Why do the Japanese have less heart disease?

We should look to the Japanese to teach us a few lessons about preventing heart disease. A Japanese male has only 65% of the risk of an American male (despite 40% of Japanese men being smokers), while a Japanese woman has 80% less risk than an American woman. While the U.S. is near the top of the list of nations with highest cardiovascular risk, Japan is the lowest.

What are they doing right?

There is no one explanation, but several. Genetics probably does not play a substantial role, by the way, as demonstrated by observations of Japanese people who emigrate to Western cultures. People of Japanese heritage living in Hawaii, for instance, develop the same cardiovascular risk as non-Japanese living in Hawaii. They also develop obesity and diabetes.

Among the factors that likely contribute to reduced risk in Japanese people:

--A style of eating that does not include a lot of sweet foods. No breakfast cereal or donuts for breakfast, for instance, but miso soup with tofu, fish, green onions, and daikon (as takuan, or pickled radish).
--Seaweed--It's probably a combination of the green phytonutrients and iodine. Typical daily iodine intake is in the neighborhood of 5000 mcg per day from nori, kombu, wakame, and other seaweed forms. (The average American obtains 125 mcg per day of iodine from diet.)
--Seafood--Fish in many forms not seen in the U.S. are popular.
--Green tea--Consumption of green tea has been confidently linked to reduced cardiovascular risk, probably via visceral fat-reducing, anti-oxidative, and anti-inflammatory effects. Although tea in Japan is often the less flavonoid-rich oolong tea, softer benefits from this form are likely.
--Soy--Tofu, miso, and soy sauce are staples. It's not clear to me whether soy is intrinsically beneficial or whether it is beneficial because it serves to replace unhealthy alternatives. (Genetic modification may change this effect.)
--Reduced exposure to cooked animal products (except seafood). This is not a saturated fat issue, but probably an advanced glycation end-product/lipoxidation issue that result from cooking.
--The lack of a "eat more healthy whole grain" mentality, the advice that has plunged the entire U.S. into the depths of a diabetes and obesity crisis (along with high-fructose corn syrup and sugar). Noodles like udon and ramen do have a place in their diet, as do some dessert foods. But the overall wheat exposure is less--no bagels, sandwiches, and breakfast cereals.
--Less overweight and obesity--The above eating style leads to less weight gain.

Japanese foods have a unique taste, consistency, and mouth-feel that go well with saltiness, thus the downside of their diet: salt consumption. On a broad scale, high salt consumption has been associated with hypertension and gastric cancer. But the tradeoff has, on the whole, been a favorable one.


One study trying to find some answers:

Dietary patterns and cardiovascular disease mortality in Japan: a prospective cohort study.

Shimazu T, Kuriyama S, Hozawa A et al.
Division of Epidemiology, Department of Public Health and Forensic Medicine, Tohoku University Graduate School of Medicine, Japan.


We prospectively assessed the association between dietary patterns among the Japanese and CVD mortality. Dietary information was collected from 40 547 Japanese men and women aged 40-79 years without a history of diabetes, stroke, myocardial infarction or cancer at the baseline in 1994.
During 7 years of follow-up, 801 participants died of CVD.

Factor analysis (principal component) based on a validated food frequency questionnaire identified three dietary patterns: (i) a Japanese dietary pattern highly correlated with soybean products, fish, seaweeds, vegetables, fruits and green tea, (ii) an 'animal food' dietary pattern and (iii) a high-dairy, high-fruit-and-vegetable, low-alcohol (DFA) dietary pattern. The Japanese dietary pattern was related to high sodium intake and high prevalence of hypertension. After adjustment for potential confounders, the Japanese dietary pattern score was associated with a lower risk of CVD mortality (hazard ratio of the highest quartile vs the lowest, 0.73; 95% confidence interval: 0.59-0.90; P for trend = 0.003). The 'animal food' dietary pattern was associated with an increased risk of CVD, but the DFA dietary pattern was not.

The Japanese dietary pattern was associated with a decreased risk of CVD mortality, despite its relation to sodium intake and hypertension.

Niacin: What forms are safe?

Niacin, or vitamin B3, remains a confusing issue for many people. It shouldn't be.

It doesn't help that most physicians and many pharmacists also do not understand the basic issues surrounding niacin. The only reason why there is any level of prevailing knowledge about niacin is that Kos Pharmaceuticals managed to "pharmaceuticalize" a niacin preparation, prescription Niaspan, that provided the revenue to fund professional "education."

Niacin can be helpful to increase HDL, reduce small LDL particles and shift them towards the more benign large particles, reduce triglycerides, and reduce lipoprotein(a).

So here's a brief description of the various forms that you will find niacin:

Immediate-release niacin--Also called crystalline niacin or just niacin. This is the original niacin that releases within minutes of ingestion. Because it releases rapidly, it triggers the most intense "hot flush." While this form of niacin works wonderfully well, is the safest, and is dirt cheap, the majority of people are simply unable to tolerate the intense flush. It also works best taken twice a day, generating two intolerable flushes per day.

Slow-release niacin--These preparations were popular in the 1980s, since the slow 12 to 24 hour pattern of release minimized the annoying hot flush. But, with prolonged use, it also became apparent that an unnaceptable frequency of liver toxicity developed. Unfortunately, this means that any niacin preparation that trickles niacin out over an extended period, including many of the slow-release preparations now sold in health food stores and pharmacies, have potential for liver toxicity. These preparations should be avoided.

6-hour release niacin--Releasing niacin more slowly than immediate-release niacin but more rapidly than slow-release niacin, 6-hour release (or what the Niaspan people call "extended-release" niacin) is nearly as effective as immediate-release niacin with approximately the same low potential for liver toxicity. It is far less liver toxic than slow-release niacin. 6-hour release niacin therefore offers the best balance between effectiveness and safety. Preparations that show this pattern of release include Niaspan ($180 per month), the poorly-named Sloniacin (about $8 per month), and Enduracin (about $7 per month) for 1000 mg per day. (Some Track Your Plaque Members have also determined that several other over-the-counter preparations have been demonstrated to share a similar pattern of release.)

