Increasingly, I’m suspicious of results from meta-analyses. Anyway, here’s the abstract of one from American Journal of Clinical Nutrition in 2020. In case you’re not familiar with the LDL-lowering, vegetarian, “portfolio diet,” click for an infographic.
Background: Many systematic reviews and meta-analyses have assessed the efficacy of dietary patterns on blood pressure (BP) lowering but their findings are largely conflicting.
Objective: This umbrella review aims to provide an update on the available evidence for the efficacy of different dietary patterns on BP lowering.
Methods: PubMed and Scopus databases were searched to identify relevant studies through to June 2020. Systematic reviews with meta-analyses of randomized controlled trials (RCTs) were eligible if they measured the effect of dietary patterns on systolic (SBP) and/or diastolic blood pressure (DBP) levels. The methodological quality of included systematic reviews was assessed by A Measurement Tool to Assess Systematic Review version 2. The efficacy of each dietary pattern was summarized qualitatively. The confidence of the effect estimates for each dietary pattern was graded using the NutriGrade scoring system.
Results: Fifty systematic reviews and meta-analyses of RCTs were eligible for review. Twelve dietary patterns namely the Dietary Approaches to Stop Hypertension (DASH), Mediterranean, Nordic, vegetarian, low-salt, low-carbohydrate, low-fat, high-protein, low glycemic index, portfolio, pulse, and Paleolithic diets were included in this umbrella review. Among these dietary patterns, the DASH diet was associated with the greatest overall reduction in BP with unstandardized mean differences ranging from -3.20 to -7.62 mmHg for SBP and from -2.50 to -4.22 mmHg for DBP. Adherence to Nordic, portfolio, and low-salt diets also significantly decreased SBP and DBP levels. In contrast, evidence for the efficacy of BP lowering using the Mediterranean, vegetarian, Paleolithic, low-carbohydrate, low glycemic index, high-protein, and low-fat diets was inconsistent.
Conclusion: Adherence to the DASH, Nordic, and portfolio diets effectively reduced BP. Low-salt diets significantly decreased BP levels in normotensive Afro-Caribbean people and in hypertensive patients of all ethnic origins.
Most data regarding the association between the glycemic index and cardiovascular disease come from high-income Western populations, with little information from non-Western countries with low or middle incomes. To fill this gap, data are needed from a large, geographically diverse population.
This analysis includes 137,851 participants between the ages of 35 and 70 years living on five continents, with a median follow-up of 9.5 years. We used country-specific food-frequency questionnaires to determine dietary intake and estimated the glycemic index and glycemic load on the basis of the consumption of seven categories of carbohydrate foods. We calculated hazard ratios using multivariable Cox frailty models. The primary outcome was a composite of a major cardiovascular event (cardiovascular death, nonfatal myocardial infarction, stroke, and heart failure) or death from any cause.
In the study population, 8780 deaths and 8252 major cardiovascular events occurred during the follow-up period. After performing extensive adjustments comparing the lowest and highest glycemic-index quintiles, we found that a diet with a high glycemic index was associated with an increased risk of a major cardiovascular event or death, both among participants with preexisting cardiovascular disease (hazard ratio, 1.51; 95% confidence interval [CI], 1.25 to 1.82) and among those without such disease (hazard ratio, 1.21; 95% CI, 1.11 to 1.34). Among the components of the primary outcome, a high glycemic index was also associated with an increased risk of death from cardiovascular causes. The results with respect to glycemic load were similar to the findings regarding the glycemic index among the participants with cardiovascular disease at baseline, but the association was not significant among those without preexisting cardiovascular disease.
In this study, a diet with a high glycemic index was associated with an increased risk of cardiovascular disease and death.
I published my first book in 2007 to extend my healing reach beyond the confines of the clinic and hospital room. I’m certain my writing has improved the health of many folks I’ll never know about, and that means more to me than any financial success I’ve had with the books.
In 2020, my net profit from writing was $937.08, which is admittedly pitiful. The prior year profit was $5,802.48. Pandemic effect, maybe? To lower my expenses in 2021, I’ll look into a private PO box instead of US Postal Service ($168/year), drop Amazon Prime ($129/year), and negotiate lower fees with Network Solutions.
I am blessed to have a hospitalist job that pays well. COVID-19 has caused major economic hardship for many of you, including unemployment.
My primary means of advertising has been blogging. Cross-posting on Facebook, Twitter, and LinkedIn has done almost nothing for book sales. A few years ago I could give my hospital patients a business card with links to my books, but my employer insisted I stop.
If you care to support my writing, buy a book. If not for yourself, then for someone you care about.
There’s a silent epidemic in folks with type 2 diabetes: 50 to 70% have non-alcoholic fatty liver disease. Non-alcoholic fatty liver disease is an important contributor to cirrhosis, i.e., scarring in the liver that impairs liver function. In the study at hand, a ketogenic diet reduced liver fat by 31% over just six days. I don’t have many details of the diet used, but it reduced carbohydrates to 20 grams/day.
