Real men don't eat carbs

Real men don't eat carbs. At least they don't eat them without eventually paying the price.

How do carbohydrates, especially those contained in "healthy whole grains," impair maleness? Several ways:

--Consume carbohydrates, especially the exceptional glucose-increasing amylopectin A from wheat, and visceral fat grows. Visceral fat increases estrogen; estrogen, in effect, opposes the masculinizing effects of testosterone. Overweight males typically have low testosterone, high estrogen, a cause for depressions, emotionality, and weight gain.

--Consume carbohydrates like wheat and visceral fat causes prolactin to be released. Increased prolactin in a male causes growth of breasts: "man boobs,""man cans," "moobs," etc. This is why male breast reduction surgery is booming at double-digit growth rates. In cities like LA, you can see billboards advertising male breast reduction surgery.

--Carbohydrates increase visceral fat that sets the stage for postprandial abnormalities, i.e., markedly increased and prolonged lipoproteins like chylomicron remnants and VLDL particles that impair endothelial function. Impaired endothelial function underlies erectile dysfunction. Eat a bagel, become impotent.

Comments (57) -

  • Ian

    4/27/2011 6:13:03 PM |

    Real men aren't terrified of an entire macronutrient because of a poor understanding of science.

  • Matt Stone

    4/27/2011 6:14:03 PM |

    Then why do I have boys (later men) doubling testosterone when switching from a very low-carb to high-wheat, high-carbohydrate diet?

  • Mike Jones

    4/27/2011 6:19:09 PM |

    Dr. Davis,

    Can you explain why I remain lean eating 15 pounds of potatoes, 2 gallons of whole milk, and close to 2 pounds of butter every week? That's in addition to regular meat, eggs, other added fats, root vegetables, beans, occasional grains, and other carb sources like fruit and molasses. I'm 6'3", 175 pounds, have never dieted, and do not exercise. My weight has never gone higher than 176 pounds.



  • Anonymous

    4/27/2011 6:48:11 PM |

    "Real men don't eat carbs."

    Are you saying half a billion Chinese men and 70 million Japanese men aren't real men?


  • Might-o'chondri-AL

    4/27/2011 7:13:59 PM |

    Prolactin secretion is held down by dopamine; with less dopamine turnover the prolactin self-regulation feedback loops are disturbed. Age has a role in the efficiency of prolactin receptors on the hypo-thalmic dopamine neurons.

    Prolactin secretion is increased by seratonin, vasopressin, cholecstokinin, Beta endorphins, angio-tensin II, thyrotropin releasing hormone, enkephalilns Leu & Met, growth factors of epidermal and fibroblast, substance P, oestradiol 17Beta, and pituitary response to prolactin-releasing peptides.

    Normal testosterone release has a  peak that inhibits prolactin for 9 -11 hours; when testosterone release is at it's lowest point in releasing cycle then estradiol gets active. Estradiol cycle is for 15 - 18 hours; and when estradiol starts to kick in the prolactin cycle of 20 - 23 hours gets going again. Estradiol in high amounts has a paradoxical effect; it lowers prolactin secretion instead of normally working toward increasing prolactin secretion.

    Prolactin has a feed back loop with testosterone; it can act on the cognate receptors in the testes Leydig cells to raise testosterone. Testosterone, for it's part, can supress the synthesis of prolactin.

    After the aged male ejaculation there is a secretion of prolactin that is sustained for about 1 hour; this is refractory, and if there is arousal without actual orgasm then that prolactin refraction does not occur. With healthy young males there is no post-orgasm prolactin perfusion; and thus their refractory phase is brief.

    Where (in brain or in periphery) the prolactin is being considered has to be born in mind; as does the context (normal or altering). Chronic high prolactin in men is associated with poor sperm fertility.

    Carb engendered insulin resistance I can see as down stream leading to more free fatty acids circulating; that, and the fact that as we age our sub-cutaneous fat cells tend to get less responsive to insulin anyway. The "freed" fatty acids cause blood albumen to release tryptophan, a substrate for synthesizing seratonin (and thus more prolactin). With age there is less need for tryptophan amino acids and so the ample western protein supply of dietary tryptophan might be a co-contributor (among others).

  • Anonymous

    4/27/2011 7:45:28 PM |

    but who was troll?

  • Martin Levac

    4/27/2011 7:55:17 PM |

    Thanks Dr Davis for great advice as usual.

    Dr Davis, have you noticed that humans somehow are arrogant enough to believe that they can eat whatever they want and still maintain good health anyway? It's like pretending a lion or cow can eat whatever it wants with no ill effect. Or maybe it's just my impression lately.

  • Might-o'chondri-AL

    4/28/2011 1:07:17 AM |

    SSRI (seratonin selective re-uptake inhibitors) entail many formulations; a number of them are associated with loss of libido (reduced sex drive), ejaculatory anorgasm, +/- 25% men get erectile dysfunction  and sometimes impotence. Seratonin is a factor increasing prolactin production by the pituitary gland.

    Carbohydrate ingestion is a popular  on-line recommendation to boost seratonin levels. The National Sleep Foundation states carbs make tryptophan more available to the brain; once tryptophan crosses the brain blood barrier we can then make seratonin from it.    

