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

Who says logical tautologies cannot have profound consequences?


Suppose someone is both depressed and aggressive, with much of the aggression and anger directed toward himself/herself. Such a person is likely at higher risk of suicide (and I believe is more likely to have been born in winter). Further suppose that this person with depression is being treated for depression and lack of sleep without drugs and the person suddenly starts sleeping much better. Would you retest him/her for depression, even if he/she claims his moods are no better?

Treating a significant improvement in sleep as a marker and forerunner of well-being, I believe you would, based on simple logic:

(depressed->poor sleep)->(not poor sleep-> not depressed).

This is the famous (a->b) -> (-b->-a)

In words, if a person is depressed, he has poor quality sleep and/or poor quantity of sleep. If he does not have poor sleep, he is not depressed. Better test!

Another view of 5 servings a day of plant food vs cancer

If we assume that those consuming 5 or more servings a day of plant foods are those who are the most health conscious, then the fact that the reduction in the risk for various types of cancer is so small that some studies flat out miss the effect argues that our health consciousness is not very accurate – we are consciously making mistakes about as often as we are choosing wisely.

The body tells us we are wrong over and over again: when are we going to listen?

The body is telling us we are wrong.

Give the body a squalene supplement and it efficiently absorbs it.

The body makes squalene and puts it to numerous good uses, but it does not make enough to meet its needs; “so” it tries to absorb whatever we give it.

Doctors prescribe statins to those who have high serum cholesterol, regardless of the reasons behind the high cholesterol. Doctors would mistakenly prescribe statins to those eating the traditional Polynesian diet.

Because statins inhibit our CoQ10 synthesis, doctors recommend that those on statins take CoQ10 (another substance the body readily absorbs “because” we do not make enough of it). What about all of the other important products made by the mevalonate pathway?

Including squalene.

Including dolichols. Want to bet the body avidly absorbs these too?

Including isoprenyls.

Including so many other useful compounds.

When are we going to get a clue? Equivalently, when are we going to take our clues from what the body is doing?

Barking up the wrong tree

If scientists were reincarnated as hunting dogs, many would be used in humorous skits because the rest of us can easily see and hear where the birds are hiding, but the scientists-turned-dogs would invariably be barking up the wrong tree.

Consider this piece of cluelessness about an important vitamin but an obviously wrong thesis:

Acta Ophthalmol. 2016 May;94(3):e170-6. doi: 10.1111/aos.12688. Epub 2015 Mar 4.

Association of vitamin C with the risk of age-related cataract: a meta-analysis.

Author information

  • 1Department of Ophthalmology, The Second Artillery General Hospital, Beijing, China.



Whether vitamin C is a protective factor for age-related cataract remains unclear. Thus, we conducted a meta-analysis to summarize the evidence from epidemiological studies of vitamin C and the risk of age-related cataract.


Pertinent studies were identified by searching in PubMed and in Webscience. The random effect model was used to combine the results. Meta-regression and subgroups analyses were used to explore potential sources of between-study heterogeneity. Publication bias was estimated using Egger’s regression asymmetry test.


Finally, 15 articles with 20 studies for vitamin C intake and eight articles with 10 studies for serum ascorbate were included in this meta-analysis. The relative risk (RR) and 95% confidence interval of cataract for the highest versus the lowest category of vitamin C intake was 0.814 (0.707-0.938), and the associations were significant in America and Asia. Significant association of cataract risk with highest versus the lowest category of serum ascorbate was found in general [0.704 (0.564-0.879)]. Inverse associations were also found between serum ascorbate and nuclear cataract and posterior subcapsular cataract.


Higher vitamin C intake and serum ascorbate might be inversely associated with risk of cataract. Vitamin C intake should be advocated for the primary prevention of cataract.


age-related cataract; meta-analysis; serum ascorbate; vitamin C

PMID: 25735187
DOI: 10.1111/aos.12688

How did I know a priori that the thesis is ridiculous? An entire civilization that must have had marginal vitamin C intake was without any significant evidence for excess cataracts.

In the long cold winters, the isolated Swiss had a diet consisting of: 2-3 servings of meat per week (none or negligible vitamin C), raw milk (some vitamin C), raw dairy products derived from milk (mostly cheese and butter, even less due to processing out the vitamin C in the liquid phase), and rye bread (no vitamin C). If these people had glassy eyes like so many peoples do around the world, would Weston Price have failed to notice the problem and report it? No.

Since vitamin C consumption is obviously not a factor in cataract development, does the following study surprise us?

Cochrane Database Syst Rev. 2012 Jun 13;(6):CD004567. doi: 10.1002/14651858.CD004567.pub2.

Antioxidant vitamin supplementation for preventing and slowing the progression of age-related cataract.

