“betcha can’t eat just one!”
“A popular U.S. brand of potato chips once promoted itself with the slogan, “betcha can’t eat just one!” Maybe that’s because potato chips, like so many foods in the American diet, can pack a mix of ingredients apt to light up people’s brain-reward neural circuitry and overpower mechanisms that are supposed to signal when we’ve had enough to eat. Researchers call this class of foods — often processed foods or sweets with alluring combinations of fat, sugar, carbohydrates and sodium — “hyper-palatable.” While a slew of films, popular books and academic studies have addressed hyper-palatable foods over the past 15 or so years, none has yet to offer a broadly accepted quantitative definition of just what constitutes a hyper-palatable food.”
New research offers specific metrics that might qualify foods as hyper-palatable — and finds most foods consumed in the United States meet these criteria.
“Extensive research has focused on hyper‐palatable foods (HPF); however, HPF are defined using descriptive terms (e.g., fast foods, sweets), which are not standardized and lack specificity. The study purpose was to develop a quantitative definition of HPF and apply the definition to the Food and Nutrient Database for Dietary Studies (FNDDS) to determine HPF prevalence in the US food system.”
“The study is the first to provide a quantitative definition of HPF to be used as a starting point for future research. Given the immense contributions of HPF to obesity risk and related health conditions, it is imperative that the research community develop and validate a specific, quantitative definition of HPF that will advance the field’s understanding of potential mechanisms that may drive overeating and obesity. The HPF definition may also be an asset to inform future food policy work. A major barrier to policy legislation on HPF is that there is no precise definition to inform regulation, and it is not feasible to limit or restrict entire categories of foods (e.g., desserts). Given the ways in which HPF are integrated into our existing food system, strong and specific scientific evidence will be needed to dislodge and eventually regulate some of the most problematic foods that are associated with extensive disease and disability in the US. The HPF definition and quantitative criteria presented in this study represent a crucial first step in this process.”
“Fazzino and her KU coauthors — Kaitlyn Rohde, research assistant at the Cofrin Logan Center and Debra K. Sullivan of the Department of Dietetics and Nutrition at the University of Kansas Medical Center — sought to define criteria for hyperpalatable foods by conducting a literature review, and then using nutrition software and applying their definition to 7,757 food items in the U.S. Department of Agriculture’s Food and Nutrient Database for Dietary Studies (FNDDS).”
In this before-after study and trial that included 214 adults who regularly drank SSBs, participants reported consuming less SSBs after a workplace sales ban and a reduction in waist circumference and sagittal diameter but no change in body mass index or insulin sensitivity. Those randomized to receive a brief motivational intervention had greater improvements.
“As rates of cardiometabolic diseases continue to rise, private employers are likely to face greater productivity losses and private health expenditures. The results of this study suggest that workplace SSB sales bans, if widely adopted, could add another layer of efficacy to existing SSB reduction strategies. At the societal level, private sector–driven change through workplace sales bans seems to offer a strategy that complements existing governmental reform efforts. Although effective, governmental reform policies, such as SSB taxation and warning labels, face significant political obstacles that private-sector sales bans do not.”
Articles about the Study
Doctors call on workplaces to ban sale of sugary drinks, The Guardian
Paper in Cell Metabolism:
It’s long been known that both “lipotoxicity” and “glucotoxicity” are associated with inflammation leading to diabetes. But it wasn’t clear which, when, and how, resulting in different factions battling for supremacy. The science of this controversy is now beginning to come into focus.
A paper two weeks ago from Softic et al. in Cell Metabolism demonstrates that fructose inhibits mitochondrial beta-oxidation through alteration of specific mitrochondrial proteins, conversely glucose stimulates it. Thus dietary sugar is more metabolically problematic than dietary starch; a finding that our group corroborated in obese children.
This paper from Nicholas et al. also in Cell Metabolism, demonstrates that because of that mitochondrial dysfunction, fatty-acylcarnitine, which should be beta-oxidized, can power the production of TH17 cytokines that in part drive that inflammation. Furthermore, one must remember that some of that fatty acid production can be derived via de novo lipogenesis using fructose as a substrate.
This paper, combined with Softic, helps bridge the gap to show that, at the molecular level, it appears to be the combination of both fat and fructose at the mitochondria that drives the inflammatory process.
The Societal Math of Processed Food (U.S.)
The food industry grosses 1.46 Trillion / yr
-657 billion is gross profit
Health care costs in the U.S. total $3.5 trillion / yr
-75% of which is chronic metabolic disease
-75% of which is preventable
Thus, $1.9 trillion / yr is wasted.
We lose triple what the food industry makes.
This is unsustainable, and explains why Medicare will be broke by 2026, and neither “Obamacare” or “Trumpcare” or “Medicare for All” can fix it (and not the NHS either).
This paper is huge. One of the arguments the food industry advances is that sugar consumption has gone down while obesity has gone up, so it can’t be sugar. This paper uses a complex statistical analysis to show that US obesity is a function of both current sugar consumption and an derivative of the sugar consumed by the previous generation going forward. In other words, it’s the economic equivalent of “epigenetics”. This is yet another nail in the coffin (as if we needed any more nails)!