    The journal "Public Health Nutrition" (Jan. 2007) details that our muscles will absorb amino acids except for tryptophan; the tryptophan builds up a "pool" in the blood to draw upon. When one is young &/or geneticly favored (among other exceptions) they are not plagued by the insulin resistance corollary of elevated free fatty acids causing their  albumen "pool" of tryptophan to head on toward excess seratonin synthesis.

    Doc likes to post provocative snippets; not footnotes we can find by searching the internet (try "Yandex" search engine if getting poor pickings). I am not fixated personally on low/no carbs, so am not advising anyone here about diet. My unsolicited observation is that age and time often confound an individual's metabolism; what was once "great" may sometimes merit reconsideration.

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    4/28/2011 8:42:32 AM |

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  • Tyson

    4/28/2011 3:15:31 PM |

    I think it would be more precise to say real men don't eat starches.  After all, vegetables are carbs, and I don't see anyone saying that veggies are bad for you....

  • CarbSane

    4/28/2011 3:58:08 PM |

    WOW!  So much misinformation in such a short post.  

    These kind of posts only undermine the nuggets of good advice you may provide.  

    By your logic the human race should not even have survived agriculture!

  • Might-o'chondri-AL

    4/28/2011 7:02:10 PM |

    Dr. Davis,
    Please post my "Endothelial dysfunction ..." comment, your
    Spam filter seems to have held it on 28th, following CarbSane's.

  • Martin Levac

    4/28/2011 7:47:59 PM |


    Every statement can be verified. Which one is not true, i.e. misinformation?

    As far as I can see, every one of those statements are true.

    @Matt Stone

    Congratulations, you have just discovered puberty (boy turns into man, doubles testosterone level in one year). You have also discovered the premature-puberty-triggering properties of wheat. It probably acts primarily through the insulin/IGF-1 pathway.

  • Steve

    4/29/2011 4:25:49 PM |

    Um...actually, non-starchy vegetables are not a carb source for humans, they convert into fat in our gut through bacterial fermentation. Vegetables are actually very low in sugars. Ruminants like cows ferment grasses into fats; they are getting most of their energy from fats.

  • David

    4/29/2011 9:28:09 PM |

    I am trying to de-program a friend that has been McDougaled.  McDougal is telling him all the scientific studies support hi-carb vegan diets.   Where can I find studies to counter these claims?  Especially about wheat.  I find Dr. Davis' articles on wheat quite compelling, but I need to show him studies.

  • BradC

    4/30/2011 1:05:53 AM |

    Facts are facts.  A man with a testimony is not at the mercy of a man with an argument.    Sugar/Carbs raise insulin levels.

    2 years lo carb hi fat.  30-50 carbs per day.  35 pounds lost.  Last VAP test was HDL 72, trig 52, LDL pattern A.  I'm 45 years old.  Exercise moderately.    I have discovered that FAT is your friend and sugar/carbs are the enemy.  Seems to work for me.

  • carb sane

    5/1/2011 10:47:11 AM |

    @Martin:  Perhaps let's start with evidence that carbs de facto  increase visceral fat.  So many of Dr. Davis' posts of late begin with either a false or unproven premise.  Some, like the recent battery acid post about oatmeal really take the cart over the cliff!

  • sss

    5/1/2011 3:17:53 PM |

    consider also: "life w/o bread" by wolfgang lutz, md, internist, wherein elevated insulin in response to carbohydrate ingestion is demonstrated to suppress testosterone and human growth hormone.  taubes also recognizes elevated insulin as a suppressant of t and hgh in gc,bc.  and sir, what a pity to see carb crank and her ilk here.  edit, please.

  • Terrence

    5/1/2011 5:50:29 PM |

    carb sane - why do YOU not respond to the others commenters here that are critical of your endlessly unsubstantiated comments (your nonsense, really)? Your insisting that  Dr Davis support HIS statements makes you look EXTREMELY hypocritical when you do not support your OWN statements.  

    Please do better. If you do not like what Dr Davis posts, you can simply stop reading his blog, and stop making silly, inane comments (that make you look like a hypocrite!).

  • Might-o'chondri-AL

    5/1/2011 6:49:21 PM |

    Dr. Davis,
    Again request you to kick out of old Spam filter my  28th April post on this thread.  When I sent it your old blog format showed it in comments section right after CarbSane's 28th posting.
    It  begins : "Endothelial dysfunction ...." and goes on to discuss particular  details related to  your premise that carbohydrates can contribute to male dysfunction.
    I don't  have it saved to re-send and won't spend time trying to recreate it .  It wasn't "X" rated and maybe some of the  guys here might find it interesting.

  • Might-o'chondri-AL

    5/1/2011 7:37:58 PM |

    CarbSane  shouldn't have to sing in the choir in order to participate and I,  for one,  hope she will continue to  comment  here.  I  request she stay on the island  ....
    I just noticed this  blog format now  uses a  "Reply" to individual commentator's posts (ex: Tyson's 28th Ap. comment got a reply underneath from Steve on 29th Ap.).  Since I follow an entire thread this is annoying; because now I can't just go to the last comment I read (or date)  and keep abreast.
    It's not like we are at a world events blog sounding of  on endless nuances.  Revisiting all the previous comments for   input is not  pleasant.  I will not use "Reply" and keep comments sequential,  like blog set up was before.

  • Might-o'chondri-AL

    5/2/2011 2:24:49 AM |

    CarbSane has pointed out that carbs do not "de facto increase visceral fat";  she did not deny that carbs are implicated in de novo lipo-genesis.  In a sense the deal with carbs   relationship to internal fats  is location, location, location; and probably time complicates  the  functional impact.

