Medicare and The Law of Unintended Consequences

This post carries on the line of conversation begun in The Origins of Heart Catheterization: Part I and Part II.



While Dr. Sones labored in the relative obscurity of his catheterization laboratory, the American public was experiencing a crisis in healthcare availability, particularly among the over-65 age group. The population of elderly in the U.S. was growing rapidly. Between 1950 and 1963, their ranks grew from 12 million to 17.5 million. The cost of hospital care was also increasing 6.7% annually, several times the rate of increase in the cost of living of the time. From 1950 to the day of Dr. Sones’ discovery, the average cost for a day in the hospital jumped from $29 to $40. As a result, private health insurance carriers were forced to increase rates, driving premiums higher and farther out of reach for many. Half of all elderly were uninsured. Many feared that, while the sophistication of medical services advanced, healthcare was becoming increasingly unavailable to many, perhaps most, Americans.

The pivotal contribution that ignited wide dissemination of healthcare technology didn’t come from a physician, nor someone in healthcare. It was spurred by a nearly-forgotten bureaucrat. Without the behind-the-scenes laboring of this one man, the present healthcare system might be quite different.

It was largely the work of Nelson H. Cruikshank, an ordained Methodist minister with a Master of Divinity degree and veteran of battling for rights of the elderly and poor deprived of health care. For 10 years, Cruikshank served as director of the AFL-CIO's Social Security Department and had been instrumental in getting the Social Security Disability act passed. Working on the side of organized labor but maintaining the public demeanor of a church pastor, Cruikshank gained a reputation as a fighter for the working man, one who didn’t back down from a political brawl. In an interview regarding the question of corporate-retained earnings for capital investment, he blasted the practice, calling it "taxation by corporation without representation. Through prices paid for consumer goods, buyers are providing capital for industries over which they have no control and from which they receive no dividends” (Time Magazine, Dec. 20, 1948).

For years, Cruikshank lobbied tirelessly on behalf of American unions to bring the new national healthcare bill, known as Medicare, to a vote on the floor of Congress. Numerous efforts at a national program had languished for a decade before Medicare was drafted, and the Medicare legislation remained bottlenecked for years in committees. Cruikshank’s relentless and forceful persuasion was instrumental in finally bringing the bill to a vote. Among the most vocal opponents Cruikshank parried was the American Medical Association (AMA), terrified that the new program would lead to loss of control over healthcare delivery and reimbursement. The AMA labeled Medicare "the most deadly challenge ever faced by the medical profession."

Cruikshank proved how tough he was when he faced off with Dr Morris Fishbein, then president of the AMA, in a radio debate. Oscar R. Ewing, attorney and Democratic political organizer under the Truman administration, offered these reminiscences of the debate:

“Dr. Fishbein described the horrible confusion that existed in the [government-run] British Health Service that had recently been established in Britain. He told of the utter confusion that he found existed when he was in England a few weeks previously; that there were long queues in every doctor's office, that doctors were overburdened with paper work; that a mother who wanted an extra allowance of milk for her sick child had to get a doctor's prescription for it and then go to the Health Department for permission to buy the milk. Dr. Fishbein painted a picture of complete confusion.

“After Dr. Fishbein had described all these horrible details he found existing when in England a few weeks earlier, Mr. Cruikshank pulled out this particular diary [published in a nationally-syndicated column called “Dr. Fishbein's Diary” ] of Dr. Fishbein in which he described his last visit to London. He had arrived in London Friday morning and that afternoon had gone out to spend the weekend with Lord and Lady so-and-so at their country place; that he'd come back to London Monday morning, had stopped by the Health Department to pick up some papers, and had gone on to catch the noon plane for Paris. So the questioner then asked, "Well, is your appraisal of the British Health Service based on those few hours in London?" The question was a stinger and pretty much discredited Dr. Fishbein.”


(Interview by Mr. J.R. Fuchs, April 29, 1969; Harry S. Truman Library Archives)



Cruikshank went on to point out that Dr. Fishbein had indeed never visited the offices of British general practitioners and had spent his brief stay in the company of British aristocracy, attending the Olympics, then making the rounds of Parisian night clubs. Fishbein stumbled through the remainder of the interview, trying unsuccessfully to cover up his gaff. Dr. Fishbein was forced out of his post as AMA president by his peers shortly following the humiliating episode.