“The majority of observational studies addressing synthetic or non-nutritive sweeteners (NNS) consumption show an association with metabolic dysregulation.”
Beyond food intake, numerous studies have shown…
weaker caloric compensation
Swithers et al., 2010
synthetic sweeteners act through the microbiome
Suez et al., 2014
reduced validity of “sweetness” to predict caloric content
Swithers et al., 2010
significant correlation between NNS consumption and weight gain in an 80,000 participants study
Stellman and Garfinkel, 1988
Other independent studies confirmed these associations, with synthetically sweetened beverage consumption being associated with a much higher incidence of metabolic syndrome (odds ratio ∼1.93) when compared to non-users
Fowler et al., 2008
Lutsey et al., 2008
and NNS consumption has been identified as a significant risk factor for metabolic disease
Blum et al., 2005
in middle-aged adults
Dhingra et al., 2007
and in the elderly
Fowler et al., 2015
One study showed that NNS consumers exhibit reduced weight gain
Schulze et al., 2004
however, these participants showed increased risk for developing diabetes in an 8-year follow-up.
Furthermore, human intervention studies have also shown that ingestion of NNS could
Tordoff and Alleva, 1990
The overall impact of NNS on metabolic health remains controversial.
“Despite inclusion in thousands of products, and consumption by billions of people, the molecular effects of ingesting synthetically sweetened food are not well understood. Moreover, there is conflicting evidence from both human and animal studies as to whether or not synthetic sweeteners interact with overall physiology or regulation of energy homeostasis.”
All the studies referenced here are cited and hyperlinked in the article.
Finally, they’ve woken up and smelled the coffee! Obesity is not the issue, metabolic health is.
But there are three other markers that are important: fasting insulin, uric acid, and ALT.
-Dr. Robert Lustig
Endocrine Daily Briefing – From the Endocrine Society
Endocrine Society Issues New Clinical Practice Guideline To Identify People At Metabolic Risk
Medscape (7/31, Busko, Subscription Publication) reports, “By screening for five simple markers – waist size, blood pressure, HDL cholesterol, triglycerides, and glucose/HbA1C – during office visits, clinicians could identify high-risk adults who need to improve their lifestyle to prevent cardiovascular disease or type 2 diabetes [T2D],” experts recommend in a “new clinical practice guideline – ‘Primary Prevention of ASCVD and T2DM in Patients at Metabolic Risk’ – issued by the Endocrine Society and published online July 31 in the Journal of Clinical Endocrinology and Metabolism.” Included in the new guideline is “the American Heart Association/American College of Cardiology Pooled Cohort Equation to calculate 10-year risk for atherosclerotic disease.”
Endocrine Today (7/31, Schaffer) reports the guideline states, “The Endocrine Society has recognized the importance of identifying individuals who are at metabolic risk so that efforts can be instituted to prevent both [atherosclerotic] CVD and [type 2 diabetes].” In particular, the guideline “addresses individuals with components of metabolic syndrome who do not yet have diagnosed atherosclerotic CVD or type 2 diabetes and the steps that can be taken to prevent these two diseases.” In addition, it “focuses on behavioral, nutritional and medical management.”
According to Endocrine News (7/31, Seaborg), “the original Endocrine Society guideline on this topic was published in 2008.” This revision, however, “takes a fresh look at metabolic risk and presents recommendations which reflect more recent trial data on blood pressure and lipids,” prioritizing “lifestyle and behavioral interventions” while discussing “new medical treatment options.” Even though “the guideline is targeted towards adults aged 40 to 75,” it “can be used to guide patients outside of this age range as well.”
How scared is the juice industry? Nothing wrong with their making a critique, just remarkable to see what lengths they will go to squelch dissent.
From the resistance… a letter received from the Juice Products Association:
It’s a trend we are all seeing – more and more studies are being conducted and published without pre-specified analysis. Researchers test connections unsystematically and publish only positive results. Our standards for how we conduct and communicate nutrition research to the public are slipping.
Last week a study was published, by the British Medical Journal that suggests that drinking 100% juice is linked with an increased risk of cancer. As you know, a person’s health is dependent upon the totality of their diet and lifestyle – not one specific food or beverage. Studies such as this one do not prove cause and effect yet that is what headlines scream.
Furthermore, these results contradict several other studies, including large U.S. cohort studies, concerning 100% fruit juice consumption and cancer, which shows no association with increased risk. In fact, 100% fruit juices contain bioactive compounds that have been shown to have anti-carcinogenic properties in some studies, (Veselkov et al. Scientific Reports. 2019;9:9237).
There were a number of limitations with the NutriNet-Santé study published last week. These include, but are not limited to:
- The study is observational and, as such, is unable to show cause and effect, only associations.
- The study was based on a French cohort and not representative of US culture, dietary patterns and eating styles. It is also not indicative of typical consumption patterns seen in the United States regarding sugary drink consumption.
