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After all my complaints about nutrition science, every now and then I hear about a study that just seems perfect.

Thanks to my NYU colleague Mitchell Moss for sending this account of the study:  Age-old Oreo mystery solved by MIT scientists: Can the cream be evenly split between both sides?

The study (published in a physics journal, no less): On Oreology, the fracture and flow of “milk’s favorite cookie. Crystal E. Owens, Max R. Fan,, A. John Hart, and  Gareth H. McKinley  Physics of Fluids 34, 043107 (2022); https://doi.org/10.1063/5.0085362

The mechanical experience of consumption (i.e., feel, softness, and texture) of many foods is intrinsic to their enjoyable consumption, one example being the habit of twisting a sandwich cookie to reveal the cream. Scientifically, sandwich cookies present a paradigmatic model of parallel plate rheometry in which a fluid sample, the cream, is held between two parallel plates, the wafers. When the wafers are counter-rotated, the cream deforms, flows, and ultimately fractures, leading to separation of the cookie into two pieces.

Method: Using a laboratory rheometer, we measure failure mechanics of the eponymous Oreo’s “creme” and probe the influence of rotation rate, amount of creme, and flavor on the stress–strain curve and postmortem creme distribution.

Results: The results typically show adhesive failure, in which nearly allw (95%) creme remains on one wafer after failure, and we ascribe this to the production process, as we confirm that the creme-heavy side is uniformly oriented within most of the boxes of Oreos…Failure mechanics further classify the creme texture as “mushy.”

Research iInnovations: We introduce Oreology (/ɔriːˈɒlədʒi/), from the Nabisco Oreo for “cookie” and the Greek rheo logia for “flow study,” as the study of the flow and fracture of sandwich cookies…Finally, we introduce and validate the design of an open-source, three-dimensionally printed Oreometer powered by rubber bands and coins for encouraging higher precision home studies to contribute new discoveries to this incipient field of study.

Multimedia: The study comes with a computer-redered animation demonstrating use of the Oreometer (definitely worth a look).

FIG. 11. This computer-rendered animation shows the assembly and use of our Oreometer including inserting the Oreo cookie into the two halves of the clamping fixture, inserting this fixture into the base, and adjusting the base separation, adding “penny castles” to the wings, adding pennies, and finally observing the fractured Oreo.

The press release: MIT engineers introduce the Oreometer

In all, the team went through about 20 boxes of Oreos, including regular, Double Stuf, and Mega Stuf levels of filling, and regular, dark chocolate, and “golden” wafer flavors. Surprisingly, they found that no matter the amount of cream filling or flavor, the cream almost always separated onto one wafer.

Comment:  Who are these people?  I love their study.  I can’t do justice to it in this brief summary.  Read it.  It’s clearly written, elegantly illustrated, and full of delicious tidbits about the construction of Oreos.

But I do have a question: When trans fats were required to be revealed on food labels, Oreo creme was no longer made with hydrogenated oils.  I think the creme in Oreos was firmer with trans fats.  I’m guessing the “mushiness” is due to higher levels of unsaturated fatty acids.  I think a historian needs to get into this.  Is the unfair distribution of creme collateral damage from making its fats healthier?

I subscribe to a newsletter, Obesity and Energetics Offerings, that often includes a section on “Headline versus Study.”  This demonstrates how  headline writers jump actual findings and draw attention-getting conclusions that the studies don’t always support.

Here are four examples, all from the UK Biobank study, an enormous epidemiologic investigation of half a million participants who filled out a dietary questionnaire, and then were followed and tested to see what diseases they developed.  These data enable investigators to link specific dietary factors to disease risk.

Such links are associations. 

This kind of study is not designed to determine whether a dietary factor causes (or prevents) a disease.  For that, other kinds of research are required.

These four examples examine associations of coffee intake with disease risk.  That’s all they do.

The headlines, however, assume causation—an epidemiologic fallacy.

I.  Headline: A Daily Dose of Coffee May Protect You from COVID-19.

Study: Self-Reported Dietary Behaviors and Incident COVID-19 in the UK Biobank.

Results: After multivariable adjustment, the odds (95% CI) of COVID-19 positivity was 0.90 (0.83, 0.96) when consuming 2–3 cups of coffee/day (vs. <1 cup/day), 0.88 (0.80, 0.98) when consuming vegetables in the third quartile of servings/day (vs. lowest quartile), 1.14 (1.01, 1.29) when consuming fourth quartile servings of processed meats (vs. lowest quartile), and 0.91 (0.85, 0.98) when having been breastfed (vs. not breastfed). Associations were attenuated when further adjusted for COVID-19 exposure, but patterns of associations remained.