Largely due to the years of behind-the-scenes maneuvering by Mr. Cruikshank, on July 30, 1965, President Lyndon Johnson signed the Social Security Amendment that enacted the Medicare program. The legislation that survived into law included Medicare Part A, the portion of the program providing payment for hospital-based diagnostic and treatment services, and Medicare Part B, allowing payment for office-based services and outpatient diagnostic tests.

Finally, after decades of political battles, a national healthcare bill had been passed. Although benefits were restricted to only those eligible for Social Security benefits, it represented a start, a first step toward greater access to healthcare for the broader American public.

At first, the full implications of the Medicare program were not apparent. But as healthcare technology advanced, including that sparked by Sones’ innovation in coronary imaging, Medicare, much as engineered in large part by Nelson Cruikshank, proved a bonanza of payment for heart procedures. Medicare also set the pace for the payment for procedures by non-government, private health insurance.

Thus the stage was set. Thanks to Medicare, over the next 40 years cardiovascular healthcare services, yielding generous revenue for practitioners and hospitals, exploded on the scene, much to the surprise of many, including the AMA. When then president of the American College of Cardiology, Dr. Charles Fisch, was asked how the passage of Medicare affected cardiology, he replied, “It made cardiologists rich, as simple as that” (American Cardiology: The History of a Specialty and Its College, W. Bruce Fye, MD). Indeed, from its introduction in 1965 to 1980, Medicare payments for health claims ballooned 10-fold from $9.6 billion to $105.7 billion, a substantial portion of which went to pay for cardiology claims.

Little did Nelson Cruikshank, ministerial defender of the working man, anticipate that the Medicare he helped engineer would prove to be the catalyst for explosive growth of the modern cardiovascular healthcare system. Ironically, the program of healthcare-for-all that Cruikshank envisioned has, over the last 40 years, soured into a self-serving system that has been corrupted by the profit motive.

In too many instances, it’s a system that uses the working man as its victim, rather than its beneficiary.

Comments (6) -

  • Scott Miller

    11/5/2008 3:47:00 PM |

    Another great historical article.  Thanks.

    Question: Now that Obama is confirmed, how do you think this will affect the medical profession?  In particular, I've heard him place some emphasis on prevention. Does this give you hope that the current sad state of government priorities will change?

  • Anonymous

    11/5/2008 5:39:00 PM |

    How I wish I had had all this information back in 2004 when my mother went through her final illness, which included catheterization and bypass, followed by a massive stroke that left her aphasic and paralyzed and on a ventilator until her last hours. At the time I trusted the doctors who said she had to have the catheterization and bypass, but now I wonder if they weren't racing to see how much Medicare and supplemental insurance money they could get thanks to her weakening heart before it gave out.

    Universal health care for all sounds like such a good idea in theory, but just how much will our taxes have to increase to finance all the medical greed of those counting on the government to pay for everything they prescribe? And I can't imagine what a mess medical care will be managed by a federal bureaucracy. I just hope the way I eat now will keep me out of the clutches of the medical establishment as much as possible.

  • Dr. William Davis

    11/6/2008 2:39:00 AM |

    Although I am hoping for positive change legislatively, I don't think that the prevention vs. catastrophic care issue can be adequately addressed by policy.

    My view is to educate the public to develop informed consumers. That is why I do what I do. We should all be trying to educate those around us on the sometimes perverse financial equation that operates in healthcare.

  • Anna

    11/6/2008 10:44:00 PM |

    I hear a lot about the astronomic costs of health care for the baby boomers (I was born at the tail end of the boomers).  I doubt there's much meaningful we can do about the health of the boomers at this point, but I do wonder a lot about what will happen to the health care of the younger generations, the ones who have and are growing up with the low fat/high carb nutrient depleted industrial foods.  They're already starting out with so many health disadvantages.