Then there are the scam products that have no useful effect at all:

Flush-free or no-flush niacin--Inositol hexaniacinate, or 6 niacin molecules bound to the sugar, inositol, has no effect in humans, at least not with the dozen or so preparations that I've seen used. Nor are there any data to document the effectiveness of flush-free niacin. It's also more expensive.

Nicotinamide--This niacin derivative likewise has no effect on the usual targets for niacin treatment.

While I used to prescribe Niaspan, the ridiculous pricing and aggressive marketing really turned me off. I now advise my patients and our online followers to use only Sloniacin or Enduracin, unless you can tolerate immediate-release niacin.

Introduction to the New Track Your Plaque book, version 2.0


Out with the old,
in with the new  



“I believe that you are suffering from what is called a fatty degeneration of the heart.”

Dr. Tertius Lydgate to Mr. Casaubon on making a diagnosis with the new medical device, the stethoscope.

George Elliot
Middlemarch, 1871





Old notions in medicine have a peculiar way of lingering.

In 1882, Dr. Robert Koch discovered the tubercle bacillus in tissues of people with “consumption.” By connecting a bacterium with the disease, he usurped the long held notion that tuberculosis was a degenerative disease caused by lack of fresh air. But, for decades after Dr. Koch’s revelation, the “bad air” belief persisted. Surgical collapse of the lung, a painful and barbaric treatment for tuberculosis, persisted well into the 1960s, years after effective antibiotics were discovered in 1947.

The medical community of the 19th century viewed mental illness as the hereditary end-product of ancestral nervousness, alcoholism, prostitution and criminal behavior, a bias that remained widespread well into the mid-20th century. Nazi physicians invoked the theory of heritable “mental degeneration” to justify wholesale extermination of schizophrenics. Electro-convulsive therapy (ECT, or “electroshock therapy”) was widely applied to treat schizophrenia, depression, homosexuality, and criminal behavior for over 30 years, gradually abandoned (at least in its original form) after years of abusive application to subdue patients, demonized in the 1975 movie, “One Flew Over the Cuckoo’s Nest,” depicting the author’s real-life experience with ECT.

Long after a theory or practice has been discredited, it can persist, refusing to die. The new and improved may not be adopted into mainstream practice for years, even decades.

Back to the 21st century: What if you realized that, by quirks of human nature and the uneven adoption of health information, your doctor practiced medicine appropriate for 1985? 1975?

While digital information nowadays is transmitted at the speed of light, disseminating as fast as it takes the next juicy tidbit to be “virally” reproduced via social networking websites, it’s the human factor that still operates with the inertia of human behavior. Habits and attitudes slow the adoption of new information in time measured not in seconds, but in years or decades.

A century ago, 20 years were required for the new technology of blood pressure measurement to be adopted after its introduction in the U.S. in 1910, since physicians were long comfortable with the practice of “pulse palpation” (feeling the pulse). (The arcane language of pulse palpation persists to this day, terms like “pulsus parvus et tardus,” the slow rising pulse of a stiff aortic valve; and the "water-hammer" pulse of a leaking aortic valve.)

The discovery of new, health-changing information today in the 21st century disseminates through the ranks of modern healthcare providers at much the same pace as measuring blood pressure did in the early 20th century.

It’s also tempting to paint American medicine as a fiefdom intent on maintaining exclusive rein over health information. Look back over the hierarchical relationship of medicine over nursing in the past century: When blood pressure measurement was adopted on a broad scale in the 1930s, it was practiced only by physicians, since nurses were deemed incapable. (Modern-day nurses should surely have a hearty laugh over this.) Stethoscopes, around even longer than blood pressure cuffs, weren’t permitted to fall into the hands of nurses until the 1960s, since the medical community feared that nurses might command too much control over patient care. Even after nurses were permitted to have their own stethoscopes, great pains were taken to be certain the nurses’ version was readily distinguishable from the “real” tool wielded by physicians; nurses’ stethoscopes were therefore labeled “nurse-o-scopes,” or “assistoscopes,” and were required to be smaller and flimsier.

Old and ineffective doesn’t always give way to new and better at once; it is slowed by habit as well as an unwillingness to relinquish control.

Somehow technology marches on. But it does so unevenly, sweeping some along in its first wave, others in its wake, some never at all.

Just as effective antibiotics to cure tuberculosis were available for 20 years while surgeons continued to remove patients’ lungs, so better solutions to heart disease are already available but not yet employed by your neighborhood physician. The primary care physician may have heard about some of the newest means to prevent heart disease, but is too overwhelmed with the day-to-day of sore throats, diarrhea, and rashes. Cardiologists, intent on inserting the next best stent or defibrillator, have little but passing interest in strategies that might halt or reverse the heart disease that can be “managed,” no matter how imperfectly, with procedural solutions like angioplasty and bypass surgery. We should bear these flawed human tendencies in mind as we explore the world of heart disease prevention.

We need look no farther than the front page of the newspaper to find evidence of the failure of present-day heart disease detection and management. Over the past several years, headlines have carried the likes of Tim Russert, Bill Clinton, Larry King, Dick Cheney, David Letterman, Tommy Lasorda, Ed Bradley, Mike Ditka, Walter Cronkite, Alberto Salazar, all heart disease sufferers. Some, like talk show host David Letterman, survived their brush with heart catastrophe and underwent successful bypass surgery. Others, like marathoners Fixx and Salazar, raised none of the conventional red flags for heart disease. All received standard, “modern” medical care . . . all the way up to their heart attack, bypass surgery, or untimely death.

