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

 

Off-topic (just came across this and felt like sharing): Effects of replacing meat with soyabean in the diet on sex hormone concentrations in healthy adult males (Habito et al., 2000)

42 healthy men aged 35-62 ate either 150 g meat or an equivalent amount of protein from tofu daily for 4 weeks, 2 week washout, then crossover.

Tofu reduced free testosterone (p=0.06) and increase estrogen (p=13)… testosterone:estrogen ratio reduced on tofu diet (p=0.06).   Effects weren’t robust, but this is a crossover study.  just sayin’

tofu

moving on: Body composition and hormonal responses to a carbohydrate-restricted diet (Volek et al., 2000)

12 healthy men switched from their habitual 48% carb diet to an 8%  carb diet for 6 weeks.  Protein intake increased from 113 to 176 g/d and fat intake nearly doubled, 32% to 61% with a lot of saturates.  Dietary cholesterol also increased from 332 mg to 741 mg/d.  A lot of dietary changes and predictable responses: 2 kg drop in body weight , 3 kg fat loss and 1 kg muscle gain… Insulin levels declined, and free testosterone increased from 0.48 to 0.53.  No effect on total testosterone… increased dietary cholesterol –> increased testosterone?  not in this study –> #SHBG.

Insulin and T

but low carb ketogenic diets specifically reduce testosterone in PCOS… 

Intensive insulin therapy increases sex hormone binding globulin in newly diagnosed type 2 diabetic patients (Tong et al., 2013)

Lower serum testosterone is independently associated with insulin resistance in non-diabetic older men: the Health In Men study (get it? H.I.M.) (Yeap et al., 2009)

In PCOS, hyperinsulinemia screws up GnRH secretion resulting in an exaggerated LH:FSH response… this increases ovarian androgen production, hirsutism.  Men don’t have ovaries, and at least one study showed LH isn’t *directly* affected by insulin [in men] (Pesant et al., 2013)… (although this doesn’t rule out subtle changes in LH pulsatility or some other rarely measured parameter).

I suspect part of the effect [in men] is mediated by aromatase.  The gyno might be permanent, but the loss of libido doesn’t have to be.

Cause or effect?  The diet stuff (above) suggests diet-induced hormonal alterations are a part of the cause.  Of course, it seems to work both ways: androgen deprivation therapy *causes* insulin resistance (Haidar 2007).  Imho, however, in practice, diet should be at least considered because it’s an easy remedy: eat better.

 

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  • http://ashsimmonds.com/ Ash Simmonds

    Confounder in the testosterone thingy is high fibre, I’m not especially knowledgable on it’s T effects and quick search says “maybe”. Plenty of evidence noting it’s deleterious effects – or should I say a complete lack of evidence proving it’s healthfulness:

    http://highsteaks.com/forum/health-nutrition-and-science/fiber-not-good-you-198.0.html

    • http://www.caloriesproper.com/ William Lagakos

      In the studies discussed above, fibre was part of the “heart-healthy low-fat diet” message. There are a lot of positive studies on certain prebiotic fibres, but they are a far cry from cereal fibres, of which I’m not a huge fan… ever since the [notorious] DART study: http://caloriesproper.com/?attachment_id=186

  • Thomas Hemming Larsen

    Isn’t fat just another fuel than carbs? Different populations have lived on either high carb of high fat diets and thrived.

    • http://www.caloriesproper.com/ William Lagakos

      Noooo! Fat and carbs elicit very different metabolic and endocrinological effects… but I do agree that many healthy peoples, particularly the indigenous ones studied by WAP, have been able to thrive on high carbohydrate diets. Those who follow Westernized high carb diets… not so much. Probably lifestyle AND dietary factors at work here.

      • Thomas Hemming Larsen

        My question was more rhetorical/philosophical. I didn’t mean that they are the same. Like today we have cars running on diesel (fat) and gasoline (carbs), they don’t have the same properties as cars but they will get you from A to B. Besides that, living on carbs 10000y ago is definitely not the same as living on carbs today.

      • Jack Kruse

        and they lived where? In between the Tropic of Capricorn and Cancer. What two things does that mean? They had a strong photoelectric effect 24/7, and they had a more stable magnetic field 24/7. At the poles the field is most chaotic. It all comes back to the photoelectric effect, magnetism, and water chemistry.

