About mljczz

I received a Ph.D. in Biochemistry in 1983 from The Ohio State University. After a sixteen year career researching and developing rapid, ultra-sensitive, quantitative DNA probe assays for the diagnosis and prognosis of deadly diseases, I have been researching and developing meals with optimal nutrition since 2000. Along the way I have also published many other books dealing with nutrition and general philosophical issues. See my Amazon, my Barnes and Noble, or my Smashwords links.

Those most responsible for America’s obesity problem –

The experts, of course.

They recommend skim milk as a healthier alternative to whole milk and to soda.

Odd that nature never figured out that skim milk is healthier than whole milk.

Odd that nature configures our digestive tract to be fully capable of absorbing 500 grams of fat a day.

Odd that the experts do not seem to realize that by skimming milk they are pushing kids to drink more soda – after all, ’tis a competitive world, and taste rules.

The experts would never think of going the other way – adding cream to whole milk to make a beverage that can compete with soda in flavor.

No – that is bad for us!

While it has higher calories and more fat, this enriched milk tastes better and is more satisfying. Soda is low in fat and low in calories, but it stimulates appetite (especially the caffeinated ones), and its own consumption, and in several different ways.

Oh, I almost forgot a reference to the current opinion of the experts:

Ward ZJ, et al. N Engl J Med. 2017;doi:10.1056/NEJMoa1703860.

November 29, 2017

More than half of U.S. children will have obesity by age 35 years if current trends continue, according to results gathered from a simulation model projecting height and weight trajectories.

“Adult obesity is linked with increased risk of diseases, such as diabetes, heart disease and cancer,” Zachary J. Ward, MPH, programmer/analyst at the Center for Health Decision Science at Harvard T.H. Chan School of Public Health, said in a press release. “Our findings highlight the importance of prevention efforts for all children as they grow up, and of providing early interventions for children with obesity to minimize their risk of serious illness in the future.”

Ward and colleagues pooled height and weight data from five nationally representative longitudinal studies totaling 176,720 observations from 41,567 children and adults to estimate the risk for adult obesity. Researchers used the data to create 1,000 virtual populations of 1 million children to age 19 years to represent the U.S. population and then projected height and weight trajectories from childhood to age 35 years.

BMI 35 kg/m2 or higher in adults and 120% or more of the 95th percentile in children were used to define severe obesity.

Researchers projected that more than half (57.3%; 95% uncertainty interval [UI], 55.2-60) of children aged 2 to 19 years will have obesity by age 35 years on the basis of current trends for BMI and obesity.

Researchers observed that the probability that children with obesity who will still be obese at age 35 years increased from 74.9% at age 2 years to 88.2% at 19 years. The probability of obesity at age 35 years in children without obesity decreased from 57.8% at age 2 years to 44.4% at 19 years. Compared with children without obesity, children with obesity had increased RRs for obesity in adulthood of 1.3 (95% UI, 1.17-1.45) at age 2 years to 1.99 (95% UI, 1.8-2.17) at age 19 years.

Severe obesity in childhood significantly increased risks for adulthood obesity at age 35 years with the chances of not being obese ranging from 21% at age 2 years to 6.1% at 19 years.

“It is critically important to implement policies and programs to prevent excess weight gain, starting at an early age,” study researcher Steven L. Gortmaker, PhD, professor of the practice of health sociology in the department of social and behavioral sciences at Harvard T.H. Chan School of Public Health, said in the release. “Plenty of cost-effective strategies have been identified that promote healthy foods, beverages and physical activity within school and community settings.” – by Amber Cox

Disclosures: The authors report no relevant financial disclosures.”


PS: don’t you just love these disclosures? To all of them, I want to append:

“and the fox reports that all of the hens are alive and well in the hen house.”



A dispositive contradiction

If proper nutrition = water + oxygen + the essential nutrients + sufficient energy, then why does an egg, for example, contain so many non-essential nutrients, nutrients that can be made from the essential nutrients?

Eggs contain water, essential nutrients, and energy sources. Oxygen is pulled through the shell and carbon dioxide is pushed out of  the shell. Heat is provided by the body of the hen. Yet eggs have so much more than this.  Why?

Could it be that proper nutrition contains large amounts of substances, which are already manufactured by the organism, but which are still needed because the organism cannot possibly make all of them in sufficient quantities?

If this is the case, then proper nutrition has been seriously misunderstood.