Like the sphygnomanometer (blood pressure) cuffs of 1910, Track Your Plaque represents an example of the new. But, unlike the simple practice of taking blood pressure in the early 20th century, Track Your Plaque represents an entirely new way to look at coronary heart disease: a new way to measure it, a new way to identify its causes, and a new way to seize control over it, often to the point of achieving reversal of the process. It also puts control over much of this process into your hands and away from hospitals, cardiologists, and heart procedures. 

I could speak of revealing “secrets,” but that’s not true. In Track Your Plaque, I simply convey information about heart disease that you were likely unaware existed, strategies that doctors fail to discuss. I assemble them into a “package” that, together, create an enormously empowering unique approach to prevent heart disease and heart attack.

Track Your Plaque also challenges the high-tech status quo, practices that occupy exalted places in the enormous cardiovascular healthcare machine that has dominated American healthcare for the past 40 years. I propose that high-tech hospital procedures should join the practice of ECT for homosexuality and insanity¾and become yet another relic of the past.

What are "normal" triglycerides?

Among the most neglected yet enormously helpful values on any standard cholesterol panel is the triglyceride value.

Triglycerides traverse the bloodstream by hitching a ride on water (serum)-soluble lipoproteins, or lipid-carrying proteins. We measure triglycerides as an indirect index of triglyceride-containing lipoproteins.

Triglycerides are a basic currency of energy. While the average American ingests around 300 mg of cholesterol per day, he or she also ingests 60,000-120,000 mg (60-120 grams) of triglycerides, i.e., 200 to 400 times greater amounts, from fat intake. Zero triglycerides in the diet or in the bloodstream is not an option.

But what represents too much triglycerides in the bloodstream? There are several observations to help us make this determination:

1) When fasting triglycerides are 133 mg/dl or greater, 80% of people will show show at least some degree of small LDL particles.

2) When fasting triglycerides are 60 mg/dl or less, most (though not all, since genetic factors enter into the picture) people will show little to no small LDL particles.

3) When fasting triglycerides are 200 mg/dl or greater, small LDL particles will dominate and large LDL particles will be in the minority or be gone entirely.

4) When triglycerides are 88 mg/dl or greater after eating, then risk for heart attack is doubled. Non-fasting triglycerides in the 400+ mg/dl range are associated with 17-fold greater risk for heart attack.



From Austin et al 1990. "Phenotype A" means that large LDL particles dominate; "phenotype B" means that small LDL particles dominate.

Note that conventional "wisdom" (i.e., NCEP ATP-3 guidelines) is that triglycerides of up to 150 mg/dl are okay, a level that virtually guarantees expression of small LDL particles and increased cardiovascular risk.

Based on observations like these, in the Track Your Plaque program we aim for fasting triglycerides of no higher than 60 mg/dl and postprandial (after-meal) triglycerides of no more than 90 mg/dl.

Curiously, while fat intake (i.e., triglyceride intake) plays a role in determining postprandial triglyceride blood levels, it's carbohydrate intake that plays a much larger role. That will be an issue for another day.

1985: The Year of Whole Grains

In 1985, the National Cholesterol Education Panel delivered its Adult Treatment Panel guidelines to Americans, advice to cut cholesterol intake, reduce saturated fat, and increase "healthy whole grains" to reduce the incidence of heart attack and other cardiovascular events.

Per capita wheat consumption increased accordingly. Wheat consumption today is 26 lbs per year greater than in 1970 and now totals 133 lbs per person per year. (Because infants and children are lumped together with adults, average adult consumption is likely greater than 200 lbs per year, or the equivalent of approximately 300 loaves of bread per year.) Another twist: The mid- and late-1980s also marks the widespread adoption of the genetically-altered dwarf variants of wheat to replace standard-height wheat.

In 1985, the Centers for Disease Control also began to track multiple health conditions, including diabetes. Here is the curve for diabetes:


Note that, from 1958 until 1985, the curve was climbing slowly. After 1985, the curve shifted sharply upward. (Not shown is the data point for 2010, an even steeper upward ascent.) Now diabetes is skyrocketing, projected to afflict 1 in 3 adults in the coming decades.

You think there's a relationship?

Have some more

Wheat, via exorphin effects, is an appetite stimulant. Eat a whole wheat bagel or bran muffin, you want another. You also want more of other foods. You also want something to eat every two hours due to widely-swinging insulin-glucose responses: blood sugar high followed by a sharp downturn that triggers a powerful impulse to eat (thus the cravings for a snack at 9 and 11 a.m. after a 7 a.m. breakfast).

If wheat is a stimulant of appetite, then removing it should yield reduced appetite and reduced calorie intake. That is precisely what happens.

When wheat products are removed from the diet--without calorie restriction, without counting fat or carbohydrate grams, no exercise program, no cleansing regimen, no skipping meals . . . nothing--calorie intake drops 350 to 400 calories per day. This calorie figure remains curiously consistent across multiple studies in which wheat was eliminated.

400 calories per day results in 21 lbs lost over 6 months, based just on calories. (3500 calories per pound lost.) That is what happens in wheat elimination diets: 21-26 lbs lost over 6 months.

Wheat is the processed food industry's nicotine, a means of ensuring repeat food purchases. It's also low-cost (subsidized by the U.S. government), high-yield, an ingredient that even has its very own withdrawal syndrome should you miss a "hit."

When MIGHT statins be helpful?

I spend a lot of my day bashing statin drugs and helping people get rid of them.

But are there instances in which statin drugs do indeed provide real advantage? If someone follows the diet I've articulated in these posts and in the Track Your Plaque program, supplements omega-3 fatty acids and vitamin D, normalizes thyroid measures, and identifies and corrects hidden genetic sources of cardiovascular risk (e.g., Lp(a)), then are there any people who obtain incremental benefit from use of a statin drug?