    • http://ashsimmonds.com/ Ash Simmonds

      The way Kurt Harris puts it:

      “Lets say a bolus of glucose and fructose from a glass of ‘healthy’ orange juice ends up as sat fat in your body.

      On the way there, it raises your insulin levels, causes insulin resistance in the liver, activates a variety of inflammatory signaling pathways, raises your triglyceride levels, increases your blood’s thrombogenicity, makes small dense LDL and helps to oxidize it, glycates your structural proteins, contributes to steatohepatosis which can destroy your liver, etc.

      The caloric equivalent from butter does exactly zero of those things.”

      And Jack Kruse:

      “Think of food as hormone information, not as a metabolic fuel.”

      Which is an important thing to do in order to internalise “healthy” eating – forget about the fuel component (calories), but understand what hormonal effect the thing you’re eating is going to have on your body – from there just consume as much of the food that does the least “bad” stuff and the most “good” stuff (as far as we know) as you need to be satisfied.

      • http://www.caloriesproper.com/ William Lagakos

        This. “Think of food as hormone information, not as a metabolic fuel.” Kudos to Jack. +1

        I haven’t read much by Kurt Harris, but to increase “sat fat in your body” you need to actually eat sat fat, preferably in the absence of sugars.

      • Thomas Hemming Larsen

        Those are some really good points which I completely agree with. Please see my comment to Bill below.

  • http://itsthewooo.blogspot.com/ Jane Plain (Woo)

    LOL I wanted to “like” this but forgot it only blog entry ;)

    Fabulous and interesting as usual Bill.

    The PCOS study graph is a bit alarming re: cortisol levels. I wonder if this was related to negative energy balance, weight loss, and if it would persist if they ate calorie adequate? This likely underlies ketotic insomnia many people report, I am very sensitive to cortisol with insomnia as are many others. However, for me, if I eat high cal keto, I sleep like baby, and if I low cal / high carb, I also have insomnia.

    Also, look at the favorable thyroid changes! So much for myth that LC explodes thyroid. I wonder if there was a specific effect of maybe just a few patients who had major improvements in thyroid secondary to gluten autoimmunity (major cause of hashimotos), or if the thyroid improvement was universal and related to eating a diet that circumvents glucose intolerance.

    Thyroid improvement all the more remarkable if the LC diet was negative energy balance and promoting wt loss which it surely was considering the insulin levels are progressively declining (a sign of wt loss and a cause).

    I suspect many PCOS women may have gluten hashimotos like thyroid changes , as you know bill low thyroid independently worsens fertility and may tip marginal PCOS cases to pathological. Many MDs anecdotally report a high correlation between pathological thyroidism and PCOS. Of course they usually get the causation wrong rather than understanding that hypothyroidism impairs fertility so any vulnerability to PCOS will be worse… and low thyroid will cause metabolic problems too of course, which can trigger PCOS.

    In PCOS the insulin excess is usually cyclical because there is a primary metabolic disoder for one reason or other (e.g. weakness synthesizing inositiol, or drug induced depletion) which leads to insulin resistance of adrenal/kidney , thus high DHEAs-> adrenal testosterone, as well as hyperinsulinemia bathing the thecal cells -> ovarian androgen excess. Once high androgens exist, glucose tolerance is even *more* poor and massive fatness results in very short order as well as way worse PCO symptom. High androgen in female -> glucose intolerance.

    Some evidence that women with PCO have poor ability to maintain sensitivity to estrogen and LH in brain, maybe implicates prenatal androgens according to animal studies. LH becomes high with cystic multiple half developed follicle because brain can’t respond to escalating E and LH with surge to induce ovulation. Although, the high responsiveness of many pCOS women to LC diets with ovulation suggests this is not true for humans or at least most PCO women. Speaking personally addressing insulin sensitivity and inositol has restored pretty much regular ovulation suggesting this is not mostly brain defect.

    • http://www.caloriesproper.com/ William Lagakos

      Regarding the thyroid changes, I suspect they were “across the board” for two reasons: 1) small standard deviations; and 2) the control group actually slid in the opposite direction… That said, I wouldn’t rule out something downstream from removing all gluten, grains, etc.

