Category Archives: fat

Lights Out! Get your melatonin.

From T.S. Wiley’s website:
“People spent summers, before electric lights, sleeping less & eating heavily in preparation for winter because the light triggered the hunger for carbohydrates. Now, light is available 24 hours a day. Heating and air-conditioning climate control our hormonal responses to consume carbohydrates now available year round. This is the scenario for obesity, Type II diabetes, and depression… In Wiley’s opinion, sleep is the best medicine.”

And Wikipedia:
“Wiley’s main thesis in Lights Out is that light is a physiological trigger that controls dopamine and hormones like cortisol. Wiley posits that with the extension of the natural day through artificial lighting, rest at the hormonal level is rarely adequate for optimum biological needs of the body. In her view, this results in both fatigue and unnatural appetite, which leads to weight gain, exhaustion, and disease. Wiley theorizes that the body’s responses are cyclical, reflecting the seasons of the year, and that the body’s needs vary seasonally. According to Wiley, during the winter months the body needs more sleep, and carbohydrates should be restricted as they would have been naturally during hunter-gatherer times.”

melatonin

Most of the first third of Wiley’s book “Lights Out: Sleep, Sugar, and Survival” centers around light exposure, melatonin, and the many, many effects of a screwed up circadian cycle.  Jane Plain and Jack Kruse have written volumes on the subject, please see their websites for more in-depth analyses and practical applications…

Much of this blog post is my take on that first third (I couldn’t wait to finish it before writing about it), plus a little input from Google, Pubmed, et al; some commentary & pseudo-fact-checking as well.  I’m going to finish the book, and hopefully it will inspire a few more blog posts as opposed to a tin foil hat.  Most of the stuff in Lights Out makes incredibly good sense, but: 1) that doesn’t mean it’s true; and 2) the strings of logic are far too long to do a proper fact-check.  But really it’s how well it makes sense (mostly) that has me intrigued.

divide and conquer

Melatonin is a sleep-inducing hormone controlled by the light-dark cycle.  It is known.  On the day-to-day, melatonin increases at night and decreases during the daytime.  From Wiley: on a seasonal level, longer days during the summer meant less melatonin overall during these months.  Since melatonin suppresses sex hormones (inconsistent? Eg, Smith et al., 2013), summer is supposed to be breeding time, so the baby is born in spring when food is plenty (I’m OK with this now, but will certainly disagree come December).  Melatonin also suppresses metabolic rate, so the decreased daylight and thus increased melatonin during the winter months helped to survive on less food (supported by Marrin et al., 2013).

Disruptions in circadian rhythms royally screws us up.  According to Wikipedia, fireplaces/candles and incandescent bulbs produce less of the melatonin-suppressive blue lights… use these at night in winter?


Antidepressant and circadian phase-shifting effects of light. (Lewy et al., 1987)
Abstract: Bright light can suppress nighttime melatonin production in humans, but ordinary indoor light does not have this effect. This finding suggested that bright light may have other chronobiologic effects in humans as well. Eight patients who regularly became depressed in the winter (as day length shortens) significantly improved after 1 week of exposure to bright light in the morning (but not after 1 week of bright light in the evening). The antidepressant response to morning light was accompanied by an advance (shift to an earlier time) in the onset of nighttime melatonin production. These results suggest that timing may be critical for the antidepressant effects of bright light.

Next:  Prolactin inhibits sex hormones, and melatonin stimulates prolactin (supported by Gill-Sharma 2009Campino et al., 2008).  Thus, less melatonin in summer means less prolactin = more sex & fertility.  She also says day sex is more likely to result in conception compared to night sex for this reason (couldn’t find a reference for or against this).

Dopamine inhibits prolactin, whereas TRH & melatonin stimulate it.  Melatonin also blunts ACTH-induced cortisol secretion (supported by Torres-Farfan 2003Campino 2008).  Winter = high melatonin, prolactin, and low cortisol & dopamine.  Summer = high dopamine & cortisol, and low melatonin & prolactin.  Prolactin is supposed to be high in winter, during pregnancy; low dopamine would support this.

