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Video Presentations on Metabolic Syndrome & LCHF

011: FAT, DIABETIC & HYPERTENSIVE? What’s Your RISK of DEATH? (The Dreadful METABOLIC SYNDROME!)

Are YOU fat, overweight or obese? Are you pre-diabetic? Is you blood sugar already high enough to be diagnosed with diabetes?

What is METABOLIC SYNDROME? Do you have it? Should you be worried about it?

Based on WHO data, METABOLIC SYNDROME is the Number 1 KILLER in the world today! Avoid it if you want to live a LONGER and HEALTHIER life!

Let's find the answers in this video!

006: The KETO Diet: WHICH FOODS are LOW CARB?

Every now and then, I encounter lots of misconceptions about which foods contain high or low carb. Thus, I see patients with Metabolic Syndrome whose blood sugar levels go up and down even when they say they are doing "keto"!

013: KETO DIET for LIFESTYLE DISEASE! (CEBUANO/VISAYAN - Ang KAAYOHAN sa KETO DIET) with Bombo Radyo

KABALO KA BA nga ang KETOGENIC DIET o "KETO DIET" makatabang sa imo ug dako para ma-prebentahan o MAPUGNGAN ang ginatawag nga "LIFESTYLE DISEASES" pareho sa HIGH BLOOD PRESSURE ug DIABETES - nga maoy mga kasagarang hinungdan sa HEART ATTACK ug STROKE?

(DO YOU KNOW that the KETOGENIC DIET or "KETO DIET" can significantly HELP YOU in PREVENTING what is called "LIFESTYLE DISEASES" like HIGH BLOOD PRESSURE and DIABETES - which are among the most common causes of HEART ATTACK and STROKE?)

Dinhi nga video nag-inistoryahay mi ug CEBUANO/BINISAYA - ug para kini jud kini sa mga BISAYA/CEBUANO pareha nimo, bisag asa man ka nga panig sa kalibutan mahikaplagan!

(In this video, we are conversing in CEBUANO/VISAYAN - this is especially for the VISAYANS, whichever part of the world you may be!)

HOWEVER, THERE ARE ENGLISH SUBTITLES for those with difficulty understanding the Cebuano language.

"Insulin at the Center: A New/Old Paradigm for Metabolic Syndrome" - Dr. Benjamin Bikman

Dr. Benjamin Bikman earned his Ph.D. in Bioenergetics and was a postdoctoral fellow with the Duke-National University of Singapore in metabolic disorders. He is currently a professor of pathophysiology and a biomedical scientist at Brigham Young University in Utah.

Dr. Bikman's professional focus as a scientist and professor is to better understand chronic modern-day diseases, with a special emphasis on the origins and consequences of obesity and diabetes, with an increasing scrutiny of the pathogenicity of insulin and insulin resistance. He frequently publishes his research in peer-reviewed journals and presents at international science meetings.

Dr. Bikman has long been an advocate of a ketogenic diet in light of the considerable evidence supporting its use as a therapy for reversing insulin resistance. His website InsulinIQ.com promotes dietary clarity, healing, and freedom through evidence-based science about insulin resistance. Employing cell-autonomous to whole-body systems, Dr. Bikman's recent efforts have focused on exploring the intimate associations between the metabolic and immune systems. 

"How Insulin Interacts with Metabolic Health" - Dr. Benjamin Bikman

Filmed on the 19th & 20th May 2023 at the Public Health Collaboration Annual Conference in Sheffield. World-renowned speakers convened to share their expertise about how we can harness the power of lifestyle to help fix healthcare together.

"The Three Faces of Metabolic Syndrome" - Dr. Robert Lustig

Robert H. Lustig, M.D., M.S.L. is Professor emeritus of Pediatrics, Division of Endocrinology at the University of California, San Francisco (UCSF). He specialises in the field of neuroendocrinology, with an emphasis on the regulation of energy balance by the central nervous system. His research and clinical practice has focused on childhood obesity and diabetes. Dr. Lustig holds a Bachelor’s in Science from MIT, a Doctorate in Medicine from Cornell University. Medical College, and a Master’s of Studies in Law from U.C. Hastings College of the Law.

Dr. Lustig has fostered a global discussion of metabolic health and nutrition, exposing some of the leading myths that underlie the current pandemic of diet-related disease. He believes the food business, by pushing processed food loaded with sugar, has hacked our bodies and minds to pursue pleasure instead of happiness; fostering today’s epidemics of addiction and depression. Yet by focusing on real food, we can beat the odds against sugar, processed food, obesity, and disease.

"Sugar, Metabolic Syndrome and Cancer" - Prof. Robert Lustig

"What is Metabolic Syndrome Anyway?" - Dr. Robert Lustig

The Science of Metabolic Syndrome

Dr. Jason Fung explains the science of metabolic syndrome and how intermittent fasting can help reverse this disease. Metabolic syndrome includes abdominal obesity, insulin resistance, high triglycerides, low HDL and hypertension but is better understood as a disease of too much insulin.

Metabolic Syndrome is Caused by Hyperinsulinemia

Metabolic syndrome is a constellation of 5 related issues, which denotes an underlying common etiology - hyperinsulinemia. It can be reversed by changing the diet.