I believe there are some groups of people who do indeed do better with statin drugs. These include:

Apoprotein E4 homozygotes

Apoprotein E2 homozygotes

Familial combined hyperlipidemia (apoprotein B overproduction and/or defective degradation)

Cholesteryl ester transfer protein homozygotes (though occasionally manageable strictly with diet)

Familial heterozygous hypercholesterolemia, familial homozygous hypercholesterolemia

Other rare variants, e.g., apo B and C variants

The vast majority of people now taking statin drugs do NOT have the above genetic diagnoses. The majority either have increased LDL from the absurd "cut your fat, eat more healthy whole grains" diet that introduces grotesque distortions into metabolism (like skyrocketing apo B/VLDL and small LDL particles) or have misleading calculated LDL cholesterol values (since conventional LDL is calculated, not measured).

As time passes, we are witnessing more and more people slow, stop, or reverse coronary plaque using no statin drugs.

Like antibiotics and other drugs, there may be an appropriate time and situation in which they are helpful, but not for every sneeze, runny nose, or chill. Same with statin drugs: There may be an occasional person who, for genetically-determined reasons, is unable to, for example, clear postprandial (after-eating) lipoproteins from the bloodstream and thereby develops coronary atherosclerotic plaque and heart attack at age 40. But these people are the exception.

Advanced topics in nutrition

Nutrition in the modern world has become an increasingly problematic topic. From genetic modification to commercialized methods of mass production, we are having to navigate all manner of complex issues in food choices, particularly if ideal health, including maximal control over coronary plaque, is among our goals.

We will therefore be releasing a series of discussions on the Track Your Plaque website in the coming months, a series I call "Track Your Plaque Advanced Topics in Nutrition." These will be, as the series title suggests, discussions for anyone interested in more than the "eat a balanced diet" nonsense that issues from "official" sources. Among the topics to be covered:

1)Advanced Glycation End-products--both endogenous and exogenous, including peripheral issues like lipoxidation and acrylamides.

2)Dietary influences on LDL oxidation--including the concept of "glycoxidation." Protection from oxidative phenomena is not just about taking antioxidants.

3) Foods you MUST eat--We've talked a lot about foods that you shouldn't eat. How about foods you should eat?

The New Track Your Plaque Guide now available

The New Track Your Plaque Guide is now available!

The Track Your Plaque program has evolved over its 8 year history. While the original Track Your Plaque book reflected the program details that got the program started back in 2003-2004, plenty has changed.

This new version of the book, what I call the program Guide, represents version 2.0 of Track Your Plaque and includes:

--Updated lipoprotein treatment strategies--including new and expanded treatment choices for small LDL and lipoprotein(a).

--An entire chapter on vitamin D and its crucial role in cardiovascular health and plaque control.

--A new and expanded diet--All the reasons why the New Track Your Plaque Diet can achieve spectacular improvement in lipids/lipoproteins, reversal of insulin resistance/pre-diabetes/diabetes, weight loss, reduction in blood pressure, etc. are discussed in considerable detail. The diet is crafted to achieve maximum control over both metabolic responses and coronary plaque.

--An entire chapter on the role of omega-3 fatty acids is included.

--A detailed discussion on the role of iodine and thyroid health--One of the newest additions to the Track Your Plaque menu of strategies is to achieve and maintain ideal thyroid health. This tips the scales in your favor for improved control over lipids/lipoproteins, weight, blood sugar, and coronary plaque.


The new guide, as well as our new Member kits that include the new Track Your Plaque Recipe Book, At-Home Lab Test kits, and nutritional supplements, are all available in the Track Your Plaque Marketplace.

Don't wet yourself

While there is more to wheat's adverse effects on human health than celiac disease, studying celiac disease provides important insights into why and how wheat--the gluten component of wheat, in this case--is so destructive to human health.

Modern wheat, in particular, is capable of causing "celiac disease" without intestinal symptoms---no cramping or diarrhea--but instead shows itself as brain injury (ataxia, dementia), peripheral nervous system damage (peripheral neuropathy), joint and muscle inflammation (rheumatoid arthritis, polymyalgia rheumatica and others), and gastrointestinal cancers.

One neurological manifestation of wheat's effect on the human brain is a condition called cerebellar ataxia. This is a condition that can affect adults (average age 48 years) and children and consists of incoordination, falls, and incontinence.

Because brain tissue has limited capacity for healing and regeneration, symptoms of cerebellar ataxia usually improve slowly and modestly with meticulous elimination of wheat and other gluten sources.

Such observations are relevant even to people without celiac disease. Celiac disease sufferers are more susceptible to such extra-intestinal phenomena, but it can also happen in people without positive celiac antibodies.



Some references:

Neurological symptoms in patients with biopsy proven celiac disease

A total of 72 patients with biopsy proven celiac disease (CD) (mean age 51 +/- 15 years, mean disease duration 8 +/- 11 years) were recruited through advertisements. All participants adhered to a gluten-free diet. Patients were interviewed following a standard questionnaire and examined clinically for neurological symptoms. Medical history revealed neurological disorders such as migraine (28%), carpal tunnel syndrome (20%), vestibular dysfunction (8%), seizures (6%), and myelitis (3%). Interestingly, 35% of patients with CD reported of a history of psychiatric disease including depression, personality changes, or even psychosis. Physical examination yielded stance and gait problems in about one third of patients that could be attributed to afferent ataxia in 26%, vestibular dysfunction in 6%, and cerebellar ataxia in 6%. Other motor features such as basal ganglia symptoms, pyramidal tract signs, tics, and myoclonus were infrequent. 35% of patients with CD showed deep sensory loss and reduced ankle reflexes in 14%. Gait disturbances in CD do not only result from cerebellar ataxia but also from proprioceptive or vestibular impairment.