    High  carbohydrate diets increase triglycerides in the liver more than dietary fat does.  High dietary fat intake, in comparison, is what increases trigs in the plasma more readily (ie: chylomicron bound trigs) than ingested carbs.

    Repeated high carb  intake can upregulate a  lipo-genesis gene, the sterol regulatory element binding protein 1c (SREBP-1c);  once  SREBP gets active this gene keys more activity of enzymes  fatty acid synthesase  and more mRNA of acetyl-CoA carboxylase .  The liver then goes on to make more triglycerides.  

    A separate affect of high carb diets is the up-regulation of the enzyme pyruvate kinase, a glycolytic enzyme.  This involves the ChoRF (carbohydrate response factor) binding to a DNA ChoRE (carbohydrate response element) and then  the protein ChREBP (carbohydrate response element binding protein) complex hypes up the liver pyruvate kinase;  fostering a pre-disposition where mitochondria are set up  to burn glucose for ATP,  and not fatty acids nor ketones.

  • Martin Levac

    5/2/2011 1:57:28 PM |

    Well a priori, it's true. Carbs increase visceral fat. What makes you believe otherwise?

  • Martin Levac

    5/2/2011 2:05:16 PM |

    Actually, the opponents of the carb hypothesis always point out how fat cells always take in fat, and always put out fat. So do the proponents of the carb hypothesis incidentally. So in effect, any substance that causes fat cells to take in fat, increases fat cells. Thus, carbs increase visceral fat. De facto, sine die, that's it for that.

    To say carbs don't increase visceral fat is to say carbs don't ever take a trip inside a fat cell at any time whatsoever never ever. How is that even more plausible?

  • Francis

    5/2/2011 7:31:50 PM |

    Ian, since you have a better understanding of science, please explain what really happens when a man consumes "healthy whole grains".

  • carb sane

    5/2/2011 7:51:40 PM |

    No, a priori it's not true.  I didn't make the assertion, Dr. Davis did.  I'm asking for the evidence in support of that.  Why should I, or anyone for that matter, be tasked with disproving an assertion?  That's not how it works Martin.  To your other post, I didn't say carbs never cause fats to be deposited in visceral depots.  That would be ridiculous.  But I've yet to see evidence that they cause increased *accumulation* of fat in same.  Have you?  I'm interested in seeing this evidence.

  • carb sane

    5/2/2011 8:08:02 PM |

    @Mito:  It appears my response to you is in moderation limbo - links?

    Here's the stripped version:  @Mito: In humans, DNL is not a significant contributor to body fat accumulation. It only becomes quantifiably significant in the context of massive carbohydrate OVERfeeding. See studies linked in these blog posts of mine: Excess carbs converted to fat?, Postprandial DNL, Nutrient Fates, Fat Futile Cycling of Carb Excesses.

    Paul Jaminet over at Perfect Health Diet had an interesting take on the subject of that last link: How does a cell avoid obesity?.

    Are high carb consuming cultures known for their moobs?

    You sound like a sentient enough being (that's a little dig at the multiplication sentient being filter here ... not a dig on you!) to use the labels function or other search stuff to find the posts if you're interested.  All of those posts on my blog contain links to the full texts of some rather nice papers.

    @Terrence:  When someone makes an assertion, the burden of proof is on them to back that up.  

    @Martin:  It's pretty lame to conflate fat deposition - that we all agree occurs continually - with fat accumulation.  By your logic, everything causes visceral fat and all you fellas would be running about needing "Bros" or was that "Manziers"?  

    Dr. Davis' claims all hinge on some special tendency for carbohydrate intake to lead to visceral fat accumulation.  It could be true.  I haven't seen much in the way of evidence though.

    Back to Mito:  You said "High carbohydrate diets increase triglycerides in the liver more than dietary fat does."  I would point out the key word "in".  Are we talking elevated circulating triglycerides produced by the liver, or are we talking hepatic triglycerides?  Two different animals.

  • Terrence

    5/2/2011 8:21:12 PM |

    carb sane said "@Terrence: When someone makes an assertion, the burden of proof is on them to back that up. "

    Exactly WHEN will YOU "back up" your empty, meaningless assertions about Dr Davis's blog? WHEN???

  • carb sane

    5/2/2011 8:51:42 PM |

    Every assertion in this post hinges on increasing visceral fat.  Dr. Davis did not provide substantiation for his assertion that eating carbs does so per se.  That's his burden, not mine for pointing out his lack of substantiation.

  • Might-o'chondria-AL

    5/2/2011 9:07:50 PM |

    Fat intake doesn't get a free pass;  depending on the amount (& type) of dietary fat it can contribute to obesity. At 10 - 20% dietary fat there is negligible contribution to weight;  it doesn't trigger intestinal gene expression related to lipid metabolism that promote  a metabolic syndrome.  

    Constant intake of 20%  fat gets PPAR  (key lipid metabolism gene) busier; and by the time regularly consuming 30% dietary fat  gene alterations have more significant  potential to affect body weight. When the diet is 45% fat then fat absorption continues to occur even further down along in the gut as genes up-regulate there to handle the high fat intake.