"Evidence Based Keto: How to Lose Weight and Reverse Diabetes" - Dr. Paul Mason

"Inflammation, Nutritional Ketosis and Metabolic Disease" - Dr. Stephen Phinney

Prediabetes and Metabolic Syndrome: Prevalence, Early Signs and the Importance of Treating Early - Dr. Sarach Hallberg, DO, MS

"The Metabolic Syndrome and Other Nutritional Disorders" - Dr. Jeffry Gerber

Dr. Jeffry N. Gerber is a board certified family physician and owner of South Suburban Family Medicine in Littleton, Colorado, where he is known as “Denver’s Diet Doctor”. He is also the co-convenor of several Low Carb Conferences in Colorado, along with Dr. Rod Tayler from Low Carb Down Under (https://lowcarbconferences.com).

Dr. Gerber has been providing personalised healthcare to his local community since 1993 and continues that tradition with an emphasis on longevity, wellness and prevention.

Nutrition and its effects on health are areas of interest for Dr. Gerber and he has been focusing on prevention and treatment programs using low-carb high fat (LCHF), Ancestral, Paleo and Primal diets to treat and prevent chronic conditions. His book on chronic disease root causes and resolution strategies (co-authored with Ivor Cummins) was released on February 27th 2018:

https://www.amazon.com/Eat-Rich-Live-...

Dr. Gerber maintains a database of patients, looking at weight loss and improved cardio-metabolic markers, demonstrating the benefits of these types of diets. He speaks frequently about these important issues to patients, the community and other health care professionals.

"The Metabolic Syndrome - A Nutritional Disease" - Dr. Jeffry Gerber

Dr. Jeffry N. Gerber is a board certified family physician and owner of South Suburban Family Medicine in Littleton, Colorado, where he is known as “Denver’s Diet Doctor”.

He has been providing personalized healthcare to the local community since 1993 and continues that tradition with an emphasis on longevity, wellness and prevention.

Nutrition and its effects on health are areas of interest for Dr. Gerber and he has been focusing on prevention and treatment programs using low-carb high fat (LCHF), Ancestral, Paleo and Primal diets to treat and prevent chronic conditions.

Dr. Gerber maintains a database of patients, looking at weight loss and improved cardio-metabolic markers, demonstrating the benefits of these types of diets. He speaks frequently about these important issues to patients, the community and other health care professionals.

What is Metabolic Syndrome (and Can Your Cure It?) 2023

Metabolic Syndrome is the condition of having Central Adiposity (belly fat), Hypertension (High Blood Pressure),  High Triglycerides, Low HDL-Cholesterol and Hyperglycemia (High Blood Sugar).  All five of these things hugely increase your risk of Heart Attack and Stroke. 

There are no pills or shots that can cure Metabolic Syndrome, NONE.  But, there is a diet which can reverse all 5 of these risk factors, and protect you from Heart Attack and Stroke. 

Big-medicine has failed to offer any solutions for metabolic syndrome, as has big-pharma. What works is fixing your diet and fixing your life. Let me show you how...

Metabolic Syndrome Solution (Cause & Cure of Syndrome X) 2023

WARNING: Metabolic Syndrome can mess you up!! 

You may have Metabolic Syndrome and not even know! Here is how metabolic syndrome is diagnosed, why it matters, and how to start to Reverse Metabolic Syndrome in a few weeks.

Millions of innocent people have Metabolic Syndrome and don't even know. Here how to find out if you have metabolic syndrome and 5 easy steps to fix metabolic syndrome.

