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Association Between Plant and Animal Protein Intake and Overall and Cause-Specific Mortality.
Huang, J, Liao, LM, Weinstein, SJ, Sinha, R, Graubard, BI, Albanes, D
JAMA internal medicine. 2020;180(9):1173-1184
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High-quality protein diets have been shown in previous studies to have health benefits, mainly due to associated fat loss. However, studies examining dietary protein sources and death has not been extensively researched and is often controversial. This cohort study of 400,000 participants aimed to examine whether plant and animal protein intake from various sources effects death rates over 16 years. The results showed that increased intakes of plant protein were associated with lower rates of death by any cause in both men and women, whereas animal protein intake was not. Plant protein intake was associated with lower death rates from heart disease and stroke combined but did not affect death rates due to heart disease alone, cancer or respiratory disease. Interestingly when substituting 3% energy from animal protein to plant protein an association with lower death rates from all causes and heart disease was observed, which was especially apparent when substituting red meat and egg protein but not white meat protein. It was concluded that dietary modifications in favour of plant protein may incur health benefits resulting in longer life. This study could be used by healthcare professionals to understand that recommending dietary changes to increase plant protein intake may increase longevity.
Abstract
Importance: Although emphasis has recently been placed on the importance of high-protein diets to overall health, a comprehensive analysis of long-term cause-specific mortality in association with the intake of plant protein and animal protein has not been reported. Objective: To examine the associations between overall mortality and cause-specific mortality and plant protein intake. Design, Setting, and Participants: This prospective cohort study analyzed data from 416 104 men and women in the US National Institutes of Health-AARP Diet and Health Study from 1995 to 2011. Data were analyzed from October 2018 through April 2020. Exposures: Validated baseline food frequency questionnaire dietary information, including intake of plant protein and animal protein. Main Outcomes and Measures: Hazard ratios and 16-year absolute risk differences for overall mortality and cause-specific mortality. Results: The final analytic cohort included 237 036 men (57%) and 179 068 women. Their overall median (SD) ages were 62.2 (5.4) years for men and 62.0 (5.4) years for women. Based on 6 009 748 person-years of observation, 77 614 deaths (18.7%; 49 297 men and 28 317 women) were analyzed. Adjusting for several important clinical and other risk factors, greater dietary plant protein intake was associated with reduced overall mortality in both sexes (hazard ratio per 1 SD was 0.95 [95% CI, 0.94-0.97] for men and 0.95 [95% CI, 0.93-0.96] for women; adjusted absolute risk difference per 1 SD was -0.36% [95% CI, -0.48% to -0.25%] for men and -0.33% [95% CI, -0.48% to -0.21%] for women; hazard ratio per 10 g/1000 kcal was 0.88 [95% CI, 0.84-0.91] for men and 0.86 [95% CI, 0.82-0.90] for women; adjusted absolute risk difference per 10 g/1000 kcal was -0.95% [95% CI, -1.3% to -0.68%] for men and -0.86% [95% CI, -1.3% to -0.55%] for women; all P < .001). The association between plant protein intake and overall mortality was similar across the subgroups of smoking status, diabetes, fruit consumption, vitamin supplement use, and self-reported health status. Replacement of 3% energy from animal protein with plant protein was inversely associated with overall mortality (risk decreased 10% in both men and women) and cardiovascular disease mortality (11% lower risk in men and 12% lower risk in women). In particular, the lower overall mortality was attributable primarily to substitution of plant protein for egg protein (24% lower risk in men and 21% lower risk in women) and red meat protein (13% lower risk in men and 15% lower risk in women). Conclusions and Relevance: In this large prospective cohort, higher plant protein intake was associated with small reductions in risk of overall and cardiovascular disease mortality. Our findings provide evidence that dietary modification in choice of protein sources may influence health and longevity.
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Ultra-Processed Diets Cause Excess Calorie Intake and Weight Gain: An Inpatient Randomized Controlled Trial of Ad Libitum Food Intake.
