Links between metabolic syndrome and the microbiome.
Evolution, medicine, and public health. 2020;2020(1):45-46
Plain language summary
Metabolic syndrome (MetS) is a cluster of co-occurring pathological conditions, characterised by insulin resistance, abdominal obesity, hypertension and dyslipidaemia One possible factor contributing to MetS risk is change in microbiome composition. Diets high in processed foods appear to alter microbiome composition in ways that promote higher fat mass and insulin resistance. Additionally, a sedentary lifestyle decreases microbiome diversity, elevating inﬂammation and metabolic disease risk. Research on how the microbiome responds to modest, attainable changes in diet and physical activity will help identify which dietary adjustments and exercise types have the greatest potential to protect patients from MetS.
Metabolic syndrome (MetS) is a cluster of harmful conditions which occur together, such as insulin resistance, abdominal obesity, and hypertension. The global prevalence of MetS is growing rapidly, with some estimates suggesting over one billion people worldwide experience increased morality and disease rates linked with this syndrome. One possible factor contributing to MetS risk is changes in microbiome composition. Approximately 100 trillion bacteria and other microbes reside in the human intestinal tract, collectively termed the gut microbiome. Humans and microbes share a long evolutionary history, with many of these microbes influencing human health outcomes. However, environmental conditions have changed dramatically with human technological innovations; many of these changes (e.g., diets high in processed foods and sedentary lifestyles) appear to impact human-microbe relationships. In general, recent changes in diet and activity patterns have been linked to decreased microbiome diversity, elevating inflammation and metabolic disease risk and likely promoting the development of MetS. Targeting patient diet or exercise patterns may therefore help doctors better treat patients suffering from MetS. Still, additional work is needed to determine how the microbiome responds to changes in patient activity and diet patterns across culturally and biologically diverse human populations.
Intramyocellular Lipids, Insulin Resistance, and Functional Performance in Patients with Severe Obstructive Sleep Apnea.
Nature and science of sleep. 2020;12:69-78
Plain language summary
Obstructive sleep apnoea syndrome (OSA) is characterized by repeated occlusion of the upper airway during sleep, resulting in periods of intermittent hypoxemia [low level of oxygen in blood]. The aim of this study was to (a) investigate the intramyocellular lipids (IMCL) and extramyocellular lipids (EMCL), biochemical data, and functional performance in patients with severe OSA versus controls, and (b) examine the correlations between intra-muscular lipid contents and biochemical and performance variables. This study is a clinical trial that recruited 20 patients with OSA and body mass index(BMI)-matched controls. Results demonstrate that patients with OSA had significantly lower IMCL and EMCL values when compared with their age-, and BMI-matched controls without OSA. Furthermore, compared with controls, patients with OSA had significantly reduced functional performance and exhibited abnormal biochemical data, including glucose and insulin levels and lipid profiles. Authors conclude that additional large-scale clinical trials are required to further explore the complex mechanism between OSA, muscle metabolism, and insulin action.
PURPOSE An increasing number of studies have linked the severity of obstructive sleep apnea (OSA) with metabolic dysfunction. However, little is known about the lipid compartments (intramyocellular [IMCL] and extramyocellular [EMCL] lipids) inside the musculature in these patients. The present study was designed to investigate the IMCL and EMCL, biochemical data, and functional performance in patients with severe OSA, and to examine the correlations between intramuscular lipid contents and test variables. PARTICIPANTS AND METHODS Twenty patients with severe OSA (apnea-hypopnea index [AHI]: ≥30/h; body mass index [BMI]: 26.05±2.92) and 20 age- and BMI-matched controls (AHI <5/h) were enrolled. Proton magnetic resonance spectroscopy was used to measure the IMCL and EMCL of the right vastus lateralis muscle. Biochemical data, including levels of fasting plasma glucose, insulin, lipid profiles, and high-sensitivity C-reactive protein (hsCRP), were measured. Insulin resistance index (IR) was calculated using the homeostasis model assessment method. Performance tests included a cardiopulmonary exercise test and knee extension strength and endurance measurements. RESULTS Patients with severe OSA had significantly (P<0.05) lower values of IMCL (14.1±5.4 AU) and EMCL (10.3±5.8 AU) compared to the control group (25.2±17.6 AU and 14.3±11.1 AU, respectively). Patients with severe OSA had significantly higher hsCRP, IR, and dyslipidemia compared with controls (all P<0.05). Furthermore, IMCL was negatively correlated with AHI, cumulative time with nocturnal pulse oximetric saturation lower than 90% (TSpO2<90%) (ρ=-0.35, P<0.05), IR (ρ=-0.40, P<0.05), glucose (ρ=-0.33, P<0.05), and insulin (ρ=-0.36, P<0.05), and positively correlated with lowest oximetric saturation (ρ=0.33, P<0.01). CONCLUSION Skeletal muscle dysfunction and metabolic abnormalities were observed in patients with OSA that did not have obesity. IMCL was positively correlated with aerobic capacity and muscular performance, but negatively correlated with AHI and IR. Large-scale clinical trials are required to explore the complicated mechanism among OSA, intramuscular metabolism, and insulin action. CLINICAL TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT00813852.