Scholarly Articles on Metabolic Syndrome in General

The IDF Definition Is Better Suited for Screening Metabolic Syndrome and Estimating Risks of Diabetes in Asian American Adults: Evidence from NHANES 2011–2016Objective: extensive effort has been made to better define metabolic syndrome (MetS). Whether current definitions accurately diagnose MetS and predict risk of cardiovascular disease (CVD) or diabetes in diverse ethnic groups remains largely unknown. The objective of this study was to compare the prevalence of MetS and risk of CVD and diabetes among Asian American adults using two MetS definitions, one proposed by the Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (ATP III) and one by the International Diabetes Federation (IDF). Methods: we obtained a nationally representative sample of 2121 Asian American adults in the noninstitutionalized civilian population of the United States from the National Health and Nutrition Examination Survey (2011–2016). We computed age-adjusted, gender-specific MetS prevalence and each MetS component using ATP III and IDF definitions. Results: based on the IDF definition, MetS prevalence was 39.26% among Asian American men and 39.66% among Asian American women included in the study sample. Based on the ATP III definition, MetS prevalence in our sample was 39.38% among men and 36.11% among women. We found good concordance between the IDF and the ATP III definitions in identifying MetS in Asian American adults. Those with MetS defined only by the IDF definition had significantly higher body mass index (BMI) and waist circumference than those with MetS defined only by the ATP III definition. The IDF definition also better predicted elevated fasting insulin. Conclusions: the IDF definition is more pertinent than the ATP III definition for screening and estimating risk of CVD and diabetes in Asian American adults. Future studies should examine differences in MetS prevalence across Asian ethnic groups to facilitate the development of culturally tailored strategies improve MetS prevention and detection in Asian Americans.
The association between glycemic index, glycemic load, and metabolic syndrome: a systematic review and dose–response meta-analysis of observational studies - European Journal of NutritionPurpose The association of glycemic index (GI) and glycemic load (GL) with metabolic syndrome (MetS) is controversial. Therefore, we conducted this first systematic review and dose–response meta-analysis of observational studies to quantify these associations. Methods We searched PubMed, EMBASE, Web of Science, and the Cochrane Library for relevant studies up to 1 April 2019. Summary odds ratios (OR) and 95% confidence intervals (CI) were calculated by a random-effects model. This study was registered with PROSPERO (CRD42019131788). Results We included eight high-quality (n = 5) or medium-quality (n = 3) cross-sectional studies in the final meta-analysis, comprising 6058 MetS events and 28,998 participants. The summary ORs of MetS for the highest versus lowest categories were 1.23 (95% CI 1.10–1.38, I2 = 0, tau2 = 0, n = 5) for dietary GI, 1.06 (95% CI 0.89–1.25, I2 = 36.2%, tau2 = 0.0151, n = 6) for dietary GL. The summary OR was 1.12 (95% CI 1.00–1.26, I2 = 0, tau2 = 0, n = 3) per 5 GI units, 0.96 (95% CI 0.83–1.10, I2 = 33.4%, tau2 = 0.0059, n = 2) per 20 GL units. Conclusions Dietary GI was positively associated with the prevalence of MetS. However, no significant association was found between dietary GL and the prevalence of MetS. Further studies with prospective design are needed to establish potential causal relationship between dietary GI and the MetS.
Postprandial Responses to a Standardised Meal in Hypertension: The Mediatory Role of Visceral Fat MassPostprandial insulinaemia, triglyceridaemia and measures of inflammation are thought to be more closely associated with cardiovascular risk than fasting measures. Although hypertension is associated with altered fasting metabolism, it is unknown as to what extent postprandial lipaemic and inflammatory metabolic responses differ between hypertensive and normotensive individuals. Linear models adjusting for age, sex, body mass index (BMI), visceral fat mass (VFM) and multiple testing (false discovery rate), were used to investigate whether hypertensive cases and normotensive controls had different fasting and postprandial (in response to two standardised test meal challenges) lipaemic, glycaemic, insulinaemic, and inflammatory (glycoprotein acetylation (GlycA)) responses in 989 participants from the ZOE PREDICT-1 nutritional intervention study. Compared to normotensive controls, hypertensive individuals had significantly higher fasting and postprandial insulin, triglycerides, and markers of inflammation after adjusting for age, sex, and BMI (effect size: Beta (Standard Error) ranging from 0.17 (0.08), p = 0.04 for peak insulin to 0.29 (0.08), p = 4.4 × 10−4 for peak GlycA). No difference was seen for postprandial glucose. When further adjusting for VFM effects were attenuated. Causal mediation analysis suggests that 36% of the variance in postprandial insulin response and 33.8% of variance in postprandial triglyceride response were mediated by VFM. Hypertensive individuals have different postprandial insulinaemic and lipaemic responses compared to normotensive controls and this is partially mediated by visceral fat mass. Consequently, reducing VFM should be a key focus of health interventions in hypertension. Trial registration: The ClinicalTrials.gov registration identifier is NCT03479866.