    Physically active people (ex: exercisers , agrarian ancestors,  hunter gatherers, youths) up-regulate AMPK  (adenosine mono-phosphate activated protein kinase); which  effectively counter-balances the effect of  regular high fat intake down-regulation of AMPK (a energy sensor in a cell when cellular energy is low) .  High fat diet retards  phosphorylation of  AMPK  gene and this stymies the mitochondrial Uncoupling Protein (UCP3);  UCP must  first activate in order to switch over to burning fat in our cells.

    With AMPK down shifted the cell house- keeper recycling step of auto-phagy is inhibited; cells accumulate debris from oxidized fats and old mishapen proteins, with cell's attendant burden of ROS (reactive oxygen species, generated  from unchecked NADPH oxidase enzymatic activity).  Palmitate fat  (for example) can cause down-regulation of AMPK and downstream  activate inflammasomes (ex: NLRP3) that contribute to adipose tissue problems;  however,  adequate K+ (potassium) ions are able to nullify the inflammasome  spark.

    Palmitate  (ex: lard = palmitate and oleate, generates ceramide molecules  ( a sphingo-glycolipid;   "sphingo" was an original typographical error instead of discoverers  chosen "sphinx-" prefix, relating to how molecule interacts biologically and enigmaticly flips it's own molecular orientation); ceramides work against insulin action in our muscles, and thus can contribute to insulin resistance (ie: risk of  pre-diabetes). Muscle ceramides are mostly made with the  fatty acids derived  from dietary fat;  in the muscle they (ceramides) increase insulin resistance . Oleic  acid, and other long chain fats,  get into intestine chylomicrons as triglycerides; their route is via mesenteric lymph transfer into the blood circulation at the left-subclavian vein (ie: don't go directly to liver).

    So, ceramides in the liver are different because they are essentially  from de-novo lipogenesis; those ceramides are not considered to directly cause of insulin resistance. In other words,  if the individual has good insulin signalling in the liver  there is still the potential for muscle insulin signalling to be made worse by constant  high fat intake.

    Lifestyle and genetics are not discussed here as mitigating factors; the dietetic strategy of eating fat to lose weight is not being parsed here .  The modern diet of abundance,  high in both fat and carbohydrates, probably  is more of a double whammy for weight gain than either die factor taken in isolation; protein is not factored in here either .

  • Martin Levac

    5/2/2011 9:17:04 PM |

    You ask why should anybody be tasked with disproving an assertion. Imagine if scientists had the same idea. Nothing would be done. If you disagree, _you_ are making an assertion. By your own logic, _you_ are tasked to prove your assertion. That's how it works miss sane.

    You say it's ridiculous to say carbs don't cause fats to be deposited in visceral depots. This means you say carbs do cause fats to be deposited in visceral depots. However, you disagree that carbs cause increased accumulation of fat in same. In effect, you disagree that carbs cause any kind of dose response of the same. Now that's ridiculous.

    As for evidence of all this, Gary Taubes Good Calories Bad Calories is as good a place to start as any. The key detail is insulin and the fact that visceral fat tissue is so much more sensitive to it than other fat tissue. To summarize, carbs drive insulin drive excess fat accumulation. Since visceral fat is more sensitive to insulin than any other kind of fat tissue, carbs drive more excess fat accumulation there than anywhere else. I'll try to find a more specific source for this if I can. But don't wait up, I could be late.

  • Might-o'chondria-AL

    5/2/2011 11:21:11 PM |

    2 times got "server" error for comments here...this is a 3rd.
    I miss the old blog set up.

  • Might-o'chondria-AL

    5/2/2011 11:49:41 PM |

    Hi CarbSane,
    13 women & 5 men with BMI = 35 +/-7 and fatty liver (non-alcoholic) followed 2 different diets (2011 study) for 2 weeks only. I think this might validate one of Doc's contentions; sorry comment seems brusque . (Unrelated: yesterday I  said "in" the liver, no circulating trigs were detailed ;  and  said "high" carbohydrate, whereas you classify "extreme" as game changer.)
    Studied group 1, restricted calories to 1,200 & 1,500 daily for women and men, respectively. Weight loss after 2 weeks was +/- 4.3% and circulating triglycerides dropped 28 (+/- 23)%
    Studied group 2, restricted carbs to maximum of 2o gr./d for both sexes and had no calorie restriction. Weight loss after 2 weeks was +/- 4.3% and circulating triglycerides dropped 55 (+/-14)%

  • Might-o'chondria-AL

    5/3/2011 12:50:44 AM |

    edit correction from me CarbSane,  
    The triglycerides  in low cal/low carb  diet comparison I cited were explicity  liver trigs,  and not circulating trigs as I skimmed from my notes; measurement of liver trigs was done by magnetic resonance spectroscopy.  I thought my synopsis was unlikely so  just traced the study back to Am. Jrnl. Clin. Nut.(; sorry about the error.

  • Dr. William Davis

    5/3/2011 1:25:21 AM |

    Hi, Might--

    Sorry, but I can't find your lost comment. I don't know what's become of it.

    I'm also just getting used to this new format.

  • Martin Levac

    5/3/2011 3:09:53 AM |

    There's much evidence that it's the lack of fat in the diet that leads to increased caloric consumption. We could still posit that it's the caloric surplus that causes obesity. But we can't discount the possibility that it's the lack of fat (and the surplus of carbs) that causes obesity, which we then compensate for by eating more, and that's what we see.