Gluten ataxia in perspective: epidemiology, genetic susceptibility and clinical characteristics

Two hundred and twenty-four patients with various causes of ataxia from North Trent (59 familial and/or positive testing for spinocerebellar ataxias 1, 2, 3, 6 and 7, and Friedreich's ataxia, 132 sporadic idiopathic and 33 clinically probable cerebellar variant of multiple system atrophy MSA-C) and 44 patients with sporadic idiopathic ataxia from The Institute of Neurology, London, were screened for the presence of antigliadin antibodies. A total of 1200 volunteers were screened as normal controls. The prevalence of antigliadin antibodies in the familial group was eight out of 59 (14%), 54 out of 132 (41%) in the sporadic idiopathic group, five out of 33 (15%) in the MSA-C group and 149 out of 1200 (12%) in the normal controls. The prevalence in the sporadic idiopathic group from London was 14 out of 44 (32%). The difference in prevalence between the idiopathic sporadic groups and the other groups was highly significant (P < 0.0001 and P < 0.003, respectively). The clinical characteristics of 68 patients with gluten ataxia were as follows: the mean age at onset of the ataxia was 48 years (range 14-81 years) with a mean duration of the ataxia of 9.7 years (range 1-40 years). Ocular signs were observed in 84% and dysarthria in 66%. Upper limb ataxia was evident in 75%, lower limb ataxia in 90% and gait ataxia in 100% of patients. Gastrointestinal symptoms were present in only 13%. MRI revealed atrophy of the cerebellum in 79% and white matter hyperintensities in 19%. Forty-five percent of patients had neurophysiological evidence of a sensorimotor axonal neuropathy. Gluten-sensitive enteropathy was found in 24%. HLA DQ2 was present in 72% of patients. Gluten ataxia is therefore the single most common cause of sporadic idiopathic ataxia.
Battery acid and oatmeal

Battery acid and oatmeal

Ever notice the warnings on your car's battery? "Danger: Sulfuric acid. Protective eyewear advised. Serious injury possible."

Sulfuric acid is among the most powerful and potentially harmful acids known. Get even a dilute quantity in your eyes and you will suffer serious burns and possibly loss of eyesight. Ingest it and you can sustain fatal injury to the mouth and esophagus. Sulfuric acid's potent tendency to react with other compounds is one of the reasons that it is used in industrial processes like petroleum refining. Sulfuric acid is also a component of the harsh atmosphere of Venus.

Know what food is the most potent source of sulfuric acid in the body? Oats.

Yes: Oatmeal, oat bran, and foods made from oats (you know what breakfast cereal I'm talking about) are the most potent sources of sulfuric acid in the human diet.

Why is this important? In the transition made by humans from net-alkaline hunter-gatherer diet to net-acid modern overloaded-with-grains diet, oats tip the scales heavily towards a drop in pH, i.e., more acidic.

The more acidic your diet, the more likely it is you develop osteoporosis and other bone diseases, oxalate kidney stones, and possibly other diseases.

Here's one reference for this effect.

Comments (38) -

  • Sly

    3/23/2011 8:21:12 AM |

    I wonder what is the best/healthiest way to alkalize your body?
    Removieng grains, of course, but what else?

  • Anne

    3/23/2011 8:42:01 AM |

    Dear Dr Davis,

    I understand that oats give an acid load to the body, but please can you explain how they are a source of sulphuric acid.

  • Kris @ Health Blog

    3/23/2011 12:18:13 PM |

    I've been reading Nutrition and Physical Degeneration by Weston Price, a dentist who travels around the world sometime around 1930-1940.

    He notices how awful the teeth of modernized people eating sugar and white flour are compared to the more "primitive" populations who don't eat those things.

    He does notice that the people who still eat a lot of rye or oats are in excellent health, while those eating sugar and wheat are awful and have very damaged teeth.

    After reading this I've put a bit of a question mark on banishing all grains, since wheat seems to be the primary culprit here. Apparently populations can live very healthy with oats and rye as a large part of their calorie intake.

    I wonder about this Oat and sulfuric acid thing, do you think this has any real consequences for us?

  • JC

    3/23/2011 12:29:06 PM |

    Alkalizing you body can lead to all kinds of problems such as yeast overgrowth.You need stomach acid to inhibit dangerous pathogens.Its a mistake to jump on the old Cayce idea of alkalilizng the body.

  • Jenny

    3/23/2011 12:44:22 PM |

    The article you cite is not a study, just a rehash of current belief. In fact, the argument that eating protein leaches calcium away from bone is one of the old wives tales used to discredit the low carb diet that hasn't stood up to actual research.

  • Peter

    3/23/2011 12:49:05 PM |

    I used to eat loads of oat bran (your suggestion), became anemic, then read someone's opinion that oat bran blocks iron absorbtion.  So I stopped eating oat bran, and the anemia went away.  Maybe coincidence, maybe not.

  • Anonymous

    3/23/2011 2:15:17 PM |

    Dr Davis:  Now that oat and oat products are off the table,and you remain in the anti sat fat camp, it would be interesting to hear what daily diet recommendations might be since you also think Omega 6 should be minimized and fruit intake watched to make sure blood sugar is not to high. What then do you recommend the diet be?  Hard to exist on just veggies, and a few nuts( to many bad for Omega 6 levels)

  • Geoffrey Levens

    3/23/2011 3:20:05 PM |

    "I wonder what is the best/healthiest way to alkalize your body?
    Removieng grains, of course, but what else?"

    The best and really only way to alkalize your body long term is to load w/ alkalizing minerals via non-starchy veg esp leafy greens.  And yes, avoid acidifying foods esp junk food, processed foods, refined carbs.

  • Dr. William Davis

    3/23/2011 3:52:24 PM |

    Commenter Geoffrey Levens, I believe, provided the right response to what foods to eat to maintain a net alkaline bias in the body.