Scholarly Articles on Metabolic Syndrome and Inflammation

Association between systemic immune-inflammation index and metabolic syndrome and its components: results from the National Health and Nutrition Examination Survey 2011–2016 - Journal of Translational MedicineBackground Metabolic syndrome (MetS), a worldwide public health problem, affects human health and quality of life in a dramatic manner. A growing evidence base suggests that MetS is strongly associated with levels of systemic immune inflammation. The present study aimed to investigate the possible relationship between the systemic immune-inflammation index (SII), a novel inflammatory marker, and MetS to provide data support for effective MetS prevention by reducing the systemic inflammatory response. Methods We included adult participants with complete SII and MetS information from the 2011–2016 National Health and Nutrition Examination Survey (NHANES). MetS was defined as using the criteria developed by the Adult Treatment Program III of the National Cholesterol Education Program. The formula for SII was as follows: SII = platelet counts × neutrophil counts/ lymphocyte counts. Weighted linear regression was used to assess differences in variables across SII quartile groups after the SII score was divided into 4 quartiles. The independent interaction between SII and MetS was investigated using weighted multivariate logistic regression analysis and subgroup analysis, and the relationship between SII levels and 5 particular MetS items was further explored in depth. Results A total of 12,402 participants, 3,489 of whom were diagnosed with MetS, were included in this study. After correcting for covariates, the results of a logistic regression of multistage weighted complex sampling data revealed that participants with higher SII scores had a higher chance of developing MetS (odds ratio (OR) = 1.33, 95% confidence interval (CI): 1.14–1.55) and that SII levels could be used as an independent risk factor to predict that likelihood of MetS onset. In the Q1–Q4 SII quartile group, the risk of developing MetS was 1.33 times higher in the Q4 group, which had the highest level of systemic immune inflammation than in the Q1 group. After adjusting for all confounding factors, SII scores were found to have a negative correlation with high-density lipoprotein cholesterol (OR = 1.29; 95% CI, 0.99–1.67, P = 0.056) and a significant positive correlation with waist circumference (OR = 2.17; 95% CI, 1.65–2.87, P < 0.001) and blood pressure (BP) (OR = 1.65; 95% CI, 1.20–2.27, P = 0.003). Gender, age, and smoking status were shown to alter the positive association between SII and MetS in subgroup analyses and interaction tests (p for interaction < 0.05). Additionally, we demonstrated a nonlinear correlation between SII and MetS. The findings of the restricted cubic spline indicated that there was an inverted U-shaped association between SII and MetS. Conclusions Our findings imply that increased SII levels are related to MetS, and SII may be a simple and cost-effective method to identify individuals with MetS. Therefore, protective measures such as early investigation and anti-inflammatory interventions are necessary to reduce the overall incidence of MetS.
Metabolic syndrome and inflammatory biomarkers: a community-based cross-sectional study at the Framingham Heart Study - Diabetology & Metabolic SyndromeBackground Prior studies reported conflicting findings on the association between metabolic syndrome and inflammatory biomarkers. We tested the cross-sectional associations between metabolic syndrome and nine inflammatory markers. Methods We measured C-reactive protein, CD40 ligand, interleukin-6, intercellular adhesion molecule-1, monocyte chemoattractant protein-1, osteoprotegerin, P-selectin, tumor necrosis factor-alpha, and tumor necrosis factor receptor-2 in 2570 Framingham Offspring Study participants free of diabetes and cardiovascular disease at examination 7. Metabolic syndrome was defined by National Cholesterol Education Program criteria. We performed multivariable linear regressions for each biomarker with metabolic syndrome as the exposure adjusting for age, sex, smoking, aspirin use, and hormone replacement. We subsequently added to the models components of the metabolic syndrome as continuous traits plus lipid lowering and hypertension treatments. We considered P < 0.05 as statistically significant. Results Metabolic syndrome was present in 984 (38%) participants and was statistically significantly associated with each biomarker (all P < 0.02) except osteoprotegerin. After adjusting for its component variables, the metabolic syndrome was associated only with P-selectin (1.06 fold higher in metabolic syndrome, 95% CI 1.02, 1.10, p = 0.005). Conclusions Metabolic syndrome was associated with multiple inflammatory biomarkers. However, adjusting for each of its components eliminated the association with most inflammatory markers, except P-selectin. Our results suggest that the relation between metabolic syndrome and inflammation is largely accounted for by its components.

Scholarly Articles on Metabolic Syndrome, Hyperinsulinemia and Insulin Resistance