    Considering many studies that show just that, that eating more fat leads to satiety which leads to eating less and losing weight simultaneously, and that hunger is an indicator of nutritional status (fuel partitioning for example: too much toward fat cells, too little toward every other cell), we can't just conclude that we grow fatter because we eat too much.

    Add to this the fact that many drugs, which contain exactly zero calories, make us fatter by themselves (and some make us leaner, ha!), and it's clear that the problem can't be expressed by calories alone.

    Ironically, you go on about physiological mechanisms to explain how fat can make us fat, but then proceed to posit that it could still be all about calories, i.e. abundance. Now that just doesn't make any sense to me. What's the physiological mechanism that controls "calories" then?

  • Jay Schwartz

    5/3/2011 6:16:12 AM |

    I enjoyed this post, but it begs the question: do real men look like Popeye?

  • Might-o'chondria-AL

    5/3/2011 6:23:47 AM |

    Hi Martin Levac,
    Just  saw your "reply" under my fat doesn't get a free pass comment; please tag me with new sequential thread comments (instead of as reply) to be sure I catch what you wrote.  I am not declaring excess weight gain is a clean cut factor of either  calorie, carb or fat intake;  genetics/epigenetics /age/pathology  will have a role in how susceptible one is to their  (carb & fat & protein) influence.  

    I don't have  any  specific formula to promote for every one. Satiation at a meal is  well worth considering as a control  factor; unfortunately,  we are able (and many have access) to not only keep eating, but also to soon " graze" on food again irregardless of our abated hunger.

    Fuel partitioning, as you mention it,  is a bit confusing to me. If your concept relates to how the body "burns" it's energy for functioning then that relates to one's underlying diet; we are set up to pump out energy in essentially distinct  mitochondrial steady states.

    Our cells don't want to be oscillating , in real time, between burning fat and glucose;  slipping in & out of phase, in real time,  is normally prevented by a high threshold  that must be exceeded to switch mitochondria over to other fuel.  In this case there must be a relatively strong OFF signal needed to get out of  the already up and running mitochondria mode,  and into the ON for a different mode for burning the other fuel.  

    The output of these types of cell signals (ie: Off/ On & On/Off  ) is a function of the previous history of trans-genetic activity (ex: genes key to burning fat or carbs and their respective cascades of genes that keep the process going) ; and this type of  threshold program is encoded on a chromosome  (like an epigenetic tweaking ).  That chromosome filters out other pulses of conflicting messenger RNA  (from typical gene transcriptions going on) that might otherwise cause other cascades leading to oscillation in the pathway of mitochondrial energy production.

    With one predominant nutrient  the dynamic is inclined toward working on a gradient; it is based on a dose response (ie: gradient of how much nutrient is put into equation)  and not just positive feedback (ie:  not just  "x" induces "y" and "y" loops through "z" to  make the action of "x" worthwhile enough  to keep doing things that way ), because  concentrations of a nutrient fine tunes the feedback response.  Biologists now call this  "hysteresis";  when a nutrient  modifies the traditional  stimulus-response relationship according to the history of past usage, and then the stimulus-response sets a high threshold (on a chromosome) for switching OFF in order to achieve a self-sustaining steady state burning the "favored" fuel.

  • Paul

    5/3/2011 7:22:19 AM |

    I have followed my own research since 2007. I started, via Dr Barry Peatfield, with Dr Broda Barnes (thyroid) and then Dr William McK Jeffries (adrenal).  Then, I found Carole Baggerly at GrassrootsHealth and Dr John Cannell at Vitamin D Council.  later still, I found Michael Pollan, Gary Taubes, Dr Mercola, Dr Kurt Harris, Dr Robert Lustig  and the wonderful Jimmy Moore with his podcast back library.  I also found Dr William Davis and this excellent blog.  

    What makes Dr William Davis special is that he does not promote just one thing (i.e. vitamin D3); instead he integrates the latest knowledge and provides guidance for a healthy lifestyle (for heart patients) covering lipids, blood sugar control, thyroid (iodine, T4, T3) and adrenal hormones (DHEA), vitamins D3, K2 and niacin, fish oil, carbohydrate restriction and grain elimination.  Whats more, as a practicing cardiologist, we get the considerable benefit of feedback from his ongoing patients.  

    I am pleased that the blog is concise and that it is not behind a paywall.  There are plenty of blogs which delve into every detail of every study, but thankfully this is not one of them.

    So, thanks to you Dr Davis.

  • Martin Levac

    5/3/2011 8:31:35 AM |


    Satiety seems to be the key factor for adherence. Like some say, hunger is not an option long term.

    Fuel partitioning is the distribution of fat between fat cells and all other cells, i.e. storage or consumption. Nutritional status would depend on this. If too much fat is shunted toward fat cells, then all other cells don't have enough and call for more. Fat cells themselves can call for more in spite of being full through their own hormonal signals. Insulin is the primary determinant for fuel partitioning. It's also the determinant of which fuel to burn.

    Incidentally, I thought that cells could switch on and off at will which fuel they burnt in their mitochondria. Since insulin is the primary determinant, and since cells can turn on and off insulin receptors, they can control their own choice of fuel. For example, if a cell contains its quota of glucose, it will turn off insulin receptors to prevent any more glucose from entering the cell. As it does so, it also causes a change in the signaling that would otherwise tell the cell to burn glucose, i.e. insulin. So while it is insulin sensitive, it burns glucose. But as soon as it's insulin resistant, it stops burning glucose and starts burning fat instead. This is normal insulin resistance, not pathological. But pathological insulin resistance applies to Dr Davis' post. Carbs cause this at some threshold.