Circadian rhythm

Dopamine is a summer hormone?  Lu et al. (2006) showed high dopaminergic activity was associated with light and wakefulness (ie, summertime).  However, Venero (2002) showed melatonin stimulated dopamine synthesis in specific brain regions, and Eisenberg (2010) showed increased dopamine synthesis in fall & winter relative to spring and summer.  Two  possible confounding factors come to mind: 1) Location, location, location!  Some of these discrepancies may be due to brain region-specific dopamine metabolism… actually, Lu is the only odd-man out, so perhaps dopamine is a winter hormone?  And 2) Wiley’s main premise is that we pwned the light… epigenetics and the like mean that we, including the people in those studies, have deeply screwed up light/dark summer/winter metabolic programs on an epigenetic level, so it’s possible those studies are riddles with artefacts.  However, Wiley also says that people get sick because they live in perpetual summer (lights on all the time = high dopamine), and Markianos (2013) showed elevated dopamine metabolites in overweight patients; in my experience these studies usually continuously enroll patients, year-round.


I’m really just blazing through abstracts here – this is why I call it “pseudo-fact-checking;” not to be confused with any degree of academic rigor.

To be continued… (no tin foil hats, I promise) (not yet at least)

Affiliate discounts: It’s 2018, join Binance and get some damn cryptoassets or download Honeyminer and get some Bitcoins for free!

Still looking for a pair of hot blue blockers? Carbonshade is offering 15% off with the coupon code LAGAKOS and Spectra479 is offering 15% off HERETrueDark is running a pretty big sale HEREIf you have no idea what I’m talking about, read this then this.

20% off some delish stocks and broths from Kettle and Fire HERE

If you want the benefits of  ‘shrooms but don’t like eating them, Real Mushrooms makes great extracts. 10% off with coupon code LAGAKOS. I recommend Lion’s Mane for the brain and Reishi for everything else

calories proper

 

Nutrition Disinformation III

but they actually get it right this time.   Big HT to George Henderson for bringing this ms to my attention.

In Nutrition Disinformation, Part I, the Mediterranean diets employed by Estruch & colleagues were discussed.  The study subjects’ need for antidiabetic drugs, insulin, and anti-platelets all increased over the course of 5 years.  The media and even the authors themselves reported the opposite, touting the benefits of Mediterranean diets.  Thus begat the Nutrition Disinformation series.

Nutrition Disinformation 2.0 was a follow-up to an older post on the Look AHEAD study, when the results were finally published.  The intensive lifestyle intervention consisted of a pharmaceutical-grade low fat diet (ie, LFD + a little bit of Orlistat), and exercise.  By the end of 10 years, medication use was modestly lower in the intensive lifestyle group compared to controls, but it was markedly increased from baseline.  Therefore, I deemed it egregious to say their intervention was “healthy.”  In the context of Nutrition Disinformation, “healthy” means you’re getting better.  The need for insulin, statins, and anti-hypertensives should decline if you’re getting better.

In part 3 of the series, Yancy must’ve been following the Nutrition Disinformation series 🙂 and decided to conduct a subgroup analysis on the patients in his previous low carb vs. low fat + Orlistat study.  Weight loss was roughly similar, but all other biomarkers improved more on low carb.  In the new publication, Yancy analyzed data selectively from the diabetic patients in his original study to generate a “Medication Effect Score (MES).”  MES is based on what percentage of  the maximum dose was a patient given, and adjusted for the median decline in HbA1c experienced by patients on said drug.  A bit convoluted, but I’m on board (at least tentatively).

Continue reading

All my organs hurt and I think I’m going blind.

People, this is how you should eat.