Mapping the knowledge structure of research on insulin resistance and metabolic syndrome: a global perspective - Translational Medicine CommunicationsBackground Insulin resistance is a major pathogenic factor that plays a crucial role in the development of metabolic syndrome and has been proposed as one of its underlying causes. Most diagnostic criteria for metabolic syndrome do not directly include insulin resistance. Furthermore, research on insulin resistance continues to provide information on the development and treatment of metabolic syndromes and related health conditions. Therefore, this bibliometric analysis aimed to investigate the current research status and identify possible future research hotspots in the area of metabolic syndrome and insulin resistance by analyzing Scopus-based studies. Methods To collect published data on metabolic syndrome and insulin resistance, this study used the Scopus database as its data source without a particular starting date but including records up to December 31, 2022. The gathered documents were then exported to VOSviewer v.1.6.18 to analyze and visualize country collaborations and identify research areas of high interest. Results The study presents an overview of 1932 records between 1988 and 2022, focusing on metabolic syndrome and insulin resistance. Of these records, 77.33% were original journal articles, while 13.30% were review articles. Additionally, 9.35% of the documents fall under other types of publication, including letters, notes, and editorials. The United States came out on top with 463 items, accounting for 23.96% of the contributions in this field, followed by Japan in second place with 119 items (6.16%). China (n = 113, 5.85%) and the United Kingdom (n = 113, 5.85%) ranked third. Most publications on metabolic syndrome and insulin resistance focus on key terms related to the pathogenesis of insulin resistance syndrome, the use of waist circumference as a crucial clinical indicator to evaluate the risk of metabolic syndrome, and the association between metabolic syndrome and oxidative stress and a pro-inflammatory state. Conclusions This study presents the first bibliometric analysis of publications focusing on metabolic syndrome and insulin resistance. The findings of this study offer a comprehensive global perspective on the research carried out on metabolic syndrome and insulin resistance and can be an invaluable source for future research.
Hyperinsulinemia and Its Pivotal Role in Aging, Obesity, Type 2 Diabetes, Cardiovascular Disease and CancerFor many years, the dogma has been that insulin resistance precedes the development of hyperinsulinemia. However, recent data suggest a reverse order and place hyperinsulinemia mechanistically upstream of insulin resistance. Genetic background, consumption of the “modern” Western diet and over-nutrition may increase insulin secretion, decrease insulin pulses and/or reduce hepatic insulin clearance, thereby causing hyperinsulinemia. Hyperinsulinemia disturbs the balance of the insulin–GH–IGF axis and shifts the insulin : GH ratio towards insulin and away from GH. This insulin–GH shift promotes energy storage and lipid synthesis and hinders lipid breakdown, resulting in obesity due to higher fat accumulation and lower energy expenditure. Hyperinsulinemia is an important etiological factor in the development of metabolic syndrome, type 2 diabetes, cardiovascular disease, cancer and premature mortality. It has been further hypothesized that nutritionally driven insulin exposure controls the rate of mammalian aging. Interventions that normalize/reduce plasma insulin concentrations might play a key role in the prevention and treatment of age-related decline, obesity, type 2 diabetes, cardiovascular disease and cancer. Caloric restriction, increasing hepatic insulin clearance and maximizing insulin sensitivity are at present the three main strategies available for managing hyperinsulinemia. This may slow down age-related physiological decline and prevent age-related diseases. Drugs that reduce insulin (hyper) secretion, normalize pulsatile insulin secretion and/or increase hepatic insulin clearance may also have the potential to prevent or delay the progression of hyperinsulinemia-mediated diseases. Future research should focus on new strategies to minimize hyperinsulinemia at an early stage, aiming at successfully preventing and treating hyperinsulinemia-mediated diseases.
Cellular and Molecular Mechanisms of Insulin Resistance - Current Tissue Microenvironment ReportsPurpose of Review Although the molecular mechanism of insulin resistance involves multiple factors and several intrinsic and extrinsic mechanisms have been identified, this comprehensive review provides key information on some of the core mechanisms and complex interactions of the molecules involved in the signaling pathways of insulin resistance. Recent Findings Diabetes Mellitus, the most common metabolic disorder, is one of the greatest global medical challenges at present. There has been a significant increase in complications associated with diabetes such as heart disorders, stroke, neuropathy, dyslipidemia, metabolic dysfunction-associated steatotic liver disease, and nephropathy. This calls for immediate strategic action to combat this complex metabolic disorder. Insulin resistance, a characteristic marker of type 2 diabetes is a condition in which the regulation of glucose metabolism in body tissues, such as the liver, adipose tissue, and skeletal muscle, becomes disrupted. It is generally associated with hyperglycemia, hyperinsulinemia, hyperlipidemia, and impaired glucose homeostasis. Summary Understanding the pathophysiological molecular mechanisms involved in insulin resistance is critical for developing new therapeutic strategies to treat this polygenic multifactorial condition. Impairment of insulin action is caused by several factors such as lipotoxicity, increased adiposity, enhanced inflammatory signaling, endoplasmic reticulum stress, adipokines, mitochondrial dysfunction, increased free fatty acids, and dysfunctional insulin signaling.