      I think the thyroid connection is most likely attributed to exactly what you’ve said in the past. Hypothyroid-like symptoms are due to low energy or nutrient intake and have little to do with the ketotic state per se. Less likely to manifest on a eucaloric or otherwise weight-maintaining ketogenic diet… although they did lose a bit (lost 3kg fat, gained 1kg muscle), so yeah, pretty remarkable.

      • Jack Cameron

        Increased intake of n-6 linoleic acid (LA) elevates endocannabinoids and predisposes mice to ectopic lipid storage and hepatic insulin resistance by promoting centrally mediated hypothyroidism; (pmid 22912404)

  • http://itsthewooo.blogspot.com/ Jane Plain (Woo)

    IN men however body fat -> estrogen -> negative feedback inhibition of testosterone via higher SHBG.

    I’ve hypothesized there is a “male PCOS ” featuring hair loss and gynecomastea related to excessive aromatization to estrogen and high SHBG, all related to insulin and body fat changes. Of course not precisely the same as PCOS but similar in that it is an insulin driven sex steroid endocrinopathy except affecting males.

    Anecdotally, overweight men are more likely bald with “breast” development I’ve observed.

    Similarly even if not PCOS (which is spectrum disorder) it is reported overweight women have higher tesosterone, an expected effect of hyperinsulinemia / ovarian hyperstimulation from insulin and perhaps subclinical PCOS.

    Acetyl-l-carnitine is a great supplement for older men because it upregulates androgen receptors and also improves LCFA oxidation as well as dopamine sensitivity. I believe studies have shown it superior to the standard low dose androgen replacement therapy for older men.

    PS sorry for epic responses as per usual. MAKE UR BLOG MOAR BORING.

    • Kindke

      isnt SHBG reduced in obesity? my feeling was that

      hyperinsulinemia -> excessive aromatase activation -> high conversion of T to E -> negative feedback at hypothalamus for LH secretion -> low T.

      • http://itsthewooo.blogspot.com/ Jane Plain (Woo)

        this is true kindke but also high bodyfat abd estrogen from t and bf -> high shbg.

        shbg is only lower in female obesity, not male

      • http://www.caloriesproper.com/ William Lagakos

        SHBG is a wild card, imo… inconsistent data from intervention and observational studies.
        https://www.ncbi.nlm.nih.gov/pubmed/17315082
        http://www.ncbi.nlm.nih.gov/pubmed/23507475
        https://www.ncbi.nlm.nih.gov/pubmed/8626841

        wild card.

        • Jack Kruse

          SHBG wild card action is tied to is molecular acrobatics. It explains why it walks the hermophrodite pathways between estrogen and testosterone.

          • Jack Kruse

            Biochemistry will never show you the magic of SHBG. When one understands the quantized mechanisms at play in melanopsin, actin, myosin, and rhodopsin you can begin to understand SHBG interaction with estrogen and testosterone. It all comes down to a transition metal at a key binding site. The primary and second structure of proteins are all controlled by nucleic acid codes. The tertiary and quaternary structure of proteins is the domain of epigenetic modifications of non coding DNA. This is where the action happens for SHBG. The primary structure of SHBG comprises tandem laminin G-like (LG) domains. The amino-terminal LG-domain includes the steroid-binding site and dimerization interface, and its tertiary structure, resolved in complex with natural and synthetic sex steroids, has revealed unanticipated mechanisms of steroid binding at the atomic level. This LG-domain interacts with fibulin-1D and fibulin- 2 in a ligand-specific manner, and this is attributed to the unique way estrogens reside within the steroid-binding site, and the ordering of an otherwise flexible loop structure covering the entrance of the steroid-binding pocket. Estrogen is designed to work in with SHBG because it is associated with a lower level of iodine in women. This changes the delocalization of electrons of Zinc’s D shell electrons. There are however two other transition metals binding sites (cation) The cation changes make SHBG resonant to different electromagnetic frequencies when different sex steroids bond to the loop ring. This mechanism enables estradiol to enhance the sequestration of plasma SHBG by the stroma of some tissues through binding to these extra-cellular matrix-associated proteins. The human SHBG amino-terminal LG-domain also contains several cation-binding sites, and occupancy of a zinc-binding site influences its affinity for estradiol. To prove to you I might be correct about this quantum SHBG dance, biochemistry still does not have the complete quaternary structure of SHBG even today. The reason? They do not realize it changes with the electromagnetic force of the environment. When you understand protein structural predictions of tertiary and quaternary structures suggest that the carboxy-terminal LG-domains extend laterally from the dimerized amino-terminal LG-domains .