There have been a lot of diet postings lately, and they are some of the healthiest diets you could imagine.  Please click the links to get the full versions, which include lifestyle tidbits, other pearls, and WHY.  And take notes.  I’ve just listed some of the foods here for the sake of brevity (and as an excuse to link to the diets).

Disclaimer: all of these diets fall somewhere on the “low carb” spectrum.  I don’t eat low carb because I have to*, I do so because it’s healthy, convenient for my lifestyle, and I rather like the foods.  *I say I don’t “have to” because I have no underlying health problems or carb-sensitive GI issues.  The people below are also far healthier than most (from what I can gather)… but if you are overweight &/or obesity-prone, or glucose-intolerant &/or diabetic, then you might want to consider following any of them.

Hyperlipid (Petro Dobromylskyj)The Optimal Diet
butter, egg yolks, cocoa, dark chocolate, macadamia nuts, sour cream, beef, green veggies.  His stats: BW stable, 28” waist, greying beard.  Peter will outlive us all.  And take over the world if he ever has the desire to do so.

Anna Fagan (Lifextension): Low Carb Paleo, probably keto
eggs, butter, avocado, cheese, shrooms, bacon, salmon, tea, coffee, nuts, sardines, lamb, pork, eggplant, cream  –> “high fat =/= fat.”  She’s currently off studying paleoanthropology somewhere in Turkey (?).

Jane Plain (ItsTheWooo): Ketogenic
cream, sour cream, nuts, butter, beef & fatty meats, pepperoni.  She, too, is rather fit.  The Scribble Pad = diet & lifestyle vs. psychoneuroendocrinology & metabolism (mixed with equal parts humor & gravitas).

Continue reading

On calorie information posted in restaurants

“This is biology, not mathematics.”

It’s law in some places.  It’s a burden on restaurants.  And it will do nothing for the cause – like trying to put out a candle by pressing the off button on your remote control.  In other words, a waste.

Here’s some of the “science” behind it.

Exhibit A.
In a study by Dumanovsky, fast-food customers were surveyed prior to and after mandatory calorie labeling in New York.  25% of the people reported “seeing calorie information,” and 10% of them said it affected their buying decision (ie, 2.5% of all fast-food consumers surveyed thought they knew enough about “calories” to be scared of them).  After the law went into effect, 64% of people noticed the calorie information, and 20% of them were affected by it (=12.8% of all fast-food consumers thought they knew enough about “calories” to be scared of them).  Sooo, the proportion of people making misinformed decisions quintupled.  Calorie Labeling = Nutrition Disinformation.  It’s misleading, and usually wrong.

Continue reading

Look AHEAD – Nutrition Disinformation 2.0

The day you’ve all been waiting for has finally arrived.  Results from the Look AHEAD study have been published.  When I first wrote about this study (HERE), it had been prematurely halted because the intervention was providing no benefits.  Everybody was in a state of shock and awe because Low Fat didn’t save lives.  But that was before we even had the data.  

Reminder: the “intensive lifestyle intervention” consisted of a Low Fat Diet & exercise.  The results?  Yes, they lost more weight than control, but they also took more Orlistat (of which I’m not a fan, see HERE for why):

orlistat

Orlistat = pharmaceutically enhanced low fat diet. 

Their normal diets were not healthy, but neither was low fat –>

med use

Medication use increased drastically in both groups.  The pundits have gone wild because medication use was lower in the intensive Low Fat group at the end of the study, but this is Nutrition Disinformation 2.0.  Eerily reminiscent of the recent Mediterranean Diet study, the conclusions are the same: keep eating poorly and the need for medications will increase.  You can call it a lot of things, but not “healthy.”  The alternative –>  How to define a “healthy” diet.  Period.


