Category Archives: marijuana

Pregnancy dieting and #moderation: just don’t be extreme

“If you can’t absorb B12, no amount of steak will help you” (more on this below)

Just like practically everyone in the field, I’m uncomfortable with the word moderation, in part because one person’s moderation can be wildly different from another’s.

Remember the Motherwell studies? In brief, they asked a group of expecting women to ditch carbs and eat a ton of meat instead (about a pound per day), and compared them with a group not given diet advice. It was designed to compare an extreme diet to an average diet (note: they didn’t assess the opposite extreme, ie, high carb vegan).

Tl;dr: babies were healthy at birth but developed a variety of health problems later in life. Perfect study design? No. Better than ALSPAC? Kinda, yeah.

 

 

In the context of today’s topic, I’ll define moderation as “not extreme” (bear with me here) (unless ALSPAC is retracted or something… which is possible given the study design.)

 

Meat consumption during pregnancy and substance misuse among adolescent offspring (Hibbeln et al., 2017) (aka ALSPAC)

 

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TRP channels in the Tx of muscle pain & cramps

NSAIDs are OK for muscle pain, but may hinder training progress in the long run (eg, Shoenfeld 2012 and Mackey 2013). The electrolyte theory of muscle cramps has been kinda debunked in some contexts (eg, Braulick et al., 2013, Miller 2014, and McKenney et al., 2015)… although I still recommend all the broths & stocks (homemade, store-bought, chicken, beef, seafood, etc.) for just about everything. 20% of Kettle & Fire broths through this link!

But even when pickle juice works (eg, Miller et al., 2010), it kicks in way sooner than if it worked via replenishing electrolytes – more likely works via the acidity activating specific ion channels.

What do we have left?

Google Image Search came through pretty epic for this…

 

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Marijuana

Marijuana is a very complex plant: many different strains with differing profiles of psychoactive, non-psychoactive, and peripherally-active compounds that impact metabolism.  Most have THC, which activates endogenous cannabinoid receptors and mimics many of the effects of smoked marijuana (eg, see studies by Hart, Wachtel, and Curran).

Do not underestimate the complexity of this plant.

 

"LOL"

“LOL”

 

I’m not ‘anti-pot’ as there are far worse drugs out there… however, some advocates make really bad “pro” arguments, like saying it’s actually healthy (or at least not harmful in any way)…
there are many independent lines of evidence which suggest otherwise, metabolically speaking.

 

MJ not crack

 

Rimonabant, the notorious pot-blocker, reduces appetite and is a fairly effective weight loss drug, but has the unfortunate side effect of doing the opposite of marijuana, psychologically speaking.  See any of the RIO studies, eg:

 

weight loss Rimonabant

 

All participants lost weight and experienced improved metabolic profiles, insulin sensitivity, etc., by blocking endogenous cannabinoid receptors.

Adverse effects?  Wellll, there’s a drug called Marinol (pure THC) that’s technically an anti-emetic (reduces the urge to vomit); it improves appetite in patients with conditions associated with anorexia or wasting.  It’s a cannabinoid agonist.  Blocking CB1 with Rimonabant induces nausea in some patients: no bueno, but not unexpected given the known effects of Marinol.  Rimonabant is also associated with depression and anxiety (in some patients); also not unexpected.

So, it’s not a good idea to block this receptor pharmacologically (for psychological reasons) or activate it recreationally (for metabolic reasons).  Obesity researchers (and big pharma no doubt) are still looking for a pot-blocker that doesn’t penetrate the brain  to avoid the negative psychological side effects (eg, Klumpers et al., 2013).

 

 

Best. Graph. Ever.  The effect of Rimonabant on how stoned participants felt after smoking pot.  Yes, “Stoned” was published in the Journal of the American Medical Association (Huestis et al., 2001).

 

Stoned

 

Indeed, Rimonabant effectively treats “cannabis intoxication” (Crippa et al., 2012).  Antagonist versus agonist 101.

 

Part II: the biological effects of cannabis, THC, marijuana, and antagonists, etc.

 

THC acts like insulin on adipocytes: increased adipogenesis, fatty acid uptake, and decreased lipolysis (eg, see studies by Teixeira and Cota).   Munchies, anyone?

Cannabinoids and mimetics/agonists induce hunger and repress satiety; cannabinoid blockers induce satiety and weight loss.  However, I actually don’t think marijuana is obesogenic aside from its anti-anorexic effects.  Cannabis use is not always associated with obesity, possibly due to confounding and/or the lack of good crossover studies (you can’t really do a proper study in healthy humans with MJ for ethical reasons).  But most rodent studies agree that cannabinoids, acting via cannabinoid receptors, induce metabolic syndrome-like effects in nearly every single tissue and on the whole-body level.

 

 

CB1 cannabinoid receptor deletion in mice leads to leanness, resistance to diet-induced obesity, and enhanced leptin sensitivity (Trillou et al., 2003).  For context, mice lacking CB1 is somewhat analogous to humans not smoking marijuana.

In liver, cannabinoid signaling induces fat accumulation and insulin resistance (Osei-Hyiaman et al., 2008).  This is absent in CB1 and liver-specific CB1 knockout models.   Mice overexpressing this receptor in liver exhibit increased insulin resistance (Liu et al., 2012).

Activating cannabinoid receptor-2 (CB2) causes insulin resistance and adipose tissue inflammation, and this is blunted in mice lacking CB2 (Deveaux et al., 2009).

 

Stoned

 

The knockouts & over-expressing rodent models, and pharmacological agonist & antagonist studies are all consistent.  That said, I still don’t think this is the worst recreational drug out there, even among “legal” ones.

 

 

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calories proper

 

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