    I'm doing what I can to get my 10 yo started in the right direction, so that he knows what are good and poor food choices that those choices do make a difference (he's already started to notice that the kids in his class with "issues" often have poor diets).   I'm trying to show him when we go on road trips through agricultural belts that the production of the grocery store foods is quite different from the kinds of local, small traditional farm foods I seek out for our family.  I can only hope he'll have the option to put that knowledge into practice when he's out on his own.

  • Anonymous

    11/7/2008 9:14:00 PM |

    One thing we baby boomers need to think about is keeping our legs strong and our balance good,
    Falls kill a lot of older people.
    So, include some balance work in with the aerobic fitness.

    Jeanne Shepard

  • Anna

    11/9/2008 8:56:00 PM |

    I agree with Jeanne about the focus on balance as a way to avoid the problems caused by falls, not to mention modifying the home to reduce things which tend to contribute to falls - "throw" rugs; inadequate hand grips on steps, showers, & tubs:, adequate lighting, and simply keeping walking surfaces clear of items.  As a good example, late last winter my 80 yo MIL suffered a fractured tibia while getting up in the night; she slipped on a magazine she left on the floor next to the bed.  Thank goodness she wasn't still living alone.

    But rather than cardio, I would focus more avoiding falls and maintaining good balance through strength and weight-bearing exercise/training.  

    Aerobic/cardio exercise is rather indirect, more time consuming, and less efficient (not to mention too much cardio can wear out the joints and cause overuse injuries).  There are plenty of baby boomers facing joint replacements thanks to too much aerobic focus in the 80s and 90s.

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In search of wheat: We bake einkorn bread

In search of wheat: We bake einkorn bread

With the assistance of dietitian and health educator, Margaret Pfeiffer,MS RD CD, author of Smart 4 Your Heart and very capable chef and breadmaker (previously, before she gave up wheat), we made a loaf of bread using Eli Rogosa's einkorn wheat. Recall that einkorn wheat is the primordial 14-chromosome wheat similar to the wild wheat harvested by Neolithic humans and eaten as porridge.

The essential question: Has wheat always been bad for humans or have the thousands of hybridization experiments of the last 50 years changed the structure of gluten and other proteins in Triticum aestivum and turned the "staff of life" into poison? I turn to einkorn wheat, the "original" wheat unaltered by human manipulations, to figure this out. While einkorn wheat is still a source of carbohydrates, is it something we might indulge in once in a while without triggering the adverse phenomena associated with modern wheat?   

Here's what we did:

This is the einkorn grain as we received it from Eli's farm. This was enough to make one loaf (approximately 3 cups).











The einkorn grain is a dark golden color. I tried chewing them. They taste slightly nutty. They soften as they sit in your mouth.





Here's Margaret putting the einkorn grain into the electric grinder.









We tried to grind the grain by hand with mortar and pestle, but this proved far more laborious than I anticipated. After about 15 minutes of grinding, this is what I got:



Barely 2 tablespoons. That's when Margaret fired up the electric grinder. (I can't imagine having to grind up enough flour by hand for an entire family. Perhaps that's why ancient cultures were thin despite eating wheat. They were just exhausted!)

We added water, salt, and yeast, then put the mix into an electric breadmaker to knead the dough and keep it warm.

We let the dough rise for 90 minutes, much longer than conventional dough. The einkorn dough "rose" very little. Margaret tells me that most dough made with conventional flour rises to double its size. The einkorn dough increased no more than 20-30%.

The einkorn dough also distinctly smelled like peanut butter.





After rising, we baked the dough at 350 degrees F for 30 minutes. This is the final product.

Because I want to gauge health effects, not taste, the bread we made had no added sugar or anything else to modify taste or physiologic effect.

On first tasting, the einkorn bread is mildly nutty and heavy. It had an unusual sour or astringent taste at the end, but overall tasted quite good.

Next: What happens when we eat it? I'm going to give the einkorn bread (I've got to make some more) to people who experience acute reactions to conventional wheat and see if the einkorn does the same. I will also assess blood sugar effects since, after all, hybridizations or no, it is still a carbohydrate.



Margaret Pfeiffer's book is available on Amazon:

Comments (6) -

  • Jim Purdy

    6/12/2010 1:41:24 PM |

    QUOTE:
    " I'm going to give the einkorn bread (I've got to make some more) to people who experience acute reactions to conventional wheat and see if the einkorn does the same."