Significant Impact of the Ketogenic Diet on Low-Density Lipoprotein Cholesterol Levels.
Plain language summary
Ketogenic diet includes food with a very low-carbohydrate and high-fat content that aims to drastically reduce carbohydrate intake and replace it with fat, hence inducing ketosis. This study is a case report which presents a case of a rapid increase, followed by a rapid correction of low-density lipoprotein cholesterol (LDL-C) in a patient following a ketogenic diet. The patient is a 56-year-old Hispanic female who showed a rapid increase in LDL-C and total cholesterol after only 30-40 days of following a ketogenic diet. She was directed to follow a balanced diet and take statin medication. Results showed that the patient's BMI, four weeks after the discontinuation of ketogenic diet, did not change despite a marked improvement in her LDL-C. Authors conclude that due to the unpredictable response of LDL-C levels to a ketogenic diet, close monitoring of patients with a high risk of cardiovascular disease should be considered.
It is well known, based on the previous research, that a ketogenic diet leads to an improvement in the lipid profile and decreases cardiovascular risk factors such as hypertension. However, recent studies have also reported increased levels of total cholesterol and low-density lipoprotein cholesterol (LDL-C) as a result of this diet. It has been postulated that this elevation in LDL-C would not likely increase cardiovascular complications due to the large LDL-C particle size. In this case report, we present a case of a rapid increase, followed by a rapid correction of LDL-C, in a patient following a ketogenic diet. A 56-year-old Hispanic female with a past medical history of hypertension and fibromyalgia presented to the outpatient clinic for evaluation of fatigue. She reported that she had been following a strict ketogenic diet along with daily regular exercise for approximately 30-40 days prior to this visit. Her diet consisted of low-carbohydrate vegetables, seafood, avocados, eggs, and coconut oil. The patient's physical exam was unremarkable. At the time of the visit, her BMI was calculated at 28 kg/m2, with a weight loss of approximately six to seven pounds since starting the ketogenic diet. Her fasting lipid profile showed a total cholesterol of 283 mg/dl, LDL-C of 199 mg/dl, high-density lipoprotein cholesterol (HDL-C) of 59 mg/dl, and triglycerides levels of 124 mg/dl. She was instructed to stop the ketogenic diet and to incorporate a balanced diet, which includes a higher amount of carbohydrates and lower fat. She was also started on high-intensity atorvastatin. However, she reported experiencing myalgias soon after initiating atorvastatin; therefore, the medication was switched to rosuvastatin 10 mg at bedtime. During her follow-up appointment, she reported not having consistently taken rosuvastatin due to the concern of worsening myalgias. Her lipid profile, after four weeks of ketogenic diet discontinuation and inconsistent use of statins, showed significant improvement resulting in a total cholesterol level of 190 mg/dl and LDL-C of 106 mg/dl. Statin therapy was discontinued, and the patient maintained optimal LDL-C levels on subsequent testing. This patient showed a rapid increase in LDL-C and total cholesterol after only 30-40 days of the ketogenic diet. Her drastic elevation in LDL-C could also be explained due to the rapid weight loss, as cholesterol in the adipose tissue is known to mobilize as the fat cells shrink. Interestingly, her BMI four weeks after the discontinuation of the ketogenic diet did not change despite a marked improvement in her LDL-C. Therefore, we believe the acute onset and resolution of hyperlipidemia was secondary to the ketogenic diet itself. This study helps to better understand expectations when recommending a ketogenic diet to patients and its consequences. There is currently no statistically significant study that proves this elevation of LDL-C would not increase cardiovascular risks. Furthermore, the necessity for statin therapy in a ketogenic diet-induced hyperlipidemia remains unknown.