  • carb sane

    5/3/2011 2:23:16 PM |

    @Martin:  I think you'll find Paul's article I linked to above (now published) rather interesting.

  • Terrence

    5/3/2011 6:06:16 PM |

    Martin Levac - do NOT expect miss sane to understand what you wrote - her mind is made up, and if anyone does not agree with her, they are wrong, wrong, WRONG, and  simply making assertions - as she endlessly asserts.

  • Might-o'chondri-AL

    5/3/2011 8:19:24 PM |

    Hi Martin Levac and anyone still reading,
    Thanx for the fuel partitioning orientation.   Maybe this elaboration will add to  your perceptions of fuel burning.

    Lipids (a.k.a. fats, fatty acids) actively induce the metabolic mechanism to preferentially burn themselves ( technically speaking for researchers : dietary fat gene transcription factor PPAR downstream induces  the pyruvate dehuydrogenase kinase 4,  PDK-4; which then reduces the levels of the enzyme pyruvate dehydrogenase and thus restrict glucose burning).

    Conversely, glucose triggers the mechanism to preferentially burn itself and by gene transcription stops lipid (fat)  burning (technically speaking for researchers:  insulin/glucose keep cell full of malonyl-CoA and this inhibits enzyme carnitine palmitoyl transferase, CPT;  fat can not get  shunted into the mitochondria fro burning). "Hysteresis"  ( explained previously and admittedly poorly)  is how there is chromosome threshold set up for controlling switching to burning one fuel vs. a different fuel;  potential to burn multiple fuels is not the same as getting to chose which fuel to burn.

    Insulin, and not just glucose, boosts glucose burning (glycolysis) and stymies fat burning (lipolysis); yet not all tissue groups have the same insulin sensitiviy. This is additionally relevant,  since say +/-  half of glucose is used by us without any involvement of insulin.

    Age is worth some precise discussion, especially since Type II diabetes is sometimes likened to advanced metabolic aging. With age the use of glucose for burning as energy increases, relative to the burning of fat & protein. This is notable in the heart, liver and brain;  while in the muscles the burning of glucose does relatively decrease compared to one's youth, but the burning of fat & protein decreases proportionately even more so.  In other words, post-prandial glucose favors burning glucose and due to hysteresis the mitochondria stay keyed to burn glucose;  even after the glucose levels drop back down to the pre-meal glucose level.

    Again, age and genetic obesity,  engender a decrease in leptin hormone response  (technically speaking for researchers: there is less hypothalmic alpha melanocyte stimulating hormone being made by  POMC,  pro-oipo-melanocortin). The increased glucose burning  generates more age related metabolic problems, such as obesity;  and  so, what we did in our youth is not always what we can  do  with impunity.

    When diet  relatively limits carbohydrates this  sets  the "hysteresis" threshold for mostly burning lipids (&/or protein) in the mitochondrial complex II;  this, however, does not mean glucose is not used as some fuel somewhere.  When blood glucose is low the atoms of Carbon from glucose burned  aren't burned in the mitochondrial complex I (technically:  don't make NADH from glycolysis); but rather, that glucose Carbon is put into the Pentose Pathway (technically:  makes NADPH ).

    Age is notorious for oxidative stress  (oxygen radicals on the loose in cells) and having low glutathione  (key anti-oxidant our cells make); glutathione, for it's part get's it's oxidant reducing power from the pentose pathway's NADPH.  Age commonly expresses less of the enzymes  that drive the production of  glutathione  (researchers:  age depletes isocitrate de-hydrogenase, the enzyme  needed for mitochondria to make NADPH  via NAP-   which interacts with glucose-6-phosphate dehydrogenase, the  rate limiting enzyme needing to be upregulated to keep the pentose pathway going).  

    In other words, age reduces our alternate pathway of glucose burning  and we get more oxidative stress  from using mitochondria complex I  for glycolysis;  mitochondria complex I burning for energy naturally spins off more  amounts of reactive oxygen molecules, these  can go on to potentially damage a cell.  A relevant example is that the shuttling of NAD+ to NADH from glucose burning in the mitochondria complex I has a potential oxidative  impact on the pancreatic Beta cells reaction over time;  youth and genetic fortune can keep cellular glutathione levels high to counter-act this Beta cell oxidative stress.

    Low blood sugar, like hypo-glycemia,  upregulates  some cell's  gene activator of GLUT 1  (glucose transporters in a cell);  this indicates the carbon atoms from glucose are not being burned in mitochondrial complex I (ie: not doing glycolysis),  but rather the pentose pathway is burning the sparse glucose.  At this point a high enough threshold has been reached to switch OFF mitochondial complex I glycolysis and the body is switching ON to use mitochondrial complex II for getting  energy by burning  fat (researchers: Beta-oxidation has prepped lipid carbon atoms to burn ) .