As a result, recommended human diets and animal chows are woefully inadequate. Many errors of interpretation and scientific artifacts have resulted from this single misconception, this gross error.

On the necessity of filtering data so as not to look like a fool

We would rather be intellectually dishonest than to be thought to be a fool. Me – I’m different; I would rather be thought a fool than commit intellectual fraud.

An illustration:

With the following requirements, could you write a sensible, peer-reviewed review of hypertension?

  1. You must begin with an admonishment about limiting salt intake.
  2. You must end by repeating the admonishment.
  3. Throughout you must hit all of the highpoints of the modern, misguided theory of hypertension.
  4. Finally, just before your conclusion, you must thoroughly discuss the hypertension studies on the Pima Indians.

If you can do this, I would like to see it. I think you would look like an idiot, which is exactly why no one even attempts this. Instead, if they even know about it, they sacrifice intellectual integrity so as not to look like a fool.

The facts are these:

  1. In their native country, eating their native diet, native Pima Indians consume as much salt as we do, while hypertension is all but non-existent among them.
  2. Lest any bonehead think this is due to genetic factors, Pima Indians who moved to the big city and adopt our Western lifestyles, transplanted Pima Indians, get hypertension about as often as we do.
  3. Not only do natives not get hypertension, native Pima Indians maintain their systole at the same level their entire natural lifespan, something rarely seen in modern America, where on average hypertension steadily increases with age.
  4. Not only that, but the systole of native Pima Indians is maintained for their lifetimes at about 100, a full 20 points lower than the accepted baseline in America, a value so low that many American doctors would be concerned about it.

Yahweh is my enemy

I hate Yahweh – with a passion. But I forgive 70×7 times the people who created this repulsive, elitist, psychotic god, who teaches us that slavery and genocide are A-OK.

To date, I have found only one thing that I share with this psychotic god –

we both hate whiners. I trust that this does not make me as psycho as Yahweh is.

PS: since Allah is Yahweh on steroids, I hate Allah more. I also forgive the people who outdid the psycho creator of the super-psycho Yahweh.

Weak or non-existent association between protein intake and Crohn’s disease

Based on the last post re: IBD, this result on Crohn’s Disease is hardly surprising.
Nutrients. 2017 May 15;9(5). pii: E500. doi: 10.3390/nu9050500.

Macronutrient Intake and Risk of Crohn’s Disease: Systematic Review and Dose-Response Meta-Analysis of Epidemiological Studies.

Author information

Department of Gastroenterology, The Central Hospital of Enshi Autonomous Prefecture, Enshi 445000, China. zenglirongenshi@sina.com.
Department of Gastroenterology, The Central Hospital of Enshi Autonomous Prefecture, Enshi 445000, China. hushenwhu@163.com.
Department of Gastroenterology, The Central Hospital of Enshi Autonomous Prefecture, Enshi 445000, China. chenpengfeienshi@sohu.com.
Department of Gastroenterology, The Central Hospital of Enshi Autonomous Prefecture, Enshi 445000, China. weiwenbinenshi@sohu.com.
Department of Gastroenterology, The Central Hospital of Enshi Autonomous Prefecture, Enshi 445000, China. tanyuanzhongenshi@sohu.com.


Dietary intake is potentially associated with the onset of Crohn’s disease (CD), but evidence from epidemiological studies has remained unclear. This study aimed to evaluate the role of macronutrient intake in the development of CD. A systematic search was conducted in PubMed and Web of Science to identify all relevant studies, and the role of macronutrients in the development of CD was quantitatively assessed by dose-response meta-analysis. Four case-control studies (a total of 311 CD cases and 660 controls) and five prospective cohort studies (238,887 participants and 482 cases) were identified. The pooled relative risks (RR) for per 10 g increment/day were 0.991 (95% confidence interval (CI): 0.978-1.004) for total carbohydrate intake, 1.018 (95% CI: 0.969-1.069) for total fat intake, and 1.029 (95% CI: 0.955-1.109) for total protein intake. Fiber intake was inversely associated with CD risk (RR for per 10 g increment/day: 0.853, 95% CI: 0.762-0.955), but the association was influenced by study design and smoking adjustment. In subtypes, sucrose intake was positively related with CD risk (RR for per 10 g increment/day: 1.088, 95% CI: 1.020-1.160). Non-linear dose-response association was also found between fiber and sucrose intake and CD risk. In conclusion, this meta-analysis suggested a lack of association between total carbohydrate, fat or protein intake and the risk of CD, while high fiber intake might decrease the risk. In subtypes, high sucrose intake might increase the risk of CD.