- Much of the data was obtained through self-reporting, which introduces errors
- The mean follow-up time (about 5 years) is very short for a cancer study
- These results cannot be applied to a general population as the cohort was overwhelmingly female (almost 79%)
Together, we can make our voices heard against bad science. I am commenting on news coverage regarding this study in order to educate the public and consumers who are confused about nutrition. I urge you to join me in speaking out against studies like this that are not based on scientific best practices and cause unnecessary consumer confusion.
For more information, visit SipSmarter.org. Please don’t hesitate to contact me directly if you have any questions, concerns, or need any other information. I would be happy to discuss.
Diane Welland MS, RD
Juice Products Association
What about fruit juice?
Fruit Juices Are Basically Just Liquid Sugar
Fruit juice products are exploding and it seems like most people believe fruit juices are healthy…they come from fruit, so they must be OK?
Unfortunately, many of the “fruit” juice products you find in the supermarket aren’t even fruit juice, just fruit flavored beverages imbued with chemicals that taste like fruit. Many of these products are basically fruit-flavored sugar water.
Even if you’re drinking 100% fruit juice (organic, natural, made in your own juicer, blah, blah, blah), it is still a problem. Fruit juice often has had the fiber taken out or destroyed and the main thing left is the sugar, now concentrated. Despite their healthy image and brilliant marketing, many fruit juice products contain the same amount of sugar as sugar-sweetened beverages.
A typical glass of orange juice contains 4 oranges. One serving of orange juice (an 8-ounce glass) contains 22 grams of sugar. By comparison, 8-ounces of Dr. Pepper (pick your soda) contains 27 grams of sugar.
One simple solution is not to drink your calories. Eat whole fruit – with the fiber. Try “spa water” recipes that use small amounts of fruit for flavoring. And when you absolutely need some juice, than make it a small glass.
How many oranges have you consumed in one sitting? The fiber in whole fruit increases satiety and also helps to metabolize the sugar in healthy ways. Since our diet is already so overloaded with sugar, big blasts of sugar tend to be bad for our metabolic health.
Review of recent study published in Cell Metabolism:
Ultra-Processed Diets Cause Excess Calorie Intake and Weight Gain: An Inpatient Randomized Controlled Trial of Ad Libitum Food Intake.
Kevin D. Hall 5 Alexis Ayuketah Robert Brychta Hongyi Cai Thomas Cassimatis Kong Y. Chen Stephanie T. Chung Elise Costa Amber Courville Valerie Darcey Laura A. Fletcher Ciaran G. Forde Ahmed M. Gharib Juen Guo Rebecca Howard Paule V. Joseph Suzanne McGehee Ronald Ouwerkerk Klaudia Raisinger Irene Rozga Michael Stagliano Mary Walter Peter J. Walter Shanna Yang Megan Zhou
Published:May 16, 2019
Comments by Dr. Robert Lustig
A calorie is a calorie is a calorie; eat less and exercise more; any calorie can be part of a balanced diet. These are the mantras of the processed food industry. But are they real or fake news?
Hall and his NIH group attempted to answer this question with a 2-week crossover demand feeding study comparing the effects of real food (NOVA system class I, developed by Monteiro et al at the University of Sao Paolo) with ultra-processed food (NOVA system class IV). Hall locked up 20 subjects at the NIH Clinical Center, threw away the key, and fed them in random order and for 2 weeks at a time an ad lib processed food diet (more carbohydrate, less fiber) or an ad lib real food diet (less carbohydrate, more fiber). The two diets were matched for presented calories, sugar, fat, fiber, and macronutrients. Hall tracked food intake, body weight, energy expenditure, and baseline and glucose-stimulated hormonal parameters.
The ultra-processed food diet resulted both in weight gain and 508 calories per day greater intake (mostly carbohydrate) than the real food diet, which resulted in weight loss. The only things that distinguished the ingestion patterns were higher carbohydrate and less fiber in the ultra-processed diet. Finally, body weight changes correlated with changes in energy intake.
Bottom line: like other studies which preceded it (eg, the DIETFITS study), this study shows that real food works, and processed food doesn’t — take it to the bank. Real food resulted in fewer calories consumed, but we can’t infer that the effect was due to increased fiber (fewer calories absorbed); decreased energy density; reductions in carbohydrate; reductions in insulin and changes in leptin signaling; feeding the microbiome; and/or increased satiety.
And what about the food industry’s real versus fake news? Can we discern if, and which, macronutrients are the bad guys? What really reduced caloric intake? Unfortunately, this study was not designed or powered to assess whether certain macronutrients (like starch, fat, fructose) altered food intake apart from its caloric equivalent. Hall is a thermodynamics guy—and a calorie is always a calorie. So, don’t expect any other seminal answers out of this one.
Commentary originally published in PracticeUpdate!
Lustig RH. Ultra-Processed Diets Cause Excess Calorie Intake and Weight Gain: An Inpatient Randomized Controlled Trial of ad Libitum Food Intake. PracticeUpdate website. Available at: https://www.practiceupdate.com/content/ultra-processed-diets-cause-excess-calorie-intake-and-weight-gain/84403/65/8/1. Accessed July 11, 2019
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