been established between chronic use of Senna products and colorectal cancer risk in humans.
The above toxicological reports suggest that Senna usage is fine if not abused (in dose) and kept relatively short, with normal doses over a prolonged period having the ability to cause some reversible abnormalities. Large doses of senna for chronic periods of time may be a risk factor for colon cancer and has biological plausibility, but has not been fully demonstrated yet
(Common misspellings for Senna alexandrina include Sena, cena, cenna, alexandria)