Conclusions: In the UK Biobank, consumption of coffee, vegetables, and being breastfed as a baby were favorably associated with incident COVID-19; intake of processed meat was adversely associated.

Caveats:  This study looked at associations of several dietary factors to Covid risk: breastfed as baby, and consumption of coffee, tea, oily fish, processed meat, red meat, fruit, and vegetables.  Based on the results, the fallacious headlines could just as easily have read:

• Vegetables may protect you from COVID-19
• Being breastfed may protect you from COVID-19
• Processed meats may increase your risk of COVID-19

The operative word is “may.”  This means that “may not” might also be appropriate.

2.  Headline: Too Much Coffee Can Cause Your Brain to Shrink, Raise Risk of Dementia by 53 Percent, Study Finds.

Study: Associations Among High Coffee Consumption, Brain Volume and Risk of Dementia and Stroke in UK Biobank.

Results: There were inverse linear associations between habitual coffee consumption and total brain (fully adjusted β per cup −1.42, 95% CI −1.89, −0.94), grey matter (β −0.91, 95% CI −1.20, −0.62), white matter (β −0.51, 95% CI −0.83, −0.19) and hippocampal volumes (β −0.01, 95% CI −0.02, −0.003), but no evidence to support an association with white matter hyperintensity (WMH) volume (β −0.01, 95% CI −0.07, 0.05). The association between coffee consumption and dementia was non-linear (Pnon-linearity= 0.0001), with evidence for higher odds for non-coffee and decaffeinated coffee drinkers and those drinking >6 cups/day, compared to light coffee drinkers. After full covariate adjustment, consumption of >6 cups/day was associated with 53% higher odds of dementia compared to consumption of 1–2 cups/day (fully adjusted OR 1.53, 95% CI 1.28, 1.83), with less evidence for an association with stroke (OR 1.17, 95% CI 1.00, 1.37, p = 0.055).

Conclusion: High coffee consumption was associated with smaller total brain volumes and increased odds of dementia.

Caveat: But why non-linear?  If coffee had these effects, shouldn’t more of it should have more of an effect?  Association, alas, does not equal causation.

3.  Headline: Your Morning Cup of Coffee May Lower Your Risk of Liver Disease.

Study: All Coffee Types are Associated with Lower Risk of Adverse Clinical Outcomes in Chronic Liver Disease: A UK Biobank Study.

Results: Compared to non-coffee drinkers, coffee drinkers had lower adjusted HRs of CLD (HR 0.79, 95% CI 0.72–0.86), CLD or steatosis (HR 0.80, 95% CI 0.75–0.86), death from CLD (HR 0.51, 95% CI 0.39–0.67) and HCC (HR 0.80, 95% CI 0.54–1.19). The associations for decaffeinated, instant and ground coffee individually were similar to all types combined.

Conclusion: The finding that all types of coffee are protective against CLD is significant given the increasing incidence of CLD worldwide and the potential of coffee as an intervention to prevent CLD onset or progression.

4.  Headline: Coffee Drinking Won’t Harm Your Health, New Study Reveals Caffeine Lowers Arrhythmia Risk.

Study: Coffee Consumption and Incident Tachyarrhythmias with Mendelian Randomization for Caffeine Metabolism in the UK Biobank.

Findings  In this large, prospective, population-based community cohort study of more than 300 000 participants, each additional daily cup of coffee was associated with a 3% reduced risk of developing an arrhythmia; these associations were not significantly modified by genetic variants that affect caffeine metabolism.

Meaning  Neither habitual coffee consumption nor genetically mediated differences in caffeine metabolism was associated with a heightened risk of cardiac arrhythmias.

Comment: Whether coffee drinking is good, bad, or indifferent to health has long been hotly debated.  For a long time, studies seemed aimed at proving coffee bad for health.  Now, studies seem aimed at showing the opposite.  The UK Biobank is expensive; its funders are largely private foundations and government agencies.  As far as I can tell, the coffee industry is not involved.  My take on all of this?  Take these epidemiological associations with a pinch of caffeine, and enjoy coffee if you like it.

Thanks to Habib Benzian for telling me about this study.

Price information influences the subjective experience of wine: A framed field experiment.  Christoph Patrick Werner, et al.  Food Quality and Preference; 2021;92:104223

Highlights

• First study manipulating wine prices using a framed field experiment.
• Blind intensity ratings differ for 3 wines of different price and expert rating.
• Blind pleasantness ratings do not differ for the same three wines.
• Pleasantness of the budget wine increased when presented with a fake higher price.

