Tag Archives: carbs

Low carbohydrate diets favorably impact testosterone levels.

It is known.  Carbohydrate restriction improves (lowers) testosterone in women with PCOS.  It works for men, too… but by “works” I mean “increases.”

Decrease of serum total and free testosterone during a low-fat high fibre diet (Hamalainen et al., 1982) 

Intervention pseudo-crossover study: 30 healthy Finnish men in their 40’s were studied on their habitual high fat diet (40%  fat), then put on a low-fat (25%) high fibre diet for 6 weeks, then switched back to high fat.  The high fat diet was also higher in saturates, P:S ratio 0.15 vs. 1.25.

free T

 

Free testosterone levels declined on the low fat diet, but they recovered after 6 weeks of going back to their high [saturated] fat dieting (p < 0.01).

Some observational data: Testosterone and cortisol in relationship to dietary nutrients and resistance exercise (Volek et al., 1997)

…fat, and in particular saturated fat, is associated with increased testosterone levels [in men]:

observational

 

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Protein Leverage Hypothesis

Inverse Carb Leverage HypothesisTM

Protein Leverage Hypothesis: Dude eats 15% protein on a 2000 kcal diet (75 g protein).  Exchange 25 grams of protein with carb, and he’s now eating 10% protein on a 2000 kcal diet (50 g protein).  Theory states Dude will increase total food intake to get back those 25 grams.

Ergo, Protein Leverage Hypothesis:

protein leverage hypothesis

Disclaimer: I don’t care much for the Protein Leverage Hypothesis.  It might be true, but that doesn’t mean it matters.  It works well in rodents, but obese patients eat tons of protein.  The rebuttal to this is that the protein in their diet is too diluted with other [empty] calories.  They’re overeating because of low protein %.

The flipside, confirmed ad nauseam in rodent studies, is that frank protein deficiency increases food intake.  Frank protein deficiency means negative nitrogen balance & tissue loss… not just skeletal muscle; organs, too.  Incompatible with survival.

Feed someone a low protein low fat diet, they get hungry.  If it’s ad libitum, they eat more.

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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)

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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).

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Calories schmalories, alcohol, and chocolate

Some calories count, others don’t.  Some calories work in some people, but not others.  Does this sound like an irrefutable Law of Nature?  No, but it is a perfectly acceptable tenet of the Laws of Energy Balance (a construct of my design).

Do alcohol calories count?  Sometimes, but not this time:

The energy cost of the metabolism of drugs, including ethanol (Pirola & Lieber 1972)

This was a study on bona fide alcoholics who participated because they were promised treatment.  Metabolic ward.  FYI, one gram of alcohol burned in a calorimeter produces ~7.1 kilocalories; alcohol = 7.1 kcal/g.

Calories required to maintain body weight (ie, = total energy expenditure) was assessed the old-fashioned way: feeding them enough calories to maintain a stable body weight – they counted calories but relied on the bathroom scale to establish a baseline.  #TPMC.  After a week of weight stability, they ISOCALORICALLY exchanged carbohydrates for alcohol, and broke CICO.

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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).

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Silent Leptin Resistance

Conventional leptin resistance has something do with obesity.  It is known.  Silent leptin resistance is … err … complicated. 

Divide and conquer

Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding (Shapiro, Scarpace, et al., 2008 AJP)

A remarkable 60% fructose diet fed to rats for 6 months had absolutely no effect on energy balance.  Nil. QED.
Fig 1

Food intake and body weight were unaffected because the levels of and sensitivity to endogenous leptin were identical in both groups.

Enter the Dragon

Enter the Dragon

“Silent Leptin Resistance” – The fructose-fed rats are, however, profoundly resistant to the satiating effects of Metreleptin (a pharmaceutical grade injectable leptin analog):

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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.

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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

Eating in the Absence of Hunger

Hat tip to Jane Plain and her ongoing series on “The physiology of body fat regulation” for citing this study as it provides a rather interesting insight into the psychoendoneuropathophysiology of the obese condition.  Eating in the Absence of Hunger.  

Caloric compensation and eating in the absence of hunger in 5- to 12-y-old weight-discordant siblings (Kral et al., 2012)

They were all full or half, weight-discordant, same-sex siblings and each sibling pair had the same mother; same mitochondrial DNA, shared a womb, etc.

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