    Who knows?  You may have a promising and prosperous future as an einkorn baker.

    Jim Purdy
    The 50 Best Health Blogs

  • Anonymous

    6/12/2010 1:52:29 PM |

    Mortar and pestle are not the best implements to grind flour. It's no wonder you couldn't get it done. Take a look at this. I have played with this kind of grinder in my childhood and its eminently doable and good exercise.

    Please post on the blood glucose effect findings.

  • Anna

    6/12/2010 2:47:33 PM |

    Have you considered incorporating wild yeasts and long fermentation time (as in days days, not minutes or hours) instead of using a single commercial strain of yeast?  In addition to the wheat having changed in recent generations, so has the yeast.  While this bread may have an ancient strain of wheat, it still seems pretty modern in other ways.

    Long fermentation times with wild yeast sourdough starter allows for fuller breakdown of the gluten protein.  Many, if not most sourdough breads on the market aren't truly sourdough fermented, but merely enhanced with sourdough starter or sour flavoring.  Commercial yeast is still used to speed dough rising and production times.  

    I haven't yet tried the "bread man's" bread below (as I also have to consider the CHO/BG issue in addition to the gluten) but if I was going to eat wheat bread again, this is the kind of bread I would try to make (he does conduct workshops, btw).  This year I drive  through LA regularly so if the timing works out on one of my trips, I may stop and try the bread sometime.  

    www.cheeseslave.com/2009/03/31/top-10-reasons-to-eat-real-sourdough-bread-even-if-youre-gluten-intolerant/

    www.yelp.com/biz/bezians-bakery-los-angeles

  • DogwoodTree05

    6/12/2010 3:13:30 PM |

    $24 + labor to yield one loaf of bread.  One would have to be a diehard bread lover to spend that time and money.  When I consider the flavor and nutrient opportunity cost of that loaf in the form of pastured meats, fresh cream, ripe berries and cherries all deliciously in season right now, that golden brown loaf doesn't look so appealing.

    I am interested in knowing how your subjects react to einkorn wheat.

  • David

    6/12/2010 3:16:56 PM |

    Fascinating experiment. I'm looking forward to seeing more on this.

  • Anonymous

    6/15/2010 2:01:42 AM |

    Too bad you didn't try making sourdough bread with it instead of conventional yeast bread.

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End-stage vitamin D deficiency

End-stage vitamin D deficiency

Let me paint a picture:

A 78-year old woman, tired and bent. She's lost an inch and a half of her original height because of collapse of several vertebra in her spine over the years, leaving her with a "dowager's hump," a stooped position that many older women assume with advanced osteoporosis. It's also left her with chronic back pain.


(Image courtesy of National Library of Medicine)

This poor woman also has arthritis in her knees, hips, and spine. All three locations add to her pain.

She also has hypertension, a high blood sugar approaching diabetes, and distortions of cholesterol values, including a low HDL and high triglycerides.

Look inside: On a simple x-ray, we see that the bones of her body are unusually transparent, with just a thin rim of bone at the outer edges, depleted of calcium. Weight-bearing bones like the spine, hips, and knees have eroded and collapsed.

On an echocardiogram of her heart (ultrasound), she has dense calcium surrounding her mitral valve ("mitral anular calcium"), a finding that rarely impairs the valve itself but is a marker for heightened potential for heart attack and other adverse events. Her aortic valve, another of the four heart valves, is also loaded with calcium. In the aortic valve, unlike the mitral valve, the collection of calcium makes the valve struggle to open, causing a murmur. The valve is rigid and can barely open to less than half of its original opening width.

If a heart scan were performed, we'd see the coronary calcification, along with calcification of the aorta, and the mitral and aortic valves.

Obviously, it's not a pretty picture. It is, however, a typical snapshot of an average 78-year old woman, or any other elderly man or woman, for that matter.

This collection of arthritis, osteoporosis, coronary and valve calcification, high blood pressure, abnormal cholesterol patterns, and pain is not unusual by any stretch. Perhaps you even recognize someone you know in this description. Perhaps it's you.