The study: The authors got 140 people to taste wines of three different price ranges with open, deceptive, or no price information, and rate them for taste.

The main result: When price information was accurate, participants’ ratings were parallel to cost.  When price information was missing or deceptive, pleasantness ratings did not differ.

Wine A is inexpensive; Wine B is more expensive and rated as medium quality; wine C is expensive and rated outstanding

The press release says it all:  “New Report Highlights How Stagnant U.S. Public Funding for Agricultural Research Threatens Food Systems.”

Stagnant public funding for agricultural research is threatening the future vitality of U.S. food systems – posing risks to farmer productivity and profitability, the steady supply of affordable food for consumers, and ultimately global food security, according to a new report.

The report, jointly commissioned by Farm Journal Foundation and the American Farm Bureau Federation and authored by the IHS Markit Agribusiness Consulting Group, highlights the vital importance of public funding for agricultural research and development (R&D).

New innovations are crucial so that farmers can increase their productivity and meet rising global demand for food, even as climate change intensifies. The world population is expected to reach 10 billion by 2050, and food production will need to increase by 60%-70% to meet rising demand. While private-sector funding for agricultural R&D has been increasing, U.S. public spending has been flat for the past decade.

Here’s the big picture.

Here’s what’s happening with USDA research funding—flat.

And here’s what’s happening with overall agricultural research.  Public funding is flat.  Industry funding is rising rapidly. 

Why is this a problem?  Because industry funds research aimed at developing and marketing profit-making products

This leaves research aimed at public health to be supported by the public.  Research is needed to

• Increase productivity
• Improve crop protection
• Promote animal health and welfare
• Prevent animal diseases
• Protect against pandemics
• Reduce effects of climate change

Industry won’t fund these research areas if there’s no profit in them.

That’s why more public funds need to go to agricultural research.

Here’s a one page summary.

Here’s the full report.

I cannot believe that we are still talking about whether vitamin C prevents colds.  No such luck.

What triggered this is a recent and quite detailed critique of a 2018 meta-analysis of studies of this question: “Extra Dose of Vitamin C Based on a Daily Supplementation Shortens the Common Cold: A Meta-Analysis of 9 Randomized Controlled Trials.”

Its conclusion:  “The combination of supplemental and therapeutic doses of vitamin C is capable of relieving chest pain, fever, and chills, as well as shortening the time of confinement indoors and mean duration.”

You can read the detailed critique of this study for yourself, but I thought this was settled years ago by one of my all-time favorite nutrition studies: Karlowski TR, Chalmers TC, Frenkel LD, Kapikian AZ, Lewis TL, Lynch JM. Ascorbic acid for the common cold. A prophylactic and therapeutic trial. JAMA 1975; 231: 1038–1042.

This fabulous study was done at NIH using NIH employees.  As the abstract puts it,

Three hundred eleven employees of the National Institutes of Health volunteered to take 1 gm of ascorbic acid or lactose placebo in capsules three times a day for nine months. At the onset of a cold, the volunteers were given an additional 3 gm daily of either a placebo or ascorbic acid.

The initial analysis of the data showed a highly significant effect of vitamin C in preventing colds or reducing symptoms.  But the trial had one major flaw: it had an usually big dropout rate.

One hundred ninety volunteers completed the study. Dropouts were defined as those who missed at least one month of drug ingestion. They represented 44% of the placebo group and 34% of those taking ascorbic acid.

These were good investigators.  They asked the dropouts why they had dropped out.  The reason: the study subjects knew (well, they thought they knew) whether they were taking vitamin C or the placebo.

The investigators reanalyzed the data according to what the study subjects thought they were taking.  Those who thought they were taking vitamin C had fewer colds and reduced symptoms—regardless of whether they were taking vitamin C or the placebo.  And those who thought they were taking the placebo had more colds and worse symptoms regardless of whether they really were taking the placebo or were actually taking vitamin C.

The authors’ cautious conclusion:

Analysis of these data showed that ascorbic acid had at best only a minor influence on the duration and severity of colds, and that the effects demonstrated might be explained equally well by a break in the double blind.

My conclusion: Vitamin C is one terrific placebo.

Nothing wrong with that, but that’s why I can’t believe investigators are still arguing about it.

I post often about conflicts of interest in nutrition research, mainly because I worry about how to  improve the quality of nutrition research studies.  Nutrition research is under attack for weaknesses well known to nutrition researchers, but recently rediscovered by critics outside the field who do not, unfortunately, propose meaningful alternatives (see this, for example).

Mainstream nutrition researchers have called for a new approach to nutrition research.