  • Martin Levac

    5/3/2011 10:54:03 PM |


    Thanks for the explanation. But I must admit that I will probably forget most of it pretty soon. I prefer to stick to simpler concepts. For example, heavy exercise depletes glycogen, which must be replenished. Cells open up more insulin receptors for this, they become insulin sensitive. If we don't eat carbs, this is done only as fast as the liver can put out glucose. If we eat carbs it's done as quickly as the carbs we eat. Considering that we can't store much more than about 2,000kcals of glycogen, mostly in the liver anyway, this is done _very_ quickly, a few minutes at most probably. As soon as that's done, cells close down their insulin receptors, they become insulin resistant. I'm just explaining what I understand, not necessarily how it really works. Anyway, as Taubes said, this effect lasts 36 hours at best, less if we eat carbs. So we could use this to prevent weight gain, but only if we don't eat carbs or not that much.

    The weight gain can be explained by the shunting of glucose toward fat cells because all other cells are now insulin resistant since they are now replete with glycogen. Even if we believe that all cells will start using glucose for fuel instead of fat when we eat carbs, we still have to explain how the insulin receptors will be opened up when the cells are already replete with glycogen, and don't want to take in any more glucose. So basically, when we eat carbs all the time, we're not dealing with the choice of glucose/fatty acids in all cells, but only in fat cells. Because only fat cells now accept glucose. Then we end up with the associated problems Dr Davis talked about like higher estrogen and prolactin to name a few.

    Does that fit in with what you know?

  • Might-o'chondri-AL

    5/4/2011 12:48:12 AM |

    Erectile dysfunction relation carbs,  a re-constructed lost comment ....

    Burning carbs (glycolysis)  for energy in the mitochondrial complex I  incurs super-oxide anions ( O2-) as  NADH generated .   Age  sees these super-oxides  anion levels increase and this can add &/or provoke pathological damage to the endothelial  vascular bed (for researchers: super-oxide locks up nitric oxide in the form of per-oxy-nitride); O2- + NO = ONOO-).

    Once endothelial dysfunction is going on the extra cellular anti-oxidant SOD (super oxide dismutase) is decreased and this compounds the situation;  little super-oxide (O2-) gets scavenged and nitric oxide (NO) gets degraded even more. NO is the main signal gas for penile erection;  NO is a downstream vasodilator allowing the extra 50 - 90 mmHg blood pressure to get into the penis.

    NO (nitric oxide  and nitric oxide  synthesase , NOS) works through a heme iron protein in hemoglobin  (researchers: via enzyme  heme oxygenase, due to NO affinity for FeII-heme protein) to act downstream on another enzyme (researchers: guanylate cyclase) to induce  a "second messenger"  inside the blood vessel's smooth muscle cells to relax and open. The "second messenger"  downstream from NO is the same molecule (researchers:  cyclic guanosine mono-phosphate, cGMP) targeted by Viagra; the drug works by stopping that "second messenger" from  degrading and thus vaso-dilation sustains erection.

    In the male genital endothelium there are the  heme enzymes for NO to work through;  although with progression of  endothelial dysfunction  the NO is  less free, and more so if  always burning glucose in the mitochondrial complex I and spinning off oxygen radical (super-oxide, O2-) to tie up the NO  .  The erection's  status  is complicated by the fact that the "second messenger" (cGMP) that works to relax/vaso-dilate blood down there
    is subject to degradation by another enzyme (researchers: phopho-di-esterase 5, PDE).

    There is yet another key enzyme (researchers: soluble guanylyl cyclase,  sGC) that is part of the cascade leading from NO to the "second messenger" (cGMP) that normally keeps the levels of the "second messenger" (cGMP) degrading enzyme (PDE-5) from getting too high. Of course, with endothelial dysfunction and less NO involved in the erectile
    cascade  there is less potential  ( less sGC)  to keep degradation enzyme (PDE-5) from knocking out the vaso-dilation;  then calcium rises inside the  blood vessel's smooth muscle cells,  less blood flows in and instead starts to flow out.

    There is a parallel/back-up signalling gas produced in the endothelium for signalling; this is CO gas, it has a feedback  loop with NO gas and can entrain a cascade that also, downstream, produces the "second messenger" (cGMP) for vaso-dilation induced erection.  The draw back is , that,  CO has 1,500 times less affinity than NO for the early step of  connecting  with  iron heme in our hemoglobin; and, not only that ,  but CO will move off of the heme slower than NO would.

    Using CO to drive the cascade  leading to downstream vaso-dilation  is  essentially  just plain slow in real time; and then too,  not enough of the intermediate enzyme (sGC)  that prevents degradation enzyme (PDE-5) is being made fast enough .  An  initial erection can be achieved in many instances through the agencies of CO &/or through a sequence of a little NO passing job on to CO;  unfortunately this erection fades and then can not be regained in a timely manner.

  • carb sane

    5/5/2011 10:25:32 AM |

    @Mito:  A loss of hepatic fat in a very short term carb restriction is a bit of a stretch to imply the reverse that carbs cause the fat accumulation per se.   There's also the problem with conflating hepatic fat with visceral fat.  Even all visceral fat doesn't appear to be the same - e.g. omental vs. retroperitoneal.

  • carb sane

    5/5/2011 10:37:41 AM |

    Oops hit post while a part of reply was highlighted so it got truncated.  Sorry so abrupt.  I believe this "reverse logic" is rampant and unfortunately used all too often to support certain contentions.  For example just because many lose weight cutting carbs doesn't make carbs fattening.  

    I also added to that last sentence:  So many studies further confuse the subject because some show it's visceral, some subQ abdominal, some both, some none wrt various metabolic factors.