Scholarly Articles on Metabolic Syndrome in Children

Metabolic syndrome among children and adolescents in low and middle income countries: a systematic review and meta-analysis - Diabetology & Metabolic SyndromeBackground Metabolic syndrome (MetS) is a clustering of cardiovascular risk factors, which is rising in the low and middle income countries (LMICs). There are various studies with inconsistent findings that are inconclusive for policy makers and program planners. Thus, this systematic review and meta-analysis aimed at estimating the pooled prevalence of MetS and its components in LMICs. Methods Electronic searches were conducted in international databases including PubMed, Web of Science, EMBASE (Elsevier), Scopus, CINAHL (EBSCOhost), Science direct (Elsevier), Food Science and Technology Abstracts (FSTA), Global Health and Medline, and other sources (World Cat, Google Scholar, and Google). The pooled estimates were computed in the random effect model. The pooled prevalence was computed using the three diagnostic methods (IDF, ATP III and de Ferranti). Publication bias was verified using funnel plot and Egger’s regression test. Subgroup and sensitivity analysis were performed to identify the possible sources of heterogeneity among the included studies. Result In this study, 142,142 children and adolescents from 76 eligible articles were included to compute the pooled prevalence of MetS and its components in LMCIs. MeTs among overweight and obese population was computed from 20 articles with the pooled prevalence of 24.09%, 36.5%, and 56.32% in IDF, ATP III and de Ferranti criteria, respectively. Similarly, a total of 56 articles were eligible to compute the pooled prevalence of MetS in the general population of children and adolescents. Hence, Mets was found in 3.98% (IDF), 6.71% (ATP III) and 8.91% (de Ferranti) of study subjects. Regarding the components of MetS, abdominal obesity was the major component in overweight and obese population and low HDL-C was the most common component in the general population. This study also revealed that males were highly affected by MetS than females. Conclusion This study illustrates that MetS among children and adolescents is an emerging public health challenge in LMICs, where the prevalence of obesity is on the move. Preventive strategies such as community and school based intervention need to be designed. Promoting physical activities and healthy eating behaviors could avert this problem.
Childhood Obesity and Cardiovascular Disease Risk - Current Atherosclerosis ReportsPurpose of Review The global epidemic of youth-onset obesity is tightly linked to the rising burden of cardiometabolic disease across the lifespan. While the link between childhood obesity and cardiovascular disease is established, this contemporary review summarizes recent and novel advances in this field that elucidate the mechanisms and impact of this public health issue. Recent Findings The review highlights the emerging data supporting the relationship between childhood adverse events, social determinants of health, and systemic and institutional systems as etiological factors. We also provide updates on new screening and treatment approaches including updated nutrition and dietary guidelines and benchmarks for pediatric obesity screening, novel pharmacological agents for pediatric obesity and type 2 diabetes such as glucagon-like 1 peptide receptor agonists, and we discuss the long-term safety and efficacy data on surgical management of pediatric obesity. Summary The global burden of pediatric obesity continues to rise and is associated with accelerated and early vascular aging especially in youth with obesity and type 2 diabetes. Socio-ecological determinants of risk mediate and moderate the relationship of childhood obesity with cardiometabolic disease. Recognizing the importance of neighborhood level influences as etiological factors in the development of cardiovascular disease is critical for designing effective policies and interventions. Novel surgical and pharmacological interventions are effective pediatric weight-loss interventions, but future research is needed to assess whether these agents, within a socio-ecological framework, will be associated with abatement of the pediatric obesity epidemic and related increased cardiovascular disease risk. Graphical Abstract
Childhood obesity and adult cardiovascular disease risk factors: a systematic review with meta-analysis - BMC Public HealthBackground Overweight and obesity is a major public health concern that includes associations with the development of cardiovascular disease (CVD) risk factors during childhood and adolescence as well as premature mortality in adults. Despite the high prevalence of childhood and adolescent obesity as well as adult CVD, individual studies as well as previous systematic reviews examining the relationship between childhood obesity and adult CVD have yielded conflicting results. The purpose of this study was to use the aggregate data meta-analytic approach to address this gap. Methods Studies were included if they met the following criteria: (1) longitudinal and cohort studies (including case-cohort), (2) childhood exposure and adult outcomes collected on the same individual over time, (3) childhood obesity, as defined by the original study authors, (4) English-language articles, (5) studies published up to June, 2015, (6) one or more of the following CVD risk factors [systolic blood pressure (SBP), diastolic blood pressure (DBP), total cholesterol (TC), high-density lipoprotein cholesterol (HDL), low-density lipoprotein cholesterol (LDL), non-high-density lipoprotein cholesterol (non-HDL), and triglycerides (TG)], (7) outcome(s) not self-reported, and (8) exposure measurements (child’s adiposity) assessed by health professionals, trained investigators, or self-reported. Studies were retrieved by searching three electronic databases as well as citation tracking. Fisher’s r to z score was calculated for each study for each outcome. Pooled effect sizes were calculated using random-effects models while risk of bias was assessed using the STROBE instrument. In order to try and identify sources of heterogeneity, random-effects meta-regression was also performed. Results Of the 4840 citations reviewed, a total of 23 studies were included in the systematic review and 21 in the meta-analysis. The findings suggested that childhood obesity is significantly and positively associated with adult SBP (Zr = 0.11; 95% CI: 0.07, 0.14), DBP (Zr = 0.11; 95% CI: 0.07, 0.14), and TG (Zr =0.08; 95% CI: 0.03, 0.13), and significantly and inversely associated with adult HDL (Zr = −0.06; 95% CI: -0.10, −0.02). For those studies that adjusted for adult body mass index (BMI), associations were reversed, suggesting that adult BMI may be a potential mediator. Nine studies had more than 33% of items that placed them at an increased risk for bias. Conclusions The results of this study suggest that childhood obesity may be a risk factor for selected adult CVD risk factors. However, a need exists for additional, higher-quality studies that include, but are not limited to, both unadjusted and adjusted measures such as BMI before any definitive conclusions can be reached. Systematic review and meta-analysis PROSPERO 2015: CRD42015019763 .
Pediatric Metabolic Syndrome Predicts Adulthood Metabolic Syndrome, Subclinical Atherosclerosis, and Type 2 Diabetes Mellitus but Is No Better Than Body Mass Index Alone | Circulation Background—The clinical utility of identifying pediatric metabolic syndrome (MetS) is controversial. This study sought to determine the status of pediatric MetS as a risk factor for adult subclinical atherosclerosis (carotid intima-media thickness [cIMT]) and type 2 diabetes mellitus (T2DM) and compare and contrast this prediction with its individual components. Methods and Results—Using data from the population-based, prospective, observational Bogalusa Heart and Cardiovascular Risk in Young Finns studies, we examined the utility of 4 categorical definitions of youth MetS and their components in predicting adult high cIMT and T2DM among 1781 participants aged 9 to 18 years at baseline (1984 to 1988) who were then examined 14 to 27 years later (2001–2007) when aged 24 to 41 years. Youth with MetS were at 2 to 3 times the risk of having high cIMT and T2DM as adults compared with those free of MetS at youth. Risk estimates with the use of high body mass index were similar to those of MetS phenotypes in predicting adult outcomes. Comparisons of area under the receiver operating characteristic curve and net reclassification index suggested that prediction of adult MetS, high cIMT, and T2DM in adulthood with the use of youth MetS was either equivalent or inferior to classification based on high body mass index or overweight and obesity. Conclusions—Youth with MetS are at increased risk of meaningful adult outcomes; however, the simplicity of screening for high BMI or overweight and obesity in the pediatric setting offers a simpler, equally accurate alternative to identifying youth at risk of developing adult MetS, high cIMT, or T2DM.