“The time has come for a national ‘moonshot’ on nutrition research,” said Dariush Mozaffarian, MD, DrPH, Dean of the Friedman School of Nutrition Science and Policy at Tufts University, chair of the session. “A strengthening of federal nutrition research has significant potential to generate new discoveries to improve and sustain the health of all Americans, reduce healthcare costs, improve health disparities, create new businesses and jobs, reinvigorate farms and rural communities, strengthen military readiness and optimize use of our natural resources.”

These researchers called for two priorities: a new authority for robust cross-governmental coordination of nutrition research; and strengthened authority and investment for nutrition research within the NIH.

It looks like they got it!  The NIH has proposed to transfer its existing Office of Nutrition Research into the NIH Director’s Office.

The National Institutes of Health (NIH) has proposed to transfer the Office of Nutrition Research (ONR) from the National Institute of Diabetes and Digestive and Kidney Diseases to the Division of Program Coordination, Planning, and Strategic Initiatives (DPCPSI) within the NIH Office of the Director. DPCPSI was created by Congress to enhance NIH-wide coordination of cross-cutting research topics.

This proposed move follows two reports from NIH about nutrition research:

• 2020-2030 Strategic Plan for NIH Nutrition Research
• Nutrition for Precision Health, powered by the All of Us Research Program

And now NIH says it is doing this!

The response from the public and the nutrition research community was overwhelmingly supportive. Such a move was also supported by the Council of Councils, an NIH advisory group, during a special meeting on December 30, 2020.

I’m pleased to share that this week, NIH has begun the official transfer of ONR to DPCPSI. This reorganization positions ONR to enhance engagement of the NIH Institutes and Centers in implementing the 2020-2030 Strategic Plan for NIH Nutrition Research to develop new collaborations and relationships focused on nutrition research within and outside NIH, and to ensure coordination of and leadership for nutrition research across the agency.

Will this strengthen the quality of nutrition research?  I certainly hope so.

Research on this virus (officially SARS CoV-2, commonly COVID-19) is pouring out and filling every medical journal I typically read.  Here are a few recent articles on food-related aspects (some of these are not yet in print).

Obesity and its Implications for COVID-19 Mortality: The authors argue that the increased prevalence of obesity in Italy older adults as compared to its prevalence in China may account for the higher mortality observed in Italy.

Obesity is associated with decreased expiratory reserve volume, functional capacity and respiratory system compliance. In patients with increased abdominal obesity, pulmonary function is further compromised in supine patients by decreased aphragmatic excursion, making ventilation more difficult. Furthermore, increased inflammatory cytokines associated with obesity may contribute to the increased morbidity associated with obesity in COVID-19 infections.

Sudden and Complete Olfactory Loss Function as a Possible Symptom of COVID-19: This is a case study of a patient infected by SARS-CoV-2 whose presenting symptom was the sudden and complete loss of the ability to smell.

Loss of smell and taste in combination with other symptoms is a strong predictor of COVID-19 infection:  “Our study suggests that loss of taste and smell is a strong predictor of having been infected by the COVID-19 virus. Also, the combination of symptoms that could be used to identify and isolate individuals includes anosmia, fever, persistent cough, diarrhoea, fatigue, abdominal pain and loss of appetite.”

COVID‐19 Related School Closings and Risk of Weight Gain Among Children:  “In short, we anticipate that the COVID‐19 pandemic will likely double out‐of‐school time this year for many children in the U.S. and will exacerbate the risk factors for weight gain associated with summer recess.”

Should COVID-19 Concern Nephrologists?  Why and to What Extent? The Emerging Impasse of Angiotensin Blockade:  This is the easiest-to-understand review of the science of this extensively studied virus I have been able to find.  It covers the basics along with detailed explanations of what this virus does, how it works, and where vaccines might operate.    To penetrate human cells, this virus seems to hijack a particular enzyme in the complicated renin-angiotensin system that regulates body fluid balance and blood pressure.

Despite these differences, several studies have reported that SARS-CoV-2 exploits the same membrane-bound angiotensin-converting enzyme 2 (ACE2) as SARS-CoV to gain access to its target cells, although it has greater binding affinity. ACE2 is a carboxypeptidase that preferentially removes carboxy-terminal hydrophobic or basic amino acids. ACE2 cleaves a single residue from angiotensin I (Ang I), generating Ang 1–9, and a single residue from angiotensin II (Ang II) to generate Ang 1–7, whose vasodilator, anti-proliferative, and anti-fibrotic functional effects oppose those of the Ang II generated by angiotensin converting enzyme (ACE).

It’s pretty exciting when a major international science journal starts a satellite journal devoted to food issues.  Welcome to Nature Food.