Crohn’s disease; disease risk; dose–response; macronutrient intake; meta-analysis

28505133 PMCID: PMC5452230

Is this the explanation of the recent increase inflammatory bowel disease?

Here the abstract of the article:

Am J Gastroenterol. 2010 Oct;105(10):2195-201. doi: 10.1038/ajg.2010.192. Epub 2010 May 11. Animal protein intake and risk of inflammatory bowel disease: The E3N prospective study. Jantchou P1, Morois S, Clavel-Chapelon F, Boutron-Ruault MC, Carbonnel F.

Author information

INSERM, UMRS, Centre for Research in Epidemiology and Population Health, Institut Gustave Roussy, Université Paris Sud, Villejuif, France.



Diet composition has long been suspected to contribute to inflammatory bowel disease (IBD), but has not been thoroughly assessed, and has been assessed only in retrospective studies that are prone to recall bias. The aim of the present study was to evaluate the role of dietary macronutrients in the etiology of IBD in a large prospective cohort.


The Etude Épidémiologique des femmes de la Mutuelle Générale de l’Education Nationale cohort consists of women living in France, aged 40-65 years, and free of major diseases at inclusion. A self-administered questionnaire was used to record dietary habits at baseline. Questionnaires on disease occurrence and lifestyle factors were completed every 24 months. IBDs were assessed in each questionnaire until June 2005, and subsequently validated using clinical and pathological criteria. We estimated the association between nutrients or foods and IBD using Cox proportional hazards models adjusted for energy intake.


Among 67,581 participants (705,445 person-years, mean follow-up since completion of the baseline dietary questionnaire 10.4 years), we validated 77 incident IBD cases. High total protein intake, specifically animal protein, was associated with a significantly increased risk of IBD, (hazards ratio for the third vs. first tertile and 95% confidence interval being 3.31 and 1.41-7.77 (P trend=0.007), and 3.03 and 1.45-6.34 (P trend=0.005) for total and animal protein, respectively). Among sources of animal protein, high consumption of meat or fish but not of eggs or dairy products was associated with IBD risk.


High protein intake is associated with an increased risk of incident IBD in French middle-aged women.

PMID: 20461067 DOI: 10.1038/ajg.2010.192
[Indexed for MEDLINE]

Re this article:

1.Has meat and fish consumption increased dramatically in the last 50 or so years among this cohort of middle aged French women? Not likely, and so while ingestion of more protein than they can digest may be a factor in development of IBD, then how could this be the underlying problem?

2a. How well are the members of this cohort digesting the protein in meat, given the widespread consumption of antacids (including H2 blockers and acid blockers), and the lack of consumption of raw foods (containing enzymes), whole foods, and digestive enzyme supplements? What role does overall under-nutrition play? Also, if undigested protein is a problem, what are the putrefactive bacteria in the bowel doing to undigested proteins? Could bacterial overgrowth of the small bowel -a side effect of acid blockers- be producing a lot of the hydrogen sulfide from sulfur amino acids?

2b. The dairy and egg protein comment is interesting re: digestibility. Meat contains connective tissue, which must be digested away to continue the digestion of the remaining protein in meat, and which itself is tougher to digest than other proteins. While rich in protein, eggs and dairy do not have connective tissue. Undigested meat stimulates the growth of putrefactive (protein-digesting) bacteria, (competitors of beneficial bacteria), and the putrefactive bacteria produce obnoxious compounds like hydrogen sulfide from these amino acids.

3. If the odds ratios are essentially the same for meat protein consumption and total protein consumption, is not the observed correlation related to total protein consumption (and likely under-digestion of protein), and not meat consumption per se? Notice that they reveal their bias, how they use meat consumption as a popular whipping boy in the abstract (essentially throwing red meat at their vegetarian colleagues) and then backtrack to the more relevant “total protein” in their conclusion.

4. In his book, Textbook of Medical Physiology, Guyton notes that the human digestive tract can absorb up to 700 grams of protein per day. But that is only if we eat all day and successfully digest all that protein. To do the latter, we must not interfere with the operations of nature by interfering with digestion; rather, we must assist nature in the digestive phase.