          • Jack Kruse
          • http://www.caloriesproper.com/ William Lagakos

            Thanks for the link, Jack.

    • http://www.caloriesproper.com/ William Lagakos

      Ha!
      Anecdote: I suspect a friend of mine might be somewhere on that “male PCOS spectrum,” but on a weird outskirt. He has a lean metabolism, like 0% body fat, a very deep voice, but has had male pattern balding since early 20′s… I always thought all of it could be explained by super high 5a-reductase activity or impaired DHT clearance. But he’s got a kid so not infertile… and no clue if there’s any gyno.

  • George

    Are they counting MUFA as a saturate? Interesting, I’ve only seen that done before in Nanji and French, where the context makes it meaningless to separate MUFA and SFA.
    So the question is, does the same context exist here? Is (omega 6) PUFA part of the pathology along with carbohydrate?
    Seems plausible to me.

    • http://www.caloriesproper.com/ William Lagakos

      lol molested n6 PUFAs are part of ALL pathologies!

      interesting, in the study you linked n3′s “fixed” androgens in PCOS… not by being n3′s, but rather by apparently blocking n6′s.

  • Jack Kruse

    Cutting many of words out: Think of food as hormone information, not as a metabolic fuel. Food captures photons and electrons from the sun. Molecular Maxwell demons in food do it. Molecular Maxwell demons take advantage of the fact that the Second Law of thermodynamics is statistical and not absolute. In this way the electromagnetic force of sunlight electrically induces the Molecular demons in us, and turns the food back into photons and electrons. First Law of thermodynamics. Energy can not be made or destroyed by transformed. Molecular demons in cytochromes steal the energy in photons and electrons excited by the sun and turn then back to their lowest energy state in molecular oxygen. Molecular demons captures the delta energy for free and couples it to reduce entropy system wide. Entropy in life, is not chaos, it is information stored in the quantum particle. Each subatomic particle is a fragment of the glass vase the “great architect” dropped in the Big Bang. Each piece forms a piece of what was the vase. Life is designed to capture photons and electrons to gain this energy for free and the information to reduce entropy to animate life. This is exactly what drives evolution, not natural selection. We evolve better entropy dumps back to the environment to become more energy efficient. As we improve, hormone panels reflect the efficiency. As information is collected life becomes aware….and conscious… within its protoplasm first, and then in its brain. Ever see a two ice dancers? Body coherence/connection due to conscious entanglement. As brain develops on the tree of life it is entangled with body. The brain becomes the librarian who can sample the consciousness throughout the entire life form. Better brain, better cognition, to tap more information to collect more energy and data. Hormones=energy+information.

    • http://ashsimmonds.com/ Ash Simmonds

      Jack – any wonder we leave some words out… LOL!

      • Jack Kruse

        Ash……for 3 yrs people have been mocking……..soon we will see who is laughing last.

        • http://ashsimmonds.com/ Ash Simmonds

          I think you’re ahead of your/our time for the most part, but most of us need bite size take-aways.

          • Jack Kruse

            agree…..but we can’t settle for a science that is not going to harvest the answers we need for our modern health conditions. I firmly believe the answer wont be in biochemistry but in QED.

    • Jack Kruse

      In QED, and in fact, in Newton’s physics, as time goes on entropy also increases. In Newton’s physics time was considered absolute and non varying. Einstein’s relativity made us all realize time was not absolute either. It was relative to who was measuring it. This implies just the act of observation can throw reality off. Quantum systems are supposed to be destroyed by the act of measurement, which brings them abruptly into the ordinary classical world. This is another reason why cause and effect might not be that important as we all think. As hard as this is to fathom, it is a consequence of nature. This one observation has had a huge effect on subatomic physics, but it did not have any effect biology or its researchers. They seem to believe “their science” is exempt from this physical fact. It should have caused them to consider the implications, because the business of biology happens at a molecular level in a cell.