Scholarly Articles on Metabolic Syndrome & ASCVD

Overview and New Insights into the Metabolic Syndrome: Risk Factors and Emerging Variables in the Development of Type 2 Diabetes and Cerebrocardiovascular DiseaseMetabolic syndrome (MetS) is considered a metabolic disorder that has been steadily increasing globally and seems to parallel the increasing prevalence of obesity. It consists of a cluster of risk factors which traditionally includes obesity and hyperlipidemia, hyperinsulinemia, hypertension, and hyperglycemia. These four core risk factors are associated with insulin resistance (IR) and, importantly, the MetS is known to increase the risk for developing cerebrocardiovascular disease and type 2 diabetes mellitus. The MetS had its early origins in IR and syndrome X. It has undergone numerous name changes, with additional risk factors and variables being added over the years; however, it has remained as the MetS worldwide for the past three decades. This overview continues to add novel insights to the MetS and suggests that leptin resistance with hyperleptinemia, aberrant mitochondrial stress and reactive oxygen species (ROS), impaired folate-mediated one-carbon metabolism with hyperhomocysteinemia, vascular stiffening, microalbuminuria, and visceral adipose tissues extracellular vesicle exosomes be added to the list of associated variables. Notably, the role of a dysfunctional and activated endothelium and deficient nitric oxide bioavailability along with a dysfunctional and attenuated endothelial glycocalyx, vascular inflammation, systemic metainflammation, and the important role of ROS and reactive species interactome are discussed. With new insights and knowledge regarding the MetS comes the possibility of new findings through further research.
Risk for cardiovascular disease associated with metabolic syndrome and its components: a 13-year prospective study in the RIVANA cohort - Cardiovascular DiabetologyBackground We aimed to investigate the association of metabolic syndrome (MetS) and its single components with cardiovascular risk and estimated their impact on the prematurity of occurrence of cardiovascular events using rate advancement periods (RAPs). Methods We performed prospective analyses among 3976 participants (age range: 35–84, 55% female) in the Vascular Risk in Navarre (RIVANA) Study, a Mediterranean population-based cohort. MetS was defined based on the modified criteria of the American Heart Association/National Heart, Lung, and Blood Institute and the International Diabetes Federation. The primary endpoint was major cardiovascular event (a composite of myocardial infarction, stroke, or mortality from cardiovascular causes). Secondary endpoints were incidence of non-fatal myocardial infarction and non-fatal stroke, cardiovascular mortality, and all-cause mortality. Cox proportional hazards models, adjusted for potential confounders, were fitted to evaluate the association between MetS and its single components at baseline with primary and secondary endpoints. Results During a median follow-up of 12.8 years (interquartile range, 12.5–13.1), we identified 228 primary endpoint events. MetS was associated with higher risk of incidence of major cardiovascular event, cardiovascular and all-cause mortality, but was neither associated with higher risk of myocardial infarction nor stroke. Compared with participants without MetS, the multivariable hazard ratio (95% confidence interval [CI]) among participants with MetS was 1.32 (1.01–1.74) with RAP (95% CI) of 3.23 years (0.03, 6.42) for major cardiovascular event, 1.64 (1.03–2.60) with RAP of 3.73 years (0.02, 7.45) for cardiovascular mortality, and 1.45 (1.17–1.80) with RAP of 3.24 years (1.21, 5.27) for all-cause mortality. The magnitude of the associations of the single components of MetS was similar than the predicted by MetS. Additionally, for each additional trait of MetS, incidence of major cardiovascular event relatively increased by 22% (1.22, 95% CI 1.09–1.36) with RAP of 2.31 years (0.88, 3.74). Conclusions MetS was independently associated with CVD risk, cardiovascular and all-cause mortality. Components of the MetS were associated with similar magnitude of increased CVD, which suggests that MetS was not in excess of the level explained by the presence of its single components. Further research should explore the association of different combinations of the components of MetS with CVD.
Metabolic Syndrome and 10-Year Cardiovascular Disease Risk in the Hoorn Study | Circulation Background— Different definitions of the metabolic syndrome have been proposed. Their value in a clinical setting to assess cardiovascular disease (CVD) risk is still unclear. We compared the definitions proposed by the National Cholesterol Education Program Adult Treatment Panel III (NCEP), World Health Organization (WHO), European Group for the Study of Insulin Resistance (EGIR), and American College of Endocrinology (ACE) with respect to the prevalence of the metabolic syndrome and the association with 10-year risk of fatal and nonfatal CVD. Methods and Results— The Hoorn Study is a population-based cohort study. The present study population comprised 615 men and 749 women aged 50 to 75 years and without diabetes or a history of CVD at baseline in 1989 to 1990. The prevalence of the metabolic syndrome at baseline ranged from 17% to 32%. The NCEP definition was associated with about a 2-fold increase in age-adjusted risk of fatal CVD in men and nonfatal CVD in women. For the WHO, EGIR, and ACE definitions, these hazard ratios were slightly lower. Risk increased with the number of risk factors. Elevated insulin levels were more prevalent in subjects with multiple risk factors, but metabolic syndrome definitions including elevated insulin level were not more strongly associated with risk. Conclusions— The metabolic syndrome, however defined, is associated with an approximate 2-fold increased risk of incident cardiovascular morbidity and mortality in a European population. In clinical practice, a more informative assessment can be obtained by taking into account the number of individual risk factors.