Look at this list again. Does it seem familiar? I'd say that the common factor that ties these seemingly unrelated conditions together is chronic and severe deficiency of vitamin D. Vitamin D deficiency leads to arthritis, osteoporosis, coronary and valve calcification, high blood pressure, abnormal cholesterol patterns, and pain.

Should we go so far as to proclaim that aging, or at least many of the undesirable phenomena of aging, are really just manifestations of vitamin D deficiency? I would propose that much of aging is really deficiency of vitamin D, chronic and severe, in its end stages.

My colleagues might propose a 30- or 40-year long randomized trial, one designed to test whether vitamin D or placebo makes any difference.

Can you wait?

Comments (7) -

  • Darren

    12/6/2007 5:43:00 PM |

    So I'm not a cancer patient but would the same 1,000 IU's / 30lbs of bodyweight be a good guideline for us as well?  

    Also he mentions blood calcium test monthly - how much of a concern is potentially elevating blood calcium for a 4K-6K IU/day intake of D3?  Would K2 reduce or increase blood calcium?  I'm just not sure it's practical for most people to get a monthly test...

  • chickadeenorth

    12/7/2007 5:12:00 AM |

    Wow interesting reads about Vit D.

    Could you help me understand more why the Vit D in softgel is better than the dry??Mainly absorption??

    Also why check the calcium levels monthly along with the 25(OH)D??

    I will support this newsletter, thanks once again.

  • Dr. Davis

    12/7/2007 11:48:00 AM |

    Softgels are oil-based; tablets are not. You can therefore force the tablet D to be absorbed by including a lot of oil, e.g., a teaspoon of olive oil. However, the absorption tends to be erratic, in my experience. Softgels are very consistent.

    We do not advocate monthly calcium levels.

  • Anonymous

    12/8/2007 1:00:00 PM |

    Just a commentary on the article,  I'm a believer in your program and as such have been telling everyone about it that will listen.  I'm a male, and I've found that convincing other males of TYP has been relatively easy.  Most guys I know now follow the TYP program somewhat to a degree.  Females I know though have been a tougher sale.  And I believe this lack of interest in TYP by females I know has probably been caused by  differences in how males and females relate to each other.

    I distribute your blog postings and this one apparently hit a cord with females.  I heard from a friend that his wife is now raiding his vitamin D bottle.  Another two female relatives have called wanting to know what vitamin D to use and where to buy.  As funny as this sounds, I think the new found interest in TYP by females I know is because of the female orientated subject in this blog.

  • Dr. Davis

    12/8/2007 1:27:00 PM |

    Interesting observation!

    Maybe there's a lesson for us to learn from your observation.

  • buy jeans

    11/3/2010 6:18:21 PM |

    In other words, the findings of this substantial observation suggest that the ranges of TSH usually regarded as normal contribute to coronary events, cardiac death, as well as lipid patterns. While several other studies have likewise shown a relationship of higher TSH/lower thyroid function with lipid abnormalities and overt heart disease, no previous study has plumbed the depth of TSH to this low level and to such a large scale.

  • Tammy Regis

    8/5/2011 8:19:10 PM |

    I like all what you wrote except you make no mention at all about muscle tissue.  Her pecs and abdomals are locked short while her neck and spinal muscles are locked long.  There is a direct mind / body connection here that Western medicine has still not caught on to.  Anyone can take a moment to think of something sad or worrisome, and take note of their posture change when they think of something happy or exciting.  A lot of people are walking dead.

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Sterols should be outlawed

Sterols should be outlawed

While sterols occur naturally in small quantities in food (nuts, vegetables, oils), food manufacturers are adding them to processed foods in order to earn a "heart healthy" claim.

The FDA approved a cholesterol-reducing indication for sterols , the American Heart Association recommends 200 mg per day as part of its Therapeutic Lifestyle Change diet, and WebMD gushes about the LDL-reducing benefits of sterols added to foods.


Sterols--the same substance that, when absorbed to high levels into the blood in a genetic disorder called "sitosterolemia"--causes extravagant atherosclerosis in young people.

The case against sterols, studies documenting its coronary disease- and valve disease-promoting effects, is building:

Higher blood levels of sterols increase cardiovascular events:
Plasma sitosterol elevations are associated with an increased incidence of coronary events in men: results of a nested case-control analysis of the Prospective Cardiovascular Münster (PROCAM) study.