Here’s the abstract:
Ketogenic diet is an effective treatment for nonalcoholic fatty liver disease (NAFLD). Here, we present evidence that hepatic mitochondrial fluxes and redox state are markedly altered during ketogenic diet-induced reversal of NAFLD in humans. Ketogenic diet for 6 [days] markedly decreased liver fat content and hepatic insulin resistance. These changes were associated with increased net hydrolysis of liver triglycerides and decreased endogenous glucose production and serum insulin concentrations. Partitioning of fatty acids toward ketogenesis increased, which was associated with increased hepatic mitochondrial redox state and decreased hepatic citrate synthase flux. These data demonstrate heretofore undescribed adaptations underlying the reversal of NAFLD by ketogenic diet and highlight hepatic mitochondrial fluxes and redox state as potential treatment targets in NAFLD.
Weight loss by ketogenic diet (KD) has gained popularity in management of nonalcoholic fatty liver disease (NAFLD). KD rapidly reverses NAFLD and insulin resistance despite increasing circulating nonesterified fatty acids (NEFA), the main substrate for synthesis of intrahepatic triglycerides (IHTG). To explore the underlying mechanism, we quantified hepatic mitochondrial fluxes and their regulators in humans by using positional isotopomer NMR tracer analysis. Ten overweight/obese subjects received stable isotope infusions of: [D7]glucose, [13C4]β-hydroxybutyrate and [3-13C]lactate before and after a 6-d KD. IHTG was determined by proton magnetic resonance spectroscopy (1H-MRS). The KD diet decreased IHTG by 31% in the face of a 3% decrease in body weight and decreased hepatic insulin resistance (−58%) despite an increase in NEFA concentrations (+35%). These changes were attributed to increased net hydrolysis of IHTG and partitioning of the resulting fatty acids toward ketogenesis (+232%) due to reductions in serum insulin concentrations (−53%) and hepatic citrate synthase flux (−38%), respectively. The former was attributed to decreased hepatic insulin resistance and the latter to increased hepatic mitochondrial redox state (+167%) and decreased plasma leptin (−45%) and triiodothyronine (−21%) concentrations. These data demonstrate heretofore undescribed adaptations underlying the reversal of NAFLD by KD: That is, markedly altered hepatic mitochondrial fluxes and redox state to promote ketogenesis rather than synthesis of IHTG.
A 2021 issue of Diabetes Care reveals the shocking prevalence of advanced liver fibrosis (scarring) in folks with type 2 diabetes: one of every six. Fibrosis may eventually lead to cirrhosis and require a liver transplant. The study at hand used vibration-controlled transient elastography to measure liver stiffness. The more fibrosis, the stiffer the liver. The measuring device “uses a pulse-echo ultrasound technique to quantify the speed of mechanically induced shear wave within liver tissue,” which correlates with the severity of fibrosis. Liver fat, i.e., steatosis, can also be quantified at the same time by measuring the ultrasonic attenuation of the echo wave.
Here’s the study abstract:
Assess the prevalence of nonalcoholic fatty liver disease (NAFLD) and of liver fibrosis associated with nonalcoholic steatohepatitis in unselected patients with type 2 diabetes mellitus (T2DM).
RESEARCH DESIGN AND METHODS
A total of 561 patients with T2DM (age: 60 ± 11 years; BMI: 33.4 ± 6.2 kg/m2; and HbA1c: 7.5 ± 1.8%) attending primary care or endocrinology outpatient clinics and unaware of having NAFLD were recruited. At the visit, volunteers were invited to be screened by elastography for steatosis and fibrosis by controlled attenuation parameter (≥274 dB/m) and liver stiffness measurement (LSM; ≥7.0 kPa), respectively. Secondary causes of liver disease were ruled out. Diagnostic panels for prediction of advanced fibrosis, such as AST-to-platelet ratio index (APRI) and Fibrosis-4 (FIB-4) index, were also measured. A liver biopsy was performed if results were suggestive of fibrosis.
The prevalence of steatosis was 70% and of fibrosis 21% (LSM ≥7.0 kPa). Moderate fibrosis (F2: LSM ≥8.2 kPa) was present in 6% and severe fibrosis or cirrhosis (F3–4: LSM ≥9.7 kPa) in 9%, similar to that estimated by FIB-4 and APRI panels. Noninvasive testing was consistent with liver biopsy results. Elevated AST or ALT ≥40 units/L was present in a minority of patients with steatosis (8% and 13%, respectively) or with liver fibrosis (18% and 28%, respectively). This suggests that AST/ALT alone are insufficient as initial screening. However, performance may be enhanced by imaging (e.g., transient elastography) and plasma diagnostic panels (e.g., FIB-4 and APRI).
Moderate-to-advanced fibrosis (F2 or higher), an established risk factor for cirrhosis and overall mortality, affects at least one out of six (15%) patients with T2DM. These results support the American Diabetes Association guidelines to screen for clinically significant fibrosis in patients with T2DM with steatosis or elevated ALT.