5. The number of IBC cases is so small in this study, just 77, they could all be eating more protein than they can digest – in essence, interfering with their digestion of protein by various means, including taking antacids, H2 blockers, or acid blockers, not eating enough raw foods containing enzymes, not taking digestive enzyme supplements, and under-nourishing their bodies with copious quantities of processed foods, making them less able to cope with the folly of under-digesting proteins.

6. If this result is general, it would be reproduced in other studies, including studies done on other populations (compare Bradford Hill’s criteria) and with similar diseases. It has not been. See:

Clin Nutr. 2017 Oct;36(5):1259-1265. doi: 10.1016/j.clnu.2016.10.009. Epub 2016 Oct 15.

Nutrients. 2017 May 15;9(5). pii: E500. doi: 10.3390/nu9050500.

Both reviews estimate the intake of macronutrients, when what is more relevant – and much harder to measure – is the digestion and absorption of macronutrients, which will only roughly correlate to total intake, a value no one knows with any certainty because people are notoriously bad at quantitative tasks like estimating how much of any particular food they consume each day and computing weekly/monthly averages.

Both reviews are on Crohn’s, one of the two most common forms of the IBDs. If high protein intake drove IBD, we would see an association in Crohn’s, and it would likely be a stronger correlation, the more severe the form of the IBD. They do not.

This irreproducibility in biological correlations is so typical, it is a rule. Guess which study/studies those with a bias against meat consumption cite?

7. Finally, notice the dietary questionnaire. Talk about recall bias! Talk about guaranteed inaccuracy! Not to mention that some people will simply put what they think they should be doing! People are reasonably good at qualitative tasks and poor at best at quantitative tasks. A person who eats very little meat relative to the average may think himself a major consumer and vice versa.

Barking up the wrong tree

When practiced properly, science is remarkable in its ability to find the right answers; however, science is rarely done properly, and thus scientists are remarkable only in their lack of ability to find the right answers.

The situation is so bad that it can be fairly said that as a rule, scientists, as a group, bark up the wrong tree.

For example:

Genetics 101: it takes thousands of years for major genetic changes to occur in the human genome. 10,000 years is a reasonable estimate.

Basic fact about major bowel disease: it has increased about 5 fold in the last 50 years or so.

If you were a scientist, would you look for the explanation of the basic fact re major bowel disease in genetic changes?

Only if you were both a scientist and a dumb ass – unfortunately, the two mostly go hand-in-hand.

What has happened in the last 50 years or so. Lots of things, both good and bad, and nothing simply good or bad.

Powerful anti-acid drugs, including antacids (Maalox, 1949), histamine H2 blockers (cimetidine, 1976), acid blockers (omeprazole, 1988), and low fat dieting (Pritikin, Pritikin Program for Diet and Exercise, 1979) have been introduced during the last 50 years or so.

Basic in vitro observation: acid plus free fatty acids is a potent germ killing combination. At a pH of 3.5 and a free fatty acid concentration of 1 mM, almost 6 logs of germ killing can occur in a test tube, over a period of an hour or so, at body temperature. To put that kind of germ killing into perspective, it is roughly as powerful as exposure of microbes to 100 ppm chlorine bleach for 30 seconds at room temperature.

Does this germ killing reaction occur in the human stomach? Don’t know. Gastric lipase has a pH optimum of around 3.5. Perhaps it does. Is it important to human health? Don’t know. Perhaps.

Could there be a connection between these rather recent developments and the increase in major bowel disease?

Probably not: Only if all of the above are true and nasty bacteria that would otherwise have been killed in the stomach without ant-acids and with a sensible and balanced diet, have aught to do with the development of bowel disease. The effect may be indirect. Germs that are normally killed in the stomach become an unwelcome immune system burden downstream. The mere preoccupation of the immune system with these living, multiplying pests may mean that something else has to give, something very basic to bowel health, something that seems highly unlikely at first thought.

Although improbable, the above idea is possible – at least a person would not be a dumb ass to suspect this, and to do some research.

If a person thinks he has thus uncovered the cause of the increase in major bowel disease, then he is still a dumb ass, because anyone with a functional brain knows that the concept of causation, the absurd idea that one thing is completely responsible for another thing, is yet another example of idiocy.

Unbalanced emotional exaggeration, a product of a mind undisciplined and un-ruled by reason  – that is causation!