Hall, KD, Ayuketah, A, Brychta, R, Cai, H, Cassimatis, T, Chen, KY, Chung, ST, Costa, E, Courville, A, Darcey, V, et al
Cell metabolism. 2019;30(1):67-77.e3
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Diets high in ultra-processed foods have been related to several poor health outcomes and even death, possibly due to properties that make them highly palatable resulting in overeating and obesity. However, to date, there are few studies that demonstrate this relationship. This randomised control trial of 20 individuals aimed to compare the effects of an ultra-processed diet to an unprocessed diet on energy intake. The results showed that the ultra-processed diet resulted in higher energy intakes due to increased carbohydrates and fat, whereas energy intake during the unprocessed diet remained stable and this was not due to differences in pleasantness of familiarity. During the ultra-processed diet participants gained weight, and lost weight during the unprocessed phase, due to increased energy intake. It was concluded that eliminating ultra-processed foods from the diet decreases energy intake resulting in weight loss. Healthcare professionals could use this study to understand the importance of recommending a diet without ultra-processed foods to decrease overeating and improve health.
Abstract
We investigated whether ultra-processed foods affect energy intake in 20 weight-stable adults, aged (mean ± SE) 31.2 ± 1.6 years and BMI = 27 ± 1.5 kg/m2. Subjects were admitted to the NIH Clinical Center and randomized to receive either ultra-processed or unprocessed diets for 2 weeks immediately followed by the alternate diet for 2 weeks. Meals were designed to be matched for presented calories, energy density, macronutrients, sugar, sodium, and fiber. Subjects were instructed to consume as much or as little as desired. Energy intake was greater during the ultra-processed diet (508 ± 106 kcal/day; p = 0.0001), with increased consumption of carbohydrate (280 ± 54 kcal/day; p < 0.0001) and fat (230 ± 53 kcal/day; p = 0.0004), but not protein (-2 ± 12 kcal/day; p = 0.85). Weight changes were highly correlated with energy intake (r = 0.8, p < 0.0001), with participants gaining 0.9 ± 0.3 kg (p = 0.009) during the ultra-processed diet and losing 0.9 ± 0.3 kg (p = 0.007) during the unprocessed diet. Limiting consumption of ultra-processed foods may be an effective strategy for obesity prevention and treatment.
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Gut dysbiosis: a potential link between increased cancer risk in ageing and inflammaging.
Biragyn, A, Ferrucci, L
The Lancet. Oncology. 2018;19(6):e295-e304
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This study looks at the important role our gut bacterial and commensal microbes play in supporting immunity and potentially reducing the risk of cancer from aging. Cancer risk increases as we age and is one of the main causes of reduced life expectancy. Our gut microbiome changes continually in response to diet, lifestyle, infection, and activation of immune responses. Gut dysbiosis is characterised by a shift towards proinflammatory commensals and a reduction of beneficial microbes, which can cause impairment and leakiness of the intestinal barrier. This is thought to trigger inflammaging or rather aging in a state of continual inflammation, where the immune system is in a heightened state of activation, and the body essentially creates an environment conducive to cancer. The gut is populated by trillions of species of bacteria which work together with our immune cells. As we age the diversity and density of these beneficial bacteria reduce. Therapies which support the balance of our commensal bacteria may prove effective at reducing rates of cancer in the elderly.
Abstract
Cancer incidence substantially increases with ageing in both men and women, although the reason for this increase is unknown. In this Series paper, we propose that age-associated changes in gut commensal microbes, otherwise known as the microbiota, facilitate cancer development and growth by compromising immune fitness. Ageing is associated with a reduction in the beneficial commensal microbes, which control the expansion of pathogenic commensals and maintain the integrity of the intestinal barrier through the production of mucus and lipid metabolites, such as short-chain fatty acids. Expansion of gut dysbiosis and leakage of microbial products contributes to the chronic proinflammatory state (inflammaging), which negatively affects the immune system and impairs the removal of mutant and senescent cells, thereby enabling tumour outgrowth. Studies in animal models and the importance of commensals in cancer immunotherapy suggest that this status can be reversible. Thus, interventions that alter the composition of the gut microbiota might reduce inflammaging and rejuvenate immune functions to provide anticancer benefits in frail elderly people.
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Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty.