Retinopathy is a fancy word meaning disease of the retina, the light detecting membrane at the back of the eyeball. About two in five folks with diabetes have some form or degree of diabetic retinopathy. The pathology is mostly in the arterial blood vessels of the retina. Keeping blood sugars under good control is one way to prevent diabetic retinopathy. Once diagnosed, it can be treated with injections, lasers, or surgery.
Here’s the abstract from a recent scientific report the looked at the ocular effects of gastric bypass surgery in obese type 2 diabetics. Over the course of 4.5 years, the risk of diabetic retinopathy was 40% less in those who had bypass surgery.
Importance Knowledge of the incidence and progression of diabetic retinopathy (DR) after gastric bypass surgery (GBP) in patients with obesity and diabetes could guide the management of these patients.
Objective To investigate the incidence of diabetic ocular complications in patients with type 2 diabetes after GBP compared with the incidence of diabetic ocular complications in a matched cohort of patients with obesity and diabetes who have not undergone GBP.
Design, Setting, and Participants Data from 2 nationwide registers in Sweden, the Scandinavian Obesity Surgery Registry and the National Diabetes Register, were used for this cohort study. A total of 5321 patients with diabetes from the Scandinavian Obesity Surgery Registry who had undergone GBP from January 1, 2007, to December 31, 2013, were matched with 5321 patients with diabetes from the National Diabetes Register who had not undergone GBP, based on sex, age, body mass index (BMI), and calendar time (2007-2013). Follow-up data were obtained until December 31, 2015. Statistical analysis was performed from October 5, 2018, to September 30, 2019.
Exposure Gastric bypass surgery.
Main Outcomes and Measures Incidence of new DR and other diabetic ocular complications.
Results The study population consisted of 5321 patients who had undergone GBP (3223 women [60.6%]; mean [SD] age, 49.0 [9.5] years) and 5321 matched controls (3395 women [63.8%]; mean [SD] age, 47.1 [11.5] years). Mean (SD) follow-up was 4.5 (1.6) years. The mean (SD) BMI and hemoglobin A1c concentration at baseline were 42.0 (5.7) and 7.6% (1.5%), respectively, in the GBP group and 40.9 (7.3) and 7.5% (1.5%), respectively, in the control group. The mean (SD) duration of diabetes was 6.8 (6.3) years in the GBP group and 6.4 (6.4) years in the control group. The risk for new DR was reduced in the patients who underwent GBP (hazard ratio, 0.62 [95% CI, 0.49-0.78]; P < .001). The dominant risk factors for development of DR at baseline were diabetes duration, hemoglobin A1c concentration, use of insulin, glomerular filtration rate, and BMI.
Conclusions and Relevance This nationwide matched cohort study suggests that there is a reduced risk of developing new DR associated with GBP, and no evidence of an increased risk of developing DR that threatened sight or required treatment.
In the study at hand, frailty was measured by exhaustion, weakness, physical activity, walking speed, and weight loss. From the Journal of the American Medical Medical Directors Association way back in 2014:
Background and objective: Low intake of certain micronutrients and protein has been associated with higher risk of frailty. However, very few studies have assessed the effect of global dietary patterns on frailty. This study examined the association between adherence to the Mediterranean diet (MD) and the risk of frailty in older adults.
Design, setting, and participants: Prospective cohort study with 1815 community-dwelling individuals aged ≥60 years recruited in 2008-2010 in Spain.
Measurements: At baseline, the degree of MD [Mediterranean Diet] adherence was measured with the Mediterranean Diet Adherence Screener (MEDAS) score and the Mediterranean Diet Score, also known as the Trichopoulou index. In 2012, individuals were reassessed to detect incident frailty, defined as having at least 3 of the following criteria: exhaustion, muscle weakness, low physical activity, slow walking speed, and weight loss. The study associations were summarized with odds ratios (OR) and their 95% confidence interval (CI) obtained from logistic regression, with adjustment for the main confounders.
Results: Over a mean follow-up of 3.5 years, 137 persons with incident frailty were identified. Compared with individuals in the lowest tertile of the MEDAS score (lowest MD adherence), the OR (95% CI) of frailty was 0.85 (0.54-1.36) in those in the second tertile, and 0.65 (0.40-1.04; P for trend = .07) in the third tertile. Corresponding figures for the Mediterranean Diet Score were 0.59 (0.37-0.95) and 0.48 (0.30-0.77; P for trend = .002). Being in the highest tertile of MEDAS was associated with reduced risk of slow walking (OR 0.53; 95% CI 0.35-0.79) and of weight loss (OR 0.53; 95% CI 0.36-0.80). Lastly, the risk of frailty was inversely associated with consumption of fish (OR 0.66; 95% CI 0.45-0.97) and fruit (OR 0.59; 95% CI 0.39-0.91).
Conclusions: Among community-dwelling older adults, an increasing adherence to the MD was associated with decreasing risk of frailty.
Did you notice another good reason to eat fish?
I wonder why the research was published in the Journal of the American Medical Medical Directors Association?