Significant adverse events:SAE

The only thing to reach statistical significance was more fractures in the intensive Low Fat group, but you didn’t read any headlines that said “Low Fat breaks bones.”  Imagine if that happened on low carb [sigh]  The next closest thing to statistical significance was increased amputations in the intensive Low Fat group :/

gem:History of CVD

Translation: if you were healthy at baseline, then you could tolerate a low fat diet.  Otherwise, not so much.  This is exactly what happened in the Women’s Health Initiative.

Ha

needless to say, none of the “possible explanations” they considered were Low fat diet Fail.

calories proper

Are carbs stored as fat?

Hint: “no”

DNL proper.

Lots of metabolism talk below, but first a brief intro.  My “muse,” if you will.

Taubes’ recent article in the BMJ (Taubes, 2013full text) generated some interesting feedback.

In the original article, Taubes basically re-states his philosophy on obesity.  Nothing new.  But one rebuttal by Cottrell got under my skin (Cottrell, 2013), and Taubes’ response was woefully inadequate.

Cottrell [sic]: “A third incorrect assertion is that obesity can be attributed to the conversion of carbohydrate to fat. This is an unsatisfactory explanation of obesity, because this route is a minor pathway to depot fat in humans, even under conditions of substantial overfeeding of sugars to obese subjects.  An unproved assumption is that the hypothetical diversion of carbohydrate energy into fat storage leaves the subject hungry, thus stimulating overeating.”

strawman

Cottrell set up a straw man and handily took it down.  The primary mechanism whereby excess carbs contribute to obesity is via insulin’s effects on adipose tissue.  Even if you’re eating very little fat, insulin will cause it to get stored.  Insulin is very good at this – it is actually far more potent at stimulating fat storage than it is at stimulating glucose uptake (eg, Insulin vs. fat metabolism FTW).  Cottrell’s straw man is that excess carbs themselves are stored as fat.  This does not occur to any appreciable extent in humans.  Here is why I believe that to be true, from one of most insightful and informative studies on the topic IMHO.

Continue reading

MOA of MCTs – black magic or something less?

MCTs provide a respectable boost in diet-induced thermogenesis (in some studies [eg, Kasai 2002  & Clegg 2012], but not others [Alexandrou 2007]), but I don’t think that’s what does it.

The alternative?  MCTs aren’t “linoleate.” (sorry for lack of suspense)

Alcohol + MCTs vs. corn oil (from Kirpich 2013):

Kirpich

Further, feed rats a diet rich in either coconut oil, olive oil, safflower oil, evening primrose oil, or menhaden oil… and eventually the fat stored in their bodies reflect those fats – eg, linoleate only accumulated in the tissues of those fed safflower & evening primrose oils (Yaqoob 1995) (expect similar results with soybean & corn oils).

Researchers constantly refer to MCTs & coconut oil as “saturated fats,” but I always thought the chain length should be recognized.  Perhaps.  But with regard to certain benefits (eg, hepatoprotection), perhaps not.

Cacao butter has a lot of stearate (a fully saturated 18-carbon fatty acid) but not much linoleate or MCTs.  This linoleate may very well be more of a detriment than stearate or MCTs are a benefit… (with regard to certain benefits [eg, hepatoprotection])Beef and chocolate

(Leslie Roberts, 1988) (she’s talking about stearate)

Continue reading

Alcohol-proof your liver. SFAs.

it probably has other benefits, too. 

Tissue lipid turnover, adipose vs. liver.

Can the saturated fat & MCTs in dark chocolate & coconut oil protect liver against the ravages of alcohol?  Tonight?

The studies discussed in “The liver is evil but need not be punished.  SFAs”  entailed chronic alcohol feeding in combination with a high saturated fat/MCT diet – the animals were given a liquid diet of complete nutrition and a LOT of booze.   Not very applicable to humans, imo [hopefully].  Which brings up the question: how long does it take for coconut oil & dark chocolate to flex their hepato-protective muscles?

wine and dark chocolate

Fortunately, [if tissue fat composition is in fact the relevant protective factor], unlike adipose fat which hangs around for years (Beynen et al., 1980 & Katan et al., 1997), liver fat appears to turn over quite rapidly.