Ferrucci, L, Fabbri, E
Nature reviews. Cardiology. 2018;15(9):505-522
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Inflammageing is a term used to describe elevated blood inflammatory markers that leads to frailty and increases an individual’s risk for heart disease, kidney disease and other physical and mental illnesses. Whether inflammageing is causal in heart disease is still uncertain. This large review of 310 papers aimed to understand the causes and role of inflammageing in heart disease and other illnesses associated with ageing. Causes of inflammageing were discussed and mechanisms are not fully understood. Genetic susceptibility, obesity, gut microbiota, gut permeability, when cells can no longer divide, and chronic infections were all implicated. The role of inflammageing in heart disease was a focus and the authors deduced that it was likely to be both causal and a result of heart disease. However, the administration of anti-inflammatories in heart disease has not always proved a successful treatment. Possible causes of inflammageing are likely to be linked and cumulative and although inflammation may cause age related diseases, its role in protecting the body means that its benefits outweigh its consequences. It was concluded that controlling inflammageing may prevent heart disease and other diseases associated with ageing. This study could be used by healthcare professionals to help understand what inflammageing is and its role in age related diseases.
Abstract
Most older individuals develop inflammageing, a condition characterized by elevated levels of blood inflammatory markers that carries high susceptibility to chronic morbidity, disability, frailty, and premature death. Potential mechanisms of inflammageing include genetic susceptibility, central obesity, increased gut permeability, changes to microbiota composition, cellular senescence, NLRP3 inflammasome activation, oxidative stress caused by dysfunctional mitochondria, immune cell dysregulation, and chronic infections. Inflammageing is a risk factor for cardiovascular diseases (CVDs), and clinical trials suggest that this association is causal. Inflammageing is also a risk factor for chronic kidney disease, diabetes mellitus, cancer, depression, dementia, and sarcopenia, but whether modulating inflammation beneficially affects the clinical course of non-CVD health problems is controversial. This uncertainty is an important issue to address because older patients with CVD are often affected by multimorbidity and frailty - which affect clinical manifestations, prognosis, and response to treatment - and are associated with inflammation by mechanisms similar to those in CVD. The hypothesis that inflammation affects CVD, multimorbidity, and frailty by inhibiting growth factors, increasing catabolism, and interfering with homeostatic signalling is supported by mechanistic studies but requires confirmation in humans. Whether early modulation of inflammageing prevents or delays the onset of cardiovascular frailty should be tested in clinical trials.
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A systematic review of attentional biases in disorders involving binge eating.
Stojek, M, Shank, LM, Vannucci, A, Bongiorno, DM, Nelson, EE, Waters, AJ, Engel, SG, Boutelle, KN, Pine, DS, Yanovski, JA, et al
Appetite. 2018;123:367-389
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Binge eating behaviour is a feature of certain eating disorders (such as binge eating disorder (BED), bulimia nervosa (BN) and binge-purge subtype of anorexia nervosa (AN). It can also be a problem for those who do not meet the criteria for an eating disorder diagnosis. The presence of binging, and a loss of control is a risk for eating disorder development, psychological distress and/or excess body weight. It is important to explore the factors that may cause or maintain binge eating behaviour. Attentional bias (AB; paying attention to some things and ignoring others) is thought to contribute to the development of eating disorders when it is maladaptive. This systematic review of 50 cross-sectional designed articles explores findings on AB to food cues, weight and shape cues and threatening cues. The review found that people with binge eating behaviour may be oversensitive to the rewarding properties of food and have increased AB for weight/shape cues, suggesting it needs to be considered when supporting people who binge. Longitudinal research is needed to explore if AB is a factor in the development of eating disorders and binge eating.
Abstract
OBJECTIVE Attentional bias (AB) may be one mechanism contributing to the development and/or maintenance of disordered eating. AB has traditionally been measured using reaction time in response to a stimulus. Novel methods for AB measurement include eye tracking to measure visual fixation on a stimulus, and electroencephalography to measure brain activation in response to a stimulus. This systematic review summarizes, critiques, and integrates data on AB gathered using the above-mentioned methods in those with binge eating behaviors, including binge eating, loss of control eating, and bulimia nervosa. METHOD Literature searches on PubMed and PsycInfo were conducted using combinations of terms related to binge eating and biobehavioral AB paradigms. Studies using AB paradigms with three categories of stimuli were included: food, weight/shape, and threat. For studies reporting means and standard deviations of group bias scores, Hedges' g effect sizes for group differences in AB were calculated. RESULTS Fifty articles met inclusion criteria and were reviewed. Individuals who binge eat in the absence of compensatory behaviors show an increased AB to food cues, but few studies have examined such individuals' AB toward weight/shape and threatening stimuli. Individuals with bulimia nervosa consistently show an increased AB to shape/weight cues and socially threatening stimuli, but findings for AB to food cues are mixed. DISCUSSION While there are important research gaps, preliminary evidence suggests that the combination of AB to disorder-specific cues (i.e., food and weight/shape) and AB toward threat may be a potent contributor to binge eating. This conclusion underscores previous findings on the interaction between negative affect and AB to disorder-specific cues. Recommendations for future research are provided.