    Most of the effects of an overly acidic lifestyle do not reach conscious perception. The calciuric effect of wheat and oats, for instance, generate no symptoms.

    Anon--

    I am not in "the anti sat fat camp." Saturated fat is part of the Track Your Plaque diet, unless you are apoprotein E4.

    By the way, the entire diet, saturated fat, wheat-free and all, is articulated in a total of nearly 100 pages of discussion on www.trackyourplaque.com, as well as the new Track Your Plaque book, version 2.0 (online now; hard copy coming in the next 2 weeks).

  • Amy

    3/23/2011 5:49:21 PM |

    I am pro-paleo and fairly anti-grain (especially wheat) -- but I have to say I take issue with your reasoning here.

    I assume you are specifically referring to Table 2 of this review article (written by a nutritionist). It lists milliequivalents of potential acid generated per 100 g of protein from the food. Oats are highest at 82.2, closely followed by eggs at 79.6; wheat is 69.4. According to your logic it would be better by far to eat wheat instead of eggs -- and I'm sure you wouldn't advise that.

    Also it is useful to think of the quantities required to obtain 100 g of protein from each food. I might easily eat 3 eggs at a meal, but I would be unlikely, if I ate oatmeal, to eat the nearly 4 cups required for the same amount of protein.

    I'm not defending oats. But as a scientist I find this particular argument against them to be weak.

  • Might-o'chondri-AL

    3/23/2011 7:37:42 PM |

    pH ranges in "normal" health is tightly controlled. Phrasing like acid/alkaline "load"/"balance" should be referenced to spot measures of the kidney dynamic. We don't have sulfuric acid sloshing against our cells.

    Cells use a lot of oxygen and kick back CO2, which we breath out. Yet, before it gets out of the cell and into blood circulation that CO2 is doing things.

    CO2, being a gas with no valent electrical charge, moves freely inside and outside our cells. We use an enzyme (carbonic anhydrase) to make it soluble (ie: so body can shift it in way body needs to). In solution it is in the form of H2CO3, carbonic acid.

    Carbonic acid is what the cells use, both inside and outside, to get ion charges (+ and -) to quickly adapt to pH fluctuations. As metabolic processes occur they naturally engender pH reactions. These pH reactions use H2CO3 (carbonic acid) to get H+, HCO3- and/or CO3-- ions, which have + and/or - interactive potential.

    It's an absolute necessity for our bodies ability to use pH to make things happen. Example: to maintain an ion neutral state for molecules needing to use a cell membrane ion channel. Membranes are designed not to let + or - charged molecules pass for good reasons; polarization and de-polarization must be regulated.

  • Helen

    3/23/2011 10:59:10 PM |

    You're killing me, Dr. Davis.  Despite your anti-oat stance and my status as a diabetic, I've found oats to be gentle to my blood sugar and, because of a number of other food intolerances, and a lack of tolerance for fat (vis a vis my blood sugars), oats make up a big part of my diet.  Now I find that I'm consuming battery acid.  

    Is there really any study correlating oat consumption per se with the diseases you mention?  I find again and again in nutrition advice (not just here) the idea that "because this contains this, it should be good/bad for you," while food and the body have such complex interrelationships it's really hard to make conclusions soley based on a food's containing a certain substance.

  • Helen

    3/23/2011 10:59:32 PM |

    (continued)

    The review you cite finds that there is insufficient evidence to suggest an upper limit for protein based on its presumed tendency to cause greater calcium excretion and that many dietary factors must be considered vis a vis urinary calcium and bone metabolism.  I think the term "not sufficiently unamibiguous" applies to your post's case against oats.

    BTW, improperly prepared oats can indeed lead to anemia.  They have to be soaked in a warm medium overnight with a phytase-containing substance (I use buckwheat flour), water, and yogurt to allow the mineral-binding phytate to get broken down.  It also allows the *phosphorous* to become bioavailable, as it is in animal sources of protein, which may mitigate the calcium-leaching effect of the oat proteins. although phosphorous is one of those things I hear contradictory things about.  One of the many.

  • steve

    3/24/2011 12:05:41 AM |

    hi Dr Davis:  I note your response that sat fat is ok except if you are Apo E 4.  Other than a blood testhow can you know?  In my case following the recommendations of this blog and others in my last NMR my LDL particle count was 64o and my small LDL was <90! Two years ago it was 1795 all small following diet of grains(plenty of oats and whole wheat and fruit). Particle size has increased from Now, eggs, meat fish,some cheese,  veggies, some potato or rice. Dark chocolate 85% and above only sweet) HDL directly measured was 64 and direct LDL was 54.  I do take Crestor and Zetia, but understand that if am Apo E 4 not likely for me to achieve these numbers even on a Statin.  Is this so?

    For me oats are for horses!
    look forward to buying your book.  Alert us when it is available.  Maybe have an Amazon link

  • Vladimir

    3/24/2011 1:12:54 AM |

    From Samuel Johnson's A Dictionary of the English Language:

    Oats: A grain, which in England is generally given to horses, but in Scotland appears to support the people.

  • Dr. William Davis

    3/24/2011 2:07:01 AM |

    Hi, Helen--

    This was not meant to indict meat. This was only about oats.

    Perhaps the confusion comes from the fact that meats yield a net acidic effect. However, the effects of animal products extend beyond acid-base effects and may impact on such things as IGF-1alpha that may blunt any pH effect.

    Some of the worst postprandial glucoses I have ever seen have been after consuming oats--no sugar, non-diabetics. This is not true in everybody, but in enough people that I've removed it from our list of foods to eat.

  • Dr. William Davis

    3/24/2011 2:07:58 AM |

    Hi, Steve--

    Great results!