  • Jack Kruse

    When a photon interacts with a material particle on our globe it lifts one electron from an electron pair to a higher level. This excited state as a rule has but a short lifetime and the electron drops back within 10–7 to 10–8 seconds to the ground state giving off its excess energy in one way or another. Life has learned to catch the photon or electron in its excited state, and then act to uncouple it from its partner and let it drop back to the ground state, through its biological semiconductors utilizing its excess energy for life processes. In this sense, you can begin to see how living organism are organized. This makes sure that all forms of life are never at the mercy of their environments, on account of the coherent energy stored within them. This explains why animals don’t have to eat constantly, leaving plenty of time for many other useful, activities of daily living. It also explains why fat likely evolved. It allowed animals to live disconnected from the Earth and sun for period of times. This was not afford to trees and plants who are 100% connected to the Earth by their roots and the sun with their leaves and canopies. Fat mass allows animals to return entropy back to the environment while providing energy when food is not present. When life is organized to store energy, no part of the system needs to be pushed or pulled into action, nor is it subject to “mechanical regulation” and control. Instead, it allows for coordinated action of all the parts. It is subject to timing, and it depends on rapid intercommunication throughout the system. The cell can thereby thought of a system of ‘excitable media’, tissues, or organs called excitable cells poised to respond specifically and disproportionately to weak low electromagnetic signals. Electromagnetic signals are the strongest forces that bind the smallest particles in nature. Because large amounts of energy stored everywhere in cells and tissues, they automatically amplify these weak electromagnetic signals, to often cause macroscopic actions. This is the simplified version to give you the essence of what I wrote in Energy and Epigenetics 6. What loads the entire system if you are following me? Sunlight. We eat electrons and photons……y’all just do not know it yet, but you will.

  • Jack Kruse

    Men and women have different Maxwell demons to account for the different results of the same quantum actions. When you understand the molecular formula does not need to change to get a different result your view point changes. Don’t believe it can happen? Look at the mechanism of action of rhodopsin, Melanopsin, actin and myosin. When you get that it can and does happen……then I can explain to you how the sex steroid hormones do their magic. You got to run from biochemistry. Everything is based on QED. When you observe something as biochemists and biology does……..you affect the ability to know. QED 101. When your target is wrong……..what good is your literature. BOOM.

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  • Thomas Hemming Larsen

    Hi Bill, I hope you had a great Danish Christmas.
    I’m not sure if this is the right post to ask my question but here goes. If one wants to gain muscle on low-carb/ketogenic diet are some fats better than others then? Firstly, I’m thinking about coconut oil which has a high amount of MCT which can’t be stored in the body so that it might be better to eat LCFA. Secondly, since saturated fat, in particular, raises testosterone does it also have some other hormonal benefits towards gaining muscle?

    • http://www.caloriesproper.com/ William Lagakos

      Thanks! You too :)

      About other hormonal benefits, I don’t know… but I tend to favor coconut oil & cocoa butter. Saturates, resistant to oxidative stress and all that jazz.

    • Chris

      Hey Tom, when testosterone levels are increased, this will most likely induce the increase in the other 2 hormones responsible for muscle growth, such as: the growth hormone and IGF-1. So I would see this as another benefit of lchf diets. ;)

      • Thomas Hemming Larsen

        Yes, higher testosterone levels are definitely good. The obvious question is then which fat raises testosterone the most :)

  • mrquetiapine

    Testosterone diffuses from the testes into the bloodstream for transport to target tissues. Approximately 1% to 2% of all testosterone circulates in the blood as free T, while the other 98% to 99% is protein-bound. Most protein-bound T is strongly associated with SHBG (60%), while the other 38% fraction is bound to albumin. Only the albumin-bound and fT forms are available for binding at target tissues, and are thus called bioavailable T (bioT).1Advancing age is accompanied with changes in testosterone binding due to an increase in SHBG.2

    References:

    Dandona P, Rosenberg MT. A practical guide to male hypogonadism in the primary care setting.Int J Clin Pract. 2010;64:682-696. PMID: 20518947.

    Kaufman J-M, T’Sojen G, Verleulen A. Androgens in male senescence. In: Nieschlag E, Behre HM, eds. Testosterone: Action, Deficiency, Substitution. Cambridge, UK: Cambridge University Press; 2012: Chapter 16.

    • http://www.caloriesproper.com/ William Lagakos

      Thanks, Mr. Quetiapine!