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Emollient use alters skin barrier and microbes in infants at risk for developing atopic dermatitis.
Glatz, M, Jo, JH, Kennedy, EA, Polley, EC, Segre, JA, Simpson, EL, Kong, HH
PloS one. 2018;13(2):e0192443
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Atopic dermatitis (AD) is a type of eczema common in babies and young children. Poor function of the skin barrier is thought to lead to changes in the composition of bacteria found on the skin. This small study investigated the effects of daily use of an emollient, Cetaphil Moisturising Cream, on the barrier function and bacterial communities on the skin of infants at risk of developing AD. After 6 months, the emollient group had a lower skin pH than the control group. The group using the emollient had more diverse skin bacterial communities than the control group. The proportion of Streptococcus salivarius was higher in the emollient versus control groups. The authors concluded that lower skin pH and increased skin bacterial diversity after long-term emollient use may reduce inflammation and lower the risk of infants developing AD.
Abstract
BACKGROUND Emollients are a mainstay of treatment in atopic dermatitis (AD), a disease distinguished by skin bacterial dysbiosis. However, changes in skin microbiota when emollients are used as a potential AD preventative measure in infants remain incompletely characterized. RESULTS We compared skin barrier parameters, AD development, and bacterial 16S ribosomal RNA gene sequences of cheek, dorsal and volar forearm samples from 6-month-old infants with a family history of atopy randomized to receive emollients (n = 11) or no emollients (controls, n = 12). The emollient group had a lower skin pH than the control group. The number of bacterial taxa in the emollient group was higher than in the control group at all sites. The Streptococcus salivarius proportion was higher in the emollient versus control groups at all sites. S. salivarius proportion appeared higher in infants without AD compared to infants with AD. A decrease in S. salivarius abundance was further identified in a separate larger population of older children demonstrating an inverse correlation between AD severity at sampling sites and S. salivarius proportions. CONCLUSIONS The decreased skin pH and the increased proportion of S. salivarius after long-term emollient use in infants at risk for developing AD may contribute to the preventative effects of emollients in high-risk infants.
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Effects of prescribed aerobic exercise volume on physical activity and sedentary time in postmenopausal women: a randomized controlled trial.
McNeil, J, Farris, MS, Ruan, Y, Merry, H, Lynch, BM, Matthews, CE, Courneya, KS, Friedenreich, CM
The international journal of behavioral nutrition and physical activity. 2018;15(1):27
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Physical activity has emerged as an important lifestyle factor for primary prevention of numerous diseases, including postmenopausal breast cancer. The aim of this two-armed randomised controlled study was to examine the effects of a year-long prescribed aerobic exercise programme on physical activity levels and sedentary time in postmenopausal women. A total of 400 postmenopausal women aged between 50 – 74 years were randomised to one of the two groups; moderate (150min of exercise/week) or high (300min of exercise/week) volumes of aerobic exercise interventions. Results showed increased activity time in total and moderate-vigorous intensity/recreational physical activity, coupled with decreased sedentary time, in response to both volumes of prescribed physical activity. However, results also showed that physical activity and sedentary time returned to baseline following study completion. Authors conclude that total physical activity time can be increased with greater volumes of prescribed exercise. Furthermore, additional support and resources may be beneficial to promote the maintenance of increased physical activity and reduced sedentary time in the long-term.