    I suggest testing apo E only when you fail to obtain the results you desire. I do not consider apo E genotype testing as a "first line" test.


    Vladimir--

    That's great!

  • Anonymous

    3/24/2011 2:21:21 AM |

    Don't we want some foods in our diet which are acidic. Is the goal to strive for 100% alkaline food consumption? I have cut down wheat dramatically but because of my active lifestyle I consume organic steel cut oats to give me a good dose of carbohydrates.

  • Jeremy

    3/24/2011 5:17:47 AM |

    Does this apply to things like apple cider vinegar as well? I understand that adding vinegar to food decreases the overall GI of the meal, so sometimes I take some apple cider vinegar with meals. Is this actually over-acidifying my diet?

  • Might-o'chondri-AL

    3/24/2011 5:28:42 AM |

    Sulphur in proteins comes from the amino acids cysteine and methonine. These sulphur aminos, along with the ammonium ions foster faster kidney filtration.
    When urination carries away positive ion rich calcium the pH can drop toward acidic.

    Sulphur (S) in the body does other things that are important. When the cells are doing "housekeeping" by internal recycling, auto-phagy (not apotosis or programmed cell death) S binds  copper, iron, mangenese & "Fenton" active metals so they can't cause problem reactions (ex: hydroxyl radicals)during auto-phagy. Oat's sustaining power from S can be applicable in this context; the battery keeps going and going....

    The amino acid cysteine's nitrogen atoms become relevant to the type of metabolic process called nitro-sylation. Sulphur(S) is the way the body moves these molecules around as a complex molecule. Cysteine protein has to shed 1 electron per each sulphur atom it has to undergo nitro-sylation.

    One way that incipient tumors are stopped is by blocking S-nitro-sylation in the cell. Some people suspect meat nitrogen acidifies the body and thus is a risk factor for cancer; it's more likely due to an amino acid trans-nitrosation propensity than the pH. If the body can get that cysteine back it's 1 electron per sulphur atom then nitro-sylation is reversable (ex: spontaneous remission reported from following some "special" regimen).

    Insulin molecules have di-sulfide(S to S) linkages; some of which join insulin's A-chain to it's B-chain. The body clears insulin by breaking it down; first step  is by exposing the di-sulfide bonds for reaction. Insulin Degrading Enzyme (IDE) does this preparatory degradation, but IDE still leaves the insulin break down in a reversible phase.

    Insulin's function of decreasing protein degradation inside the cell is one reason for the body to hedge on it's (insulin's) clearing (ie: hold at reversible phase). A cell might be moving toward auto-phagy (ex: protein recycling) and have to hold off the process due to a life-threatening development. (Protein di-sulfide isomerase enzyme is what can finish the process and put insulin's trichloracetic acids into  irreversably soluble particles.)  

    Human genetic variants of splicing IDE are involved in hypo-glycemia  and hyper-glycemia. Those individuals can't regulate insulin and have their post-prandial blood sugar respond "normally". Doc mentions (above) variable response to oats he's dealt with.

    Type II diabetics have chronic inflammation and this leads to the molecule S-nitroso-glutathione formation. Elevated circulating free fatty acids are another activator of s-nitoso-glutathione; and as such can also inhibit insulin clearance.

    The cysteine protein loses 2electrons for every sulphur atom it has in order to glutation-ylate. In order to reverse S-nitroso-glutathione those 2 electons have to be restored to the cysteine wing of the molecule. Then the glutathione is free from the sulphurous nitrogen amino acid.

    With higher levels of free glutathione the body increases the solubility of insulin. Which is why Type II diabetics who eat lots of  vegetables (as opposed to tubers and grains)see some benefit; the veggies provide electrons to donate to and reverse the excessive glutathonylation. It's not about veggies "fixing" pH - that's done in cells via CO2 and carbonates, etc .

  • Might-o'chondri-AL

    3/24/2011 5:47:03 AM |

    typo errors alert for:
    methionine, glutathione, glutathion-ylate, glutathion-ylation, S-nitroso-glutathione

  • CarbSane

    3/24/2011 10:10:03 AM |

    Aww c'mon Doc!  

    2 large eggs contain 140 cals and 12g protein = approx 9.6 mEq SAA

    A 140 cal serving of plain oatmeal contains just under 5.5g protein = approx  4.5 mEq SSA.

  • revelo

    3/24/2011 4:21:37 PM |

    Johnson: "Oats: A grain, which in England is generally given to horses, but in Scotland appears to support the people."

    Boswell: "And that is why England is renowed for her horses and Scotland is renowned for her men."

  • Dr. William Davis

    3/24/2011 6:52:34 PM |

    It sounds to me like acid-base issues require an entire separate series of discussions all of their own.

    An issue for the future.

  • Might-o'chondri-AL

    3/24/2011 11:49:43 PM |

    (Sulfphur = S) S-nitroso-glutathione inhibits insulin degradation and impedes the insulin degrading enzyme (IDE) doing it's job. However, there is a "weak" acid that can partially annul that effect of S-nitroso-glutathione; that acid is ascorbate (commonly called vitamin C).

    Type II diabetics have notably low levels of ascorbate in their blood. There was a lot of 1990s
    European research indicating vitamin C gave diabetics better blood sugar control; and some researchers got no beneficial results.

    For each 1 mol of Ascorbate it was calculated there was +/- 0.5 mol glutathione increase. The more glutathione free from S-nitroso-glutathione molecule there is more of insulin's tri-chlor-acetic acid (from the insulin A-chain) made soluble.

