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two inquisitive chicksby: Chris Clancey

Alcohol, universal inhibition unburdener and ubiquitous recreational drug extraordinaire, is a substance we all would love to hate, if only it didn’t go so damn well with everything from bars to ball-games to back-yard cook-outs—and just about everything in between. So just what is the health and body composition conscious drinker to do? Tee-totaling is clearly no fun, and also tends to summon the awkward “so what’s your deal?” Rather, moderation and ‘picking your battles’ (or maybe just blackouts) seems to be the better course of action. But is there anything else one can do to decrease the damage to ones’ liver and leanness so common with ethanol-indulgence?

You bet your bottom dollar-draft there is, and its name is Sesathin™.

Sesathin™, a naturally-occurring, damn-near-miracle sesame lignan, is pretty much damage control in a pill (or liquid lecithin suspension) from all the chief metabolic harms of cocktail hour. How so you ask? Well, let’s break it down then.

Alcohol, also known as ethanol, is a nutritively dense substance that provides 7.1 calories per gram (1), almost twice that of a gram of protein or carbohydrate. Considering most drinks contain roughly 12g of ethanol, you’re looking at about 84kcals from the alcohol content alone in your average drink. Obviously, if you’re drinking a beer or sipping a Mai Tai, you’re going to have to factor in some carb-calories too (and don’t even get me started on Orgasms and White Russians). And generally, once you pop a shot, the fun don’t stop until you’ve put down easily five hundred to a thousand-plus calories—not exactly ideal if you’re watching your waistline, particularly if you’re a frequent (we call them “recreational”) drinker. Even if we grant the Microsomal Ethanol Oxidizing System and the other systems in the body that metabolize alcohol some degree of inefficiency, alcohol is definitely not giving you a free-ride calorically (2,3,4).

Moreover, alcohol’s chief metabolic byproduct, acetate, will directly suppress fat-oxidation in the short-term (5,6). Even worse perhaps, is research showing that alcohol consumption not only directly increases fat storage via a modest activation of the hepatic de novo lipogenesis pathway (5,7), but likely also increases adipogenesis (the creation of fat cells) from stem cells through an upregulation of PPARgamma2 (8). All told, acute ethanol intake in humans has been shown to reduce whole-body lipid-oxidation by a whopping 73%, while systematic lipolysis is virtually halved (5). Couple that with upregulated fat-storage potential, a whopping increase in cortisol secretion (9,10), temporary insulin resistance which is then compensated for by a resultant hypersecretion of insulin (11), acute hypertriglyceridemia (12,13) and a 3 a.m. trip to Wendy’s because dude, you’re starving, and unless you’ve got miracle genetics, your abs are going to be looking to duck and cover from your lifestyle under a nice layer of stored lipids.

Unfortunately, the ills don’t exactly end there with alcohol. High levels of consumed alcohol will also cause a build-up of toxic (and reactant) metabolic intermediates like acetaldehyde from the alcohol dehydrogenase reaction (14), metabolic acidosis (15), and the inhibition of hepatic (liver) fatty acid metabolism because of a heightened demand for NAD+ (16,17), which often results in the detrimental accumulation of fatty acids (fatty) liver (18) and heightened VLDL (19,20). Generally, liver enlargement and fatty-acid buildup can be reversed once the alcohol is withdrawn (17). All the same, if one’s consumption is frequent enough, the resultant cell death and inflammation from these hepatic alterations can develop into full-blown and occasionally fatal clinical conditions like alcoholic hepatitis or cirrhosis of the liver (21,22). Finally, if I haven’t already brought my health-conscious drinking audience to the verge of tears, alcohol is also immunosuppressive (23,24), as the ingestion of ethanol blunts the body’s ability to properly produce IL-1, IL-6, and TNF-alpha (24) and antigen specific T-cells (25), two critical facets to the body’s immune response (26).

As you can plainly see, Sesathin clearly has its work cut out for it. Luckily for us however, it rises to the challenge admirably, combating the negative effects of alcohol through numerous pathways.

We first talked about body composition, where Sesathin truly shines as a dietary supplement. Alcohol drops the body’s fatty-acid oxidation rates by 73%? Well, Sesathin’s potent PPARalpha activation (the same mechanism that the omega-3 fatty acids in fish oil work through, only far stronger) increases fat-oxidation 10-fold over baseline in skeletal muscle (27). Even better, it has similar properties in the liver, where it markedly decreases triglyceride (TG) formation and increases TG uptake and fatty acid oxidation (27,28,29). As mentioned earlier, alcohol’s ability to blunt fat oxidation and cause the accumulation of fatty acids in the liver are two of its worst side-effects, and Sesathin directly antagonizes both. In fact, whereas the upregulation of PPARgamma (in this case by ethanol) strongly promotes fat gain, the upregulation of PPARalpha-mediated gene-expression does the exact opposite in the body: it promotes leanness, accelerates fat metabolism, and decreases fat storage (30,31,32).

But Sesathin’s ownage of alcohol-prompted pathologies goes even further, thanks to its strong anti-oxidant, anti-inflammatory, blood-lipid improving, and insulin-sensitizing properties. Alcohol increases oxidative stress and causes the build-up of toxic metabolites. Sesathin decreases oxidative stress and inhibits the metabolism of the anti-oxidant/anti-inflammatory compound vitamin E (33,34,35,36). In fact, the actives in Sesathin have been clinically proven to protect the liver from damage induced by both the toxic chemical carbon tetrachloride, and, you guessed it, alcohol overdose (37).

Additionally, the ingredients in Sesathin positively modulate insulin sensitivity and blood lipid levels (27,35), a dynamic which ought to seriously come in handy against the insulin resistance and hyperlipidemia so commonly seen with ethanol ingestion in humans. Plus, Sesathin’s anti-inflammatory, PPARalpha activating, and phospholipid membrane-permeating properties will also put a check on increases in inflammatory cytokines and the formation of the prostaglandin PGE2. This means that Sesathin will also help counteract the immunosuppressive effects of alcohol, and should theoretically boost immune-function, even during and after inebriation. And, in what seems like a gift from above, Sesathin may even decrease hangovers, since it antagonizes the very inflammatory prostaglandins that ethanol consumption has been shown to increase (38). Anybody know why popping Aspirin like Skittles is like, “Hangover Home-Remedies 101” for anybody who hit the bar a little too hard the night before? Because Aspirin is a non-steroidal anti-inflammatory (NSAID) drug that inhibits the formation of those same inflammatory prostaglandins known for contributing to soreness and headaches. How glorious is that??

So the next time you decide to go bottoms up, don’t forget your Sesathin™, easily the best all-in-one protective against the ills of intoxication since M.A.D.D. Don’t forget to drink responsibly. Cheers all.


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SesaThin and Alcohol