Abstract
BACKGROUND Physical activity has emerged as an important lifestyle factor for primary prevention of numerous diseases, including postmenopausal breast cancer. No study to date has assessed the acute and long-term effects of year-long aerobic exercise programs differing in prescribed exercise volume on physical activity and sedentary time in postmenopausal women. Therefore, we aimed to examine the effects of two moderate-vigorous intensity exercise doses on total, light and moderate-vigorous intensity physical activity times, and sedentary time in postmenopausal women during the year-long intervention and one year later. METHODS The Breast Cancer and Exercise Trial in Alberta (BETA) was a two-center, two-arm, 12-month randomized controlled trial that included 400 previously inactive postmenopausal women randomized to either 150 (MODERATE) or 300 (HIGH) minutes/week of aerobic exercise. Physical activity and sedentary time were assessed at baseline, 6- (intervention mid-point), 12- (prior to end of intervention) and 24-months (follow-up) with waist-mounted accelerometers (Actigraph GTX3®). Self-reported activity and sedentary time at baseline, 12- and 24-months was also assessed (Past Year Total Physical Activity Questionnaire and SIT-Q). Intention-to-treat analyses were conducted using linear mixed models and adjusted for baseline variables. RESULTS Both physical activity interventions led to increases in objective and subjective measures of total and moderate-vigorous intensity/recreational physical activity time, coupled with decreases in sedentary time, at 6- and 12-months compared to baseline. Additionally, greater increases in accelerometry-derived total physical activity time at 6- and 12-months, and self-reported recreational activity time at 12-months, compared to baseline were noted in the HIGH versus MODERATE groups. Decreases in total, light and moderate-vigorous intensity physical activity time, and an increase in sedentary time, in both groups were noted at 24-months compared to 12-months. A decrease in light intensity physical activity time in both groups at 24-months compared to baseline was also noted. CONCLUSION These findings have important health implications, suggesting that total physical activity time can be increased with greater volumes of prescribed exercise, but that additional support and resources could be used to promote the maintenance of these high levels of aerobic exercise participation following study completion. TRIAL REGISTRATION clinicaltrials.gov identifier: NCT01435005 (BETA Trial). Registred September 15th 2011 (retrospectively registered).
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Fast food fever: reviewing the impacts of the Western diet on immunity.
Myles, IA
Nutrition journal. 2014;13:61
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This 2014 review delves into the impact that an over-indulgence in foods high in sugar, salt, saturated fats, genetically modified foods, gluten and artificial sweeteners may have on our immune system. The modern western diet is generally characterised as being abundant in these nutrient-poor foods, which exert an unhealthful impact on the body. They report that sugars increase inflammatory markers and reduce white blood cell production. Artificial sweeteners appear to be less inflammatory however data is limited. There is some suggestion that saccharin and sucralose interfere with digestive enzymes and are implicated in Inflammatory Bowel Disease. High salt may increase inflammatory cytokines. Saturated fats and high omega 6 fatty acids from vegetable oils increase inflammatory immune markers such as C-Reactive protein. Omega 3 polyunsaturated fats are generally associated with anti-inflammatory effects and regulating immune mediators. Gluten inappropriately activates an immune T-cell response. GM foods may have protective effects against malnutrition but have been shown to induce an allergic response in some cases. There is also concern that genetic modifications can be internalised by our gut bacteria and passed on to offspring. The review concludes that poor dietary choices are encoded into our gut and increase inflammation, and thus reduce our immune resilience to control infection.
Abstract
While numerous changes in human lifestyle constitute modern life, our diet has been gaining attention as a potential contributor to the increase in immune-mediated diseases. The Western diet is characterized by an over consumption and reduced variety of refined sugars, salt, and saturated fat. Herein our objective is to detail the mechanisms for the Western diet's impact on immune function. The manuscript reviews the impacts and mechanisms of harm for our over-indulgence in sugar, salt, and fat, as well as the data outlining the impacts of artificial sweeteners, gluten, and genetically modified foods; attention is given to revealing where the literature on the immune impacts of macronutrients is limited to either animal or in vitro models versus where human trials exist. Detailed attention is given to the dietary impact on the gut microbiome and the mechanisms by which our poor dietary choices are encoded into our gut, our genes, and are passed to our offspring. While today's modern diet may provide beneficial protection from micro- and macronutrient deficiencies, our over abundance of calories and the macronutrients that compose our diet may all lead to increased inflammation, reduced control of infection, increased rates of cancer, and increased risk for allergic and auto-inflammatory disease.