Sterols can be recovered from diseased aortic valves:
Accumulation of cholesterol precursors and plant sterols in human stenotic aortic valves.

Sterols are incorporated into carotid atherosclerotic plaque:
Plant sterols in serum and in atherosclerotic plaques of patients undergoing carotid endarterectomy.




Though the data are mixed:

Moderately elevated plant sterol levels are associated with reduced cardiovascular risk--the LASA study.

No association between plasma levels of plant sterols and atherosclerosis in mice and men.




The food industry has vigorously pursued the sterol-as-heart-healthy strategy, based on studies conclusively demonstrating LDL-reducing effects. But do sterols that gain entry into the blood increase atherosclerosis regardless of LDL reduction? That's the huge unanswered question.

Despite the uncertainties, the list of sterol-supplemented foods is expanding rapidly:




Each Nature Valley Healthy Heart Bar contains 400 mg sterols.












HeartWise orange juice contains 1000 mg sterols per 8 oz serving.













Promise SuperShots contains 400 mg sterols per container.














Corozonas has an entire line of chips that contain added sterols, 400 mg per 1 oz serving.














MonaVie Acai juice, "Pulse," contains 400 mg sterols per 2 oz serving.














Kardea olive oil has 500 mg sterols per 14 gram serving.










WebMD has a table that they say can help you choose "foods" that are sterol-rich.

In my view, sterols should not have been approved without more extensive safety data. Just as Vioxx's potential for increasing heart attack did not become apparent until after FDA approval and widespread use, I fear the same may be ahead for sterols: dissemination throughout the processed food supply, people using large, unnatural quantities from multiple products, eventually . . . increased heart attacks, strokes, aortic valve disease.

Until there is clarification on this issue, I would urge everyone to avoid sterol-added "heart healthy" products.


Some more info on sterols in a previous Heart Scan Blog post: Are sterols the new trans fat? .

Comments (10) -

  • TedHutchinson

    3/14/2009 3:10:00 PM |

    Margarine and Phytosterolemia

    Stephan Wholehealthfoodsource also has a recent interesting blog on this topic.

  • Anne

    3/16/2009 2:19:00 AM |

    The more I read about processed foods, the more I stick to whole foods. I was part of the trans fat experiment. I am not willing to take part in the sterol test.

  • Rick

    3/16/2009 5:43:00 AM |

    Most medical blogs, though useful, give us a "Choose your guru" kind of model. This post exemplifies an approach that can be summarised as: "Here's what I think, and why; you can follow my recommendations, or you can do your own research; and what's more I'll give you some pointers to get you started." Great stuff. Thank you.

    On the issue of plant sterols, the standard argumentation appears to be: "Cholesterol is bad. Anything that displaces cholesterol must be good. We're not interested in what the substances displacing cholesterol might be doing." Unfortunately, the argument is usually tacit; otherwise, it would be immediately obvious how misguided this line of thought is.

  • renegadediabetic

    3/16/2009 1:33:00 PM |

    Here they go again.  They try to solve a non-existant problem and just make things worse.

    There's big $$$$$$ in cholesterol and this is all about $$$$$, not health.

  • Anna

    3/17/2009 3:43:00 AM |

    I rarely shop in regular supermarkets anymore (farm subscription for veggies, meat bought in bulk for the freezer, eggs from a local individual, fish from a fish market, freshly roasted coffee from a local coffee place, etc.).  What little else I need comes from quirky Trader Joe's (dark chocolate!), the fish market, farmer's markets, a small natural foods store, or mail order.  

    When I do need to go into one of the many huge supermarkets near me, not being a regular shopper there, I never know where anything is, so I have to ramble a bit around the aisles before I find what I'm looking for (and I almost always can grab a hand basket, instead of a trolley cart).  

    It's almost like being on another planet!  There's always so many new products (most of them I hesitate to even call food).   It's really a shock to the senses now to see how much stuff supermarkets sell that I wouldn't even pick up to read the label, let alone put in a cart or want to taste.  I'm not even tempted by 99% of the tasting samples handed out by the sweet senior ladies in at Costco anymore (only thing I remember tasting at Costco in at least 6 mos was the Kerrygold  Irish cheese, because I know their cows have pasture access and it's real food).