For example, a single shot of radiolabeled oleate is cleared out of the liver within a few days, whereas it lingers significantly longer in adipose of rats (Iritani et al., 2005).  And this is actually enhanced in rats fed a higher fat diet.fat-free diet

Similarly, a study on diet-induced changes in liver fat in humans showed that after only 3 days of low carb dieting, liver fat significantly declined in 5/10 patients, and in all of them by day 10 (Hollingsworth et al., 2006):liver fat time course

Shoutout to Mike Eades for directing me to this study.  Whatever happens after 3-10 days, I suspect, will reflect the new dietary pattern – you are what you eat?  :/

I don’t put too much stock in generic nutrition textbooks, but those data are rather close to estimates put forth by Frayn, Arner, and Yki-Jarvinen (2006, free full text):Frayn

Translation: while a single meal of dark chocolate and coconut oil may not acutely protect the liver from alcohol [tonight], a few days’ worth just might.

Others?

Red meat.   While the saturated fat content of red meat is expected to similarly bolster liver resistance to oxidative stress, another component – carnitine (of the recent TMAO infamy) – may also provide some benefit by enhancing liver fat turnover (Kepka et al., 2011 sorry no full text, so only in theory).  Taurine, also found in red meat, also prevents some alcohol-induced liver pathologies [in rats] (Kerai et al., 1998 & Pushpakiran et al., 2005).

Coffee, too (Gallus et al., 2002Tverdal et al., 2003; Klatsky et al., 2006; Lopez-Garcia et al., 2008Sugiyama et al., 2010).  Probably has more to do with prevention of lipid peroxidation via antioxidant polyphenols.  just sayin’     …compared to the SFA’ers, would those on a high PUFA diet benefit more from coffee in this regard?

The culprit isn’t red meat or TMAO, its cigarettes & sedentary obese HFCS PUFA empty calories – the bona fide confounding factors in most anti-nutrition propaganda.

 

calories proper

 

Become a Patron!

 

 

Molested fats, Op. 139

or
Trans fats, part IV

Proceed with caution, this is an exploratory post.  Replacing CakesCookiesPiesPastriesBreadCerealsBiscuitsPizzaMuffins with [insert any whole food item here] is just a good idea.  And more reasons to eat dark chocolate.

In Inflammatory, trans, or linoleate? the idea was explored that it might not be the theorized textbook pro-inflammatory end products of omega-6 fats that give them a bad rap, but rather the foods that contain them – ie, “cakes, cookies, pies, and pastries” (Kris-Etherton et al., 2012 NHANES), or “bread, cereals, cakes, biscuits, pies, pizza, and muffins” (Meyer et al., 2003 from down under).

dark chocolate

Further, what starts out as an omega-6 fat can easily become peroxidized or isomerized into an oxidized or trans fat, respectively, via industrial molestation or just plain old cooking (eg, Romero et al., 1998, Marmesat et al., 2012, & Minami et al., 2012) – even just a few minutes in the microwave (Herzallah et al., 2005)!  I don’t know exactly what all of these end products are for sure, but they might look something like this:ox linoleate

Thus, the culprit may not be native Dc9,c1218:2n6 linoleate.

Continue reading

Liver is evil but need not be punished. SFAs.

What to serve with a liquid lunch, and a recipe for chocolate.

It’s like a feed forward downward spiral.  If you don’t eat saturated fat & MCTs prior to imbibing, then liver intentionally makes more PUFAs for the alcohol-induced burning ROS to molest.  Liver is evil but need not be punished.  SFAs.

Brief background: (Kirpich et al., 2011 & 2013)

Researchers studying alcohol in rodents know where they’re going and like to get there fast.  70 drinks per day fast.  Granted, rats metabolize faster than humans so it’s likely a little less… but a little less than 70 is still a lot of sauce.

Continue reading