    2007 data after 16 weeks for  43 adults(24 men & 19 women), aged +/- 52 year old, with Type II diabetics of +/- 7.5 years diagnosed as having diabetes who supplemented 1000 mg/day vitamin C (average for both sex):
    insulin before = 16.91 +/- 3.1 uU/ml
    insulin after  =  8.77 +/- 1.3 uU/ml
    HbA1c % before =  8.82 +/- 1.3
    HbA1c % after  =  7.66 +/- 1.3
    fasting blood sugar (mg/dl),
            before = 169.33 +/-34.03
    fasting blood sugar (mg/dl),
            after  = 144.80 +/-33.44

    A seperate comparable group of 41subjects, who supplemented with 500 mg/day vitamin C for 16 weeks, showed no benefit in the same parameters. So insulin, Hb1Ac and fasting blood sugar had no statistically significant improvement with the lower dose.

    There is however evidence, from other investigations, that some diabetic individuals who take supplements of vitamin C have their blood sugar actually go up even higher. I suspect this is related to individual genetics; and another indication diabetes is not a uniform disease awaiting one single cure.

  • Might-o'chondri-AL

    3/25/2011 4:43:20 AM |

    Acidity inside the cell is sometimes necessary. At the onset of auto-phagy  sulphur (S) keeps metals from reacting  dangerously. It temporarily "stashes" them in one of the vacuole compartments inside the cell.

    Acidic pH is instigated by the protein Vascular Regulatory Subunit 1 H (V1H; a.k.a. Nef binding protein 1) and is powered by ATP energy. This takes the form of an enzyme called V1H-ATPase; it's action is to lower (acidify) the pH inside the auto-phagy cell.

    This function of V1H makes it possible for things to shift around inside that cell and mediate the steps whereby components get "stashed" (endo-cytosis). This extends to the damaged proteins  slated for recycling; they get processed in a "safe" compartment inside the cell.

    Once the inner endo-some &/or lyso-some compartment pH acidifies to a set ( pre-programmed) low the protease enzymes (protein cleavers) upregulate for action. The di-sulfide (S-S) bonds of damaged proteins cleave and those proteins open up their uniquely convoluted configuration (unfold).

    Unfolded proteins are then "digested" and their components recylced, into new and unblemished proteins. It's an economical saving of energy not to have to assemble a new cell and improve the efficiency of an existing cell whose proteins were "wearing" out.

    When auto-phagy is done, and new protein(s) made, that protein(s) is sent out into the same cell and the cell pH rises back to normal. Being integral to survival, this (auto-phagy) is not dependant on pH from foods in the diet of a relatively healthy person.

  • body lift

    3/25/2011 10:04:35 AM |

    Your information may be very useful for me. Oats consumption is perhaps one of the best natural remedies for eczema. Oats are rich in fiber, fats, saponins, proteins and polysaccharides.

  • Anonymous

    3/25/2011 7:49:17 PM |

    Dr. Bernstein recommends limiting vit c supplements to 250mg/day.

  • paul

    3/26/2011 1:15:14 AM |

    You sir .... are a fear monger, and after this article, I am UNSUBSCRIBING to your blog!

    I don't know what happened to you, but you seem to be over time developing paranoia, and now instilling it in your faithful readers ...

    Maybe you should consult with a chemist before publishing such a reckless article trying to demonize perhaps one of the most balanced foods for people with blood sugar or cholesterol problems.

    THIS DOCTOR IS A QUACK PEOPLE!!! Talk to a chemist about what kind of damage oats are doing to your body - not this tinfoil-hat-wearing fraud!!!

    Our bodies need to be not to alkaline, and not too acidic ... sulfates and sulfuric acid help to counter the effects of alkalinity, and are necessary in moderate amounts in our diets!!!  

    UNSUBSCRIBED!!!

  • meta

    3/28/2011 6:39:21 PM |

    Your post showed up on my google reader recommended reads. this article sounds so hokey and weird.
    I don't know what you learned in physiology class in med school.. or did you pay someone to do your assignments for you back then?
    So weird I won't even attempt to refute, there is no head or tail to the amount of wrong in your article. To compare acid in oats with acid in car battery?
    Are you intellectually handicapped as you are so unable to make a decent analogous example?

  • karl

    3/29/2011 3:31:37 AM |

    A bit over the top - Oatmeal is loaded with carbs, but many foods contain similar substances that are toxic - our digestive system has evolved to deal with the chemical arms race brought to us by the plant kingdom.

    I'm all for reducing carbohydrates but this borders on disinformation..

    Almonds contain a bit of cyanide.. etc..

  • microdermabrasion

    6/24/2011 2:59:21 PM |

    Interference and you may suffer fatal injuries in the mouth and esophagus. Strong tendency of sulfuric acid to react with other compounds is one of the reasons used in industrial processes such as oil refineries.

  • Dion

    9/1/2011 7:50:43 PM |

    I have been eating oatmeal/porridge for breakfast with honey and Brazil nuts for three months. My total cholesterol has droppped from 251 to 199, my triglycerides from 305 to 72. My HDL is 58 and my LDL is 127.  I don't know if these are good figures but my doctor was surprised by the drop. The only change in my diet was the oatmeal. I'm Irish and porridge was a traditional breakfast food when people were thinner.

  • Dr. William Davis

    9/2/2011 2:17:23 AM |

    Hi, Dion--While these are great changes, it does not mean that you have fully eliminated, or at least substantially decreased, small LDL. To know, it requires specific measurement.

  • Dion

    10/3/2011 11:02:01 PM |

    I'm following a wheat-free diet since reading your book but am still a bit unsure about stopping the oatmeal porridge. If I have a bowl at 8am, I don't feel hungry until 2pm. Surely this is not representative of a high carb food effect, at least for me?

  • Dr. William Davis

    10/4/2011 2:38:20 AM |

    Sure doesn't sound like it. You might be among the metabolically "gifted."

  • Ginger_gal

    10/19/2011 3:44:07 PM |

    The best way to alkalize is by eating vegetables and some fruits.  If not eating them, then make smoothies with greens in them....spinach, lettuce, etc.

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