  • Martin Levac

    5/5/2011 12:08:43 PM |

    @Carb Sane

    Yes, this "reverse logic" is rampant. But we call it "implication". Like so "this evidence implies that conclusion". Science is full of such "reverse logic". And, it's proof that scientists use their brains to figure out how things work. It also helps scientists devise tests to refute those implied conclusions. That's also how science works.

    Incidentally, for the subject we're discussing here, there is _direct_ evidence that carbs cause excess fat accumulation. No need to refer to the previous evidence, or the previous implications, or the previous conclusions. In fact, there's about 150 years of it.

    Now you're attempting to bring confusion yourself by pointing out how different fat tissue respond differently. We already know about that. It does not refute anything Dr Davis said about carbs. Carbs still cause excess fat accumulation, and all the other nasty stuff he mentioned.

  • Might-o'chondri-AL

    5/5/2011 7:36:58 PM |

    Hi CarbSane,
    Read me clearly:  I don't write that a carb automatically  always causes an iota of body fat;  and  I don't give a pass to dietary fat.    Doc, unlike me, has  a clinical practice to base his declarations on;  I am merely trying to understand any science that might validate his point(s).

    Denmark " Inter99 Study"  of 3,164 adults with normal glucose tolerance tracked over 5 years data is interpreted in journal "Diabetic Medicine",, April 2009, vol. 26, issue 4, pg. 377-383.  Synopsis is:  2 hour post glucose (2hrPG; using oral glucose tolerance test as the glucose load) has  a relationship to overall degree of obesity; whereas fasting blood sugar has more of a relationship to larger abdominal/waist circumference.    

    Doc's contention is carbs can raise the blood glucose and this contributes to getting fat;  which (2hrPG) the Inter99 study links to % obesity.   One  can argue  the issue from another direction;  namely that incipient obese fat, from any number of assorted causes  (ie: not carb induced) can , down the line,  cause the situation whereby 2hrPG ( blood sugar response) then goes on to predict waist circumference and BMI.

    Omental adipose tissue is  considered as part of the  regulatory loop  of insulin sensitivity.  One of the causes of lipids (fatty acids, fats) going into the omental adipose cells (and liver cells) is when sub-cutaneous fat can't hold all the lipids presented to it (sub-cutaneous fat).

    Size matters too, since large adipocytes produce more pro-inflammatory cytokines;  thus,  an individual with  factors  limiting pre-adipocytes from differentiating into functional adipocytes  is at risk of pumping up their  existing adipocytes.  This  is one way dietary excess  is modified by the metabolic coping  of each individual;  in other words not every obese person  is going to get Type II diabetes.

    Omental macrophages, and their cytokines, are associated with greater liver inflammation; and an altered pattern of  fibrosis in the liver.  The omental macrophage risk to the liver exists even if there is no insulin resistance;  ie:   not only Type II diabetics but the obese  can have  liver risks.

  • Hans Keer

    5/8/2011 4:36:25 AM |

    Real men avoid grains (lectins, gluten, anti-nutrients), that's for sure. But that does not mean that they have to avoid all carbohydrates. Especially starches and glucose are, when cosumed in correspondence with your lifestyle, tolerated perfectly by the human body. It's time to get more specific doctor Davis. We cannot just keep advocating GCBC. VBR Hans

  • carb sane

    5/9/2011 1:37:00 PM |

    Martin, Dr. Davis made the specific assertion that carbs cause visceral fat accumulation (implied to a greater degree than fats or protein).  Where's the evidence for that?  Eating leads to fatty acids moving into fat cells and getting deposited.  That's not "fat accumulation" though.  Accumulation involves net deposition vs. mobilization and that is determined by how much carb, fat and protein someone consumes.   The statement "Carbs still cause excess fat accumulation, and all the other nasty stuff he mentioned." is unsubstantiated.  It is repeated over and over in the low carb echo chamber, but there's no evidence for it.

  • Jonathan

    5/12/2011 9:43:29 PM |

    What has happened?!?  This comment section is ridiculous!  You trolls need your own site or forum to go nuts on and bash Dr. Davis there.  Or better yet, meet each other somewhere, throw your weight around in person, and claim your position as the smartest person in the world.

  • Renfrew

    5/17/2011 8:42:12 AM |

    Hi Dr. Davis,

    what is happening? No new post lately. On vacation? Sick? Tired?
    I miss your musings and posts!

  • FDK

    5/21/2011 4:21:29 AM |

    All - I think we should periodically go back to how our particular bodies evolved ..... (e.g Why/How do bears get fat before the winter).  Single season - meaning only available once per year - items are typically high in Carbs... Berries, Fruits, Roots, etc... Green leafy veggies are low in carbs... Grains from grasses are once per year.... highly processes they are acres of starch to our army of enzimes and produce huge insulin response... even Bears never had the availablity of wheat flour... otherwise they would have gotten fat enough, soon enough without having to go up and down all those mountain slopes looking for huckleberries and ants....

    Man ... as usual ... is very efficient at what he does.....

  • Nat Purcell

    6/25/2011 4:34:03 PM |

    You're an idiot and a charlatan.

  • Nunya

    9/1/2011 5:50:13 PM |

    Because on that list potatoes are pretty much the only thing listed that is actually bad and you probably burn more calories than you take in.