    What's really shocking to me is how large some sections of the markets have become in recent years.  While Americans got larger, so did some sections of the supermarket (hint - good idea to limit the consumption of products from those areas).  Meat and seafood counters have shrunk, though.  Produce areas seem to be about the same size as always (but more of it is pre-prepped and RTE in packaging.

    But the chilled juice section is h-u-g-e!  And no, I don't think there is a Florida orange grove behind the cases.  Come on, how much juice do people need?  Juice glasses used to be teeny tiny, for a good reason.  To me it looks like a long wall stocked full of sugar water.  Avoiding that section will put a nice dent in the grocery expenses.

    The yogurt case is also e-n-o-r-m-o-u-s!   Your 115 yo Bulgarian "grandmother" wouldn't know what to make of all these "pseudo-yogurts"!  Chock full of every possible variety, but very little fit to eat.  The only yogurts I'll look at are made with plain whole milk, without added gums, emulsifiers, or non-fat milk solids, and live cultures (I mostly buy yogurt now and then to refresh my starter culture at home).  I can flavor them at home if needed.   The sterols are showing up in processed yogurts, too, along with patented new strains of probiotic cultures (I'll stick to my old fashioned, but time-proven homemade lacto-cultured veggies and yogurt instead).

    I found the same "cooler spread" in the butter & "spread" section.  The spread options were just grotesque sounding.  Actually, the butter options weren't much better, as many were blended with other ingredients to increase spreadability, reduce calories or cholesterol/saturated fat, etc.  A few plain butters were enhanced with "butter flavor" - say what?  And on no package could it be determined if the butter came from cows that were naturally fed on pasture or on grain in confined pens.

  • fizzog

    3/19/2009 12:31:00 PM |

    Are sterols the same as plant stanol esters, as in Benecol (http://www.benecol.co.uk/new/light-nutrition-information.htm)?

  • Anonymous

    3/21/2009 6:14:00 PM |

    Is beta-sitosterol, found in anti-BPH supplements in the amount of about 500 mg., okay?

  • Klimbsac

    4/11/2009 5:40:00 AM |

    I recently came accross your blog and have been reading along. I thought I would leave my first comment. I dont know what to say except that I have enjoyed reading. Nice blog. I will keep visiting this blog very often.


    Joannah

    http://myscones.com/

  • Tony

    7/23/2009 9:51:32 PM |

    One of your articles cited concludes:

    "However, the role of dietary plant sterols in the development of atherosclerotic plaque is not known."

    Basically, there is no evidence that adsorption of sterols into serum did anything negative here. The presence of sterols is not a smoking gun.

    I take your warning as a caution, but I am not sure I believe you any more than the opposite side of this story, and yet I am by example proof that sterols have reduced my bad cholesterol levels.

    By the way, the Promise Active Supershots actually have 2 GRAMS of sterols, not 400 mg as you stated. Also, that product is being taken off the market at the end of August 2009 due to lack of market response (so I am told by Unilever).

  • buy jeans

    11/3/2010 3:20:34 PM |

    This study, piled on top of the worrisome literature that precede it, are enough for me: No more tin cans (which are lined with BPA), no more hard plastics labeled with recycling code #7 or #3, no more polycarbonate water bottles (the hard ones, often brightly colored). Microwaveable-safe may also mean human-unsafe, as highlighted by this damning assurance from the Tupperware people that BPA is not a health hazard.

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Real men don't eat carbs

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?  

    http://180degreehealth.blogspot.com/2011/03/natural-testosterone-enhancement.html

  • 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.

    Thanks,

    Mike

  • 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?

    -DIANA

  • 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.

  • salvinder

    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 |

    @Carbsane

    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  ....
    Unrelated:  
    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. "
    PRECISELY, carb sane PRECISELY!

    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, et.al) 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.(ajcn.org/content93/5/1048); 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 |

    @Might-o'chondria-AL

    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 |

    @Might-o'chondri-AL

    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!
    Cheers,
    Renfrew

  • 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.

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