SesaThin™ is a lignan naturally present in sesame oil. It possesses extraordinary potential in the fight for a lean body, owing to its potent effects on lipid oxidation and storage. And, to top it off, it also acts strongly as an anti-oxidant and anti-inflammatory. Thus, making SesaThin™ perhaps the most important new supplement this decade for achieving superior body composition and health.
The first study that struck me with SesaThin™, when I became aware of it 4 years ago, was one showing it to elevate fatty acid oxidation by as much as 10-fold, mediated via PPAR-alpha activation, the same as fibrates and fish oil (10535395). Not only is fat is what we want to get rid of, but increased fatty acid utilization is strongly correlated with leanness. It is also correlated with related health factors, particularly those involved in the pathogenesis of Metabolic Syndrome X, such as insulin sensitivity, blood lipids, and atherosclerosis (14608009, 11452220).
Thus, this compound was obviously of great, great interest. In recent years, numerous other studies have come out supporting its remarkable effects on fat oxidation. Fatty acid oxidation is typically increased by reduced calorie and/or carbohydrate diets, as well as exercise. But, remarkably, SesaThin™ actually increases these markers in the fed state, when glucose is readily available (15158759, 12015159).
What this means is that with SesaThin™, you suddenly have one of those coveted “fast metabolisms” like the people we all hate so very much.
Obviously, all else being equal, a big increase in fat burning is going to leave less available for storage. But SesaThin™ goes further than that. It directly antagonizes lipid synthesis and storage. Diets containing the lignan lowered the activity of a multitude of lipogenic enzymes to one-half, and lowered mature SREBP-1 (one of the most important lipogenic genes) protein to less than one-that of animals fed a lignan-free diet (12015159, 11750882. )
And, while there are no direct studies, it very likely inhibits DGAT1, which is necessary for the final step in fat storage. This has been observed for fellow PPAR-alpha activators TTA and EPA. (10493929). In addition, the drug simvastatin, which shares inhibition of 3-HMG coA reductase with SesaThin™, also lowered DGAT1 activity (1856608) (12031956)
Appetite and Metabolic Control
In addition to combating the storage of body fat, the reduced lipid synthesis does something else that might be even more important. Namely, by reducing serum lipid levels, it will help to maintain (or bring back) high leptin and insulin sensitivity.
Initially, muscle, adipose, and the brain are quite good at taking up and utilizing these nutrients, either by using for fuel or storing them. Unfortunately, cells eventually start to become full — and, a full sell is a nutrient insensitive cell. So, insulin signaling starts to decrease (i.e. you become insulin resistant).
Leptin shares a large number of signallling pathways and mechanisms with insulin (14506627, 12674509), and its sensitivity goes down pretty much in unison (15467824, 15208705). And, indeed leptin and insulin resistance is strongly correlated with triglyceride levels (10193869, 10878682).
Both leptin and insulin are potent mediators of the adipostat (10612703). There secretion is proportional to body fat and nutrient intake (especially glucose), and they robustly reduce food intake and body weight by directly stimulating receptors locally in the brain.(15533772).
So when their signalling get screwed up, the brain starts constantly thinking it needs food — even when you are overfed and getting fatter and fatter.
Recall DGAT1 from our last section. It catalyzes the final step in triglyceride formation. DGAT1 deficiency increases the response to leptin infusion in genetic models of obesity and insulin resistance (12130553). It also decreases levels of tissue triglycerides, as would be expected, as well as increasing sensitivity to insulin and to leptin, while protecting against obesity, in a model of severe leptin resistance (11956242). Further evidence of the negative consequences of excess triglyceride is that an increase in triglyceride via lipid infusion increasing the expression of appetite stimulating peptides in the hypothalamus (15117877)
Fibrates, PPAR-alpha agonists like SesaThin™, have been found to decrease serum glucose, insulin, and leptin levels as in diet-induced obesity (15114521). They also improved insulin sensitivity and the diabetic condition of MKR mice, which have a mutation in the IGF-1 receptor, leading to type II diabetes and related pathologies (12829645)
SesaThin’s potent protective effects on central appetite and metabolic control centers will be most welcomed for improved nutrient partitioning for anyone over 15% body fat or who is overeating/bulking. And, for those who are closer to the obese side, it is a Godsend.
In addition to obesity and insulin/leptin resistance, SesaThin™ has been shown to have a number of other mechanism positive for health. It reduces the formation and secretion of TG’s and cholesterol, from the liver (10575634, 8829994, 9072406). It increased the good HDL cholesterol, while decreasing the very bad VLDL (9072406). It was found to be modestly, but significantly hypocholestemic (cholesterol lowering) in humans at less than 100mg per day (8724120)
It also possesses potent anti-oxidant activity, in vivo (15631503). It reduces lipid peroxidation in response to exercise (12968212), fish oil feeding (14598914), and reduces oxidative stress in response to alcohol (15665483), and salt (12968212). It also increases vitamin E levels by inhibiting its metabolism (11061988) . In combination, they synergistically reduce oxidative stress (15526409, 14598914).
Chronic ingestion attenuates elevation in blood pressure, oxidative stress and blood clotting in hypertension prone rats (15649279) mediated through its antioxidant activity and protection/maintenance of proper functioning of endothelial elements, including nitric oxide (NO) (10993201)
It also prevents superoxide production and hypertension in response corticosteroid treatment (14646147, 12230131), which is great news in the high stress modern world.
It is also an anti-inflammatory. It inhibits LPS-induced IL-6 production by suppression of p38 MAPK signal pathway and NF-kappaB activation. Sesamin decrease PGE2 (9610840) as well as TNF-alpha (10966903)
In addition to being greatly beneficial for general health, these factors make it a must use for those with certain lifestyles – particularly high stress, anabolic steroid users, as regular stimulant or alcohol users and abusers.
SesaThin™ also appears almost to have been made specifically for the low-carb dieter. Carbohydrates increase lipogenesis and serum TG levels (11894744). One of the main mediators is the protein SREBP-1, which we mentioned earlier. Glucose, sucrose, and fructose feeding cause SREBP-1c induction. And, this expression increases over time with continuous availability of these nutrients (14988238). SesaThin™ lowered mature SREBP-1 to 1/5 of normal levels (11750882).
Increased burning of fatty acids (which we have covered) is associated with increased production of ketones. And, sure enough, SesaThin also increases ketone production. (10575634 (9655371). And, again, SesaThin does its magic, even in the fed state.
Thus, with SesaThin™ one can reap the metabolic benefits of ketosis without being quite as strict about carbohydrates. Likewise, for cyclical dieters, you can get back into ketosis much faster after your reefed.
To summarize, SesaThin™:
- Increases fat burning
- Decreases fat storage
- Combats elevated cholesterol
- Potent anti-oxidant
- Potent anti-inflammatory
- Stimulant free