Author information

  • 1MetroWest Medical Center, Framingham, Massachusetts, USA. milan@milanmathew.com.



Age-related cataract is a major cause of visual impairment in the elderly. Oxidative stress has been implicated in its formation and progression. Antioxidant vitamin supplementation has been investigated in this context.


To assess the effectiveness of antioxidant vitamin supplementation in preventing and slowing the progression of age-related cataract.


We searched CENTRAL (which contains the Cochrane Eyes and Vision Group Trials Register) (The Cochrane Library 2012, Issue 2), MEDLINE (January 1950 to March 2012), EMBASE (January 1980 to March 2012), Latin American and Caribbean Literature on Health Sciences (LILACS) (January 1982 to March 2012), Open Grey (System for Information on Grey Literature in Europe) (www.opengrey.eu/), the metaRegister of Controlled Trials (mRCT) (www.controlled-trials.com), ClinicalTrials.gov (www.clinicaltrials.gov) and the WHO International Clinical Trials Registry Platform (ICTRP) (www.who.int/ictrp/search/en). There were no date or language restrictions in the electronic searches for trials. The electronic databases were last searched on 2 March 2012. We also checked the reference lists of included studies and ongoing trials and contacted investigators to identify eligible randomized trials.


We included only randomized controlled trials in which supplementation with one or more antioxidant vitamins (beta-carotene, vitamin C and vitamin E) in any form, dosage or combination for at least one year was compared to another antioxidant vitamin or to placebo.


Two authors extracted data and assessed trial quality independently. We pooled results for the primary outcomes, i.e., incidence of cataract and incidence of cataract extraction. We did not pool results of the secondary outcomes – progression of cataract and loss of visual acuity, because of differences in definitions of outcomes and data presentation. We pooled results by type of cataract when data were available. We did not perform a sensitivity analysis.


Nine trials involving 117,272 individuals of age 35 years or older are included in this review. The trials were conducted in Australia, Finland, India, Italy, the United Kingdom and the United States, with duration of follow-up ranging from 2.1 to 12 years. The doses of antioxidant vitamins were higher than the recommended daily allowance. There was no evidence of effect of antioxidant vitamin supplementation in reducing the risk of cataract, cataract extraction, progression of cataract or in slowing the loss of visual acuity. In the pooled analyses, there was no evidence of effect of beta-carotene supplementation in reducing the risk of cataract (two trials) (relative risk (RR) 0.99, 95% confidence interval (CI) 0.91 to 1.08; n = 57,703) or in reducing the risk of cataract extraction (three trials) (RR 1.00, 95% CI 0.91 to 1.10; n = 86,836) or of vitamin E supplementation in reducing the risk of cataract (three trials) (RR 0.97, 95% CI 0.91 to 1.04; n = 50,059) or of cataract extraction (five trials) (RR 0.98, 95% CI 0.91 to 1.05; n = 83,956). The proportion of participants developing hypercarotenodermia (yellowing of skin) while on beta-carotene ranged from 7.4% to 15.8%.


There is no evidence from RCTs that supplementation with antioxidant vitamins (beta-carotene, vitamin C or vitamin E) prevents or slows the progression of age-related cataract. We do not recommend any further studies to examine the role of antioxidant vitamins beta-carotene, vitamin C and vitamin E in preventing or slowing the progression of age-related cataract. Costs and adverse effects should be weighed carefully with unproven benefits before recommending their intake above recommended daily allowances.

PMID: 22696344
PMCID: PMC4410744
DOI: 10.1002/14651858.CD004567.pub2
[PubMed – indexed for MEDLINE]

Free PMC Article


Anyone knowing Weston Price’s observational data would not even have done this meta-analysis. A complete waste of time – killer counterexamples are real and smart scientists save time by paying attention to them.



Deducing our body’s programs one by one

Who says that biology is purely inductive? Nonsense- there are deductions to be had.

Consider the workings of our digestive system, far from perfect, but better than we know because we are doing so many harmful things to our system and then blaming our system for not adapting to our errors on the fly.

Our digestion is strongly acidic, as is that of every vertebrate tested. Calcium has to be solubilized. That probably drove this, but that is only the beginning.

That switch to acidic digestion during the evolution of vertebrates necessitated a gut that is adapted to acidophilus organisms and is likely averse to certain acidophobic organisms.

Since bacteria, yeast, and fat are present in our foods, and it appears that free fatty acids plus stomach acid is a strong germ killer, nature made use of the slight advantage that acidophilus organisms would have in that environment and sacrificed the rest of the microbes, some of which would be downright harmful, and sacrificed a large proportion of acidophilus as well, and harvested their enzymes, getting better digestion, less bloating, more nutrients and better intestinal motility in the process.