Scholarly Articles on Metabolic Syndrome & NAFLD/MASLD

Beneficial Effects of the Ketogenic Diet on Nonalcoholic Fatty Liver Disease (NAFLD/MAFLD)The prevalence of nonalcoholic fatty liver disease (NAFLD) is likely to be approaching 38% of the world’s population. It is predicted to become worse and is the main cause of morbidity and mortality due to hepatic pathologies. It is particularly worrying that NAFLD is increasingly diagnosed in children and is closely related, among other conditions, to insulin resistance and metabolic syndrome. Against this background is the concern that the awareness of patients with NAFLD is low; in one study, almost 96% of adult patients with NAFLD in the USA were not aware of their disease. Thus, studies on the therapeutic tools used to treat NAFLD are extremely important. One promising treatment is a well-formulated ketogenic diet (KD). The aim of this paper is to present a review of the available publications and the current state of knowledge of the effect of the KD on NAFLD. This paper includes characteristics of the key factors (from the point of view of NAFLD regression), on which ketogenic diet exerts its effects, i.e., reduction in insulin resistance and body weight, elimination of fructose and monosaccharides, limitation of the total carbohydrate intake, anti-inflammatory ketosis state, or modulation of gut microbiome and metabolome. In the context of the evidence for the effectiveness of the KD in the regression of NAFLD, this paper also suggests the important role of taking responsibility for one’s own health through increasing self-monitoring and self-education.

Scholarly Articles on Metabolic Syndrome & GERD

Scholarly Articles on Metabolic Syndrome & LCHF

Carbohydrate restriction improves the features of Metabolic Syndrome. Metabolic Syndrome may be defined by the response to carbohydrate restriction - Nutrition & MetabolismMetabolic Syndrome (MetS) represents a constellation of markers that indicates a predisposition to diabetes, cardiovascular disease and other pathologic states. The definition and treatment are a matter of current debate and there is not general agreement on a precise definition or, to some extent, whether the designation provides more information than the individual components. We consider here five indicators that are central to most definitions and we provide evidence from the literature that these are precisely the symptoms that respond to reduction in dietary carbohydrate (CHO). Carbohydrate restriction is one of several strategies for reducing body mass but even in the absence of weight loss or in comparison with low fat alternatives, CHO restriction is effective at ameliorating high fasting glucose and insulin, high plasma triglycerides (TAG), low HDL and high blood pressure. In addition, low fat, high CHO diets have long been known to raise TAG, lower HDL and, in the absence of weight loss, may worsen glycemic control. Thus, whereas there are numerous strategies for weight loss, a patient with high BMI and high TAG is likely to benefit most from a regimen that reduces CHO intake. Reviewing the literature, benefits of CHO restriction are seen in normal or overweight individuals, in normal patients who meet the criteria for MetS or in patients with frank diabetes. Moreover, in low fat studies that ameliorate LDL and total cholesterol, controls may do better on the symptoms of MetS. On this basis, we feel that MetS is a meaningful, useful phenomenon and may, in fact, be operationally defined as the set of markers that responds to CHO restriction. Insofar as this is an accurate characterization it is likely the result of the effect of dietary CHO on insulin metabolism. Glucose is the major insulin secretagogue and insulin resistance has been tied to the hyperinsulinemic state or the effect of such a state on lipid metabolism. The conclusion is probably not surprising but has not been explicitly stated before. The known effects of CHO-induced hypertriglyceridemia, the HDL-lowering effect of low fat, high CHO interventions and the obvious improvement in glucose and insulin from CHO restriction should have made this evident. In addition, recent studies suggest that a subset of MetS, the ratio of TAG/HDL, is a good marker for insulin resistance and risk of CVD, and this indicator is reliably reduced by CHO restriction and exacerbated by high CHO intake. Inability to make this connection in the past has probably been due to the fact that individual responses have been studied in isolation as well as to the emphasis of traditional therapeutic approaches on low fat rather than low CHO.We emphasize that MetS is not a disease but a collection of markers. Individual physicians must decide whether high LDL, or other risk factors are more important than the features of MetS in any individual case but if MetS is to be considered it should be recognized that reducing CHO will bring improvement. Response of symptoms to CHO restriction might thus provide a new experimental criterion for MetS in the face of on-going controversy about a useful definition. As a guide to future research, the idea that control of insulin metabolism by CHO intake is, to a first approximation, the underlying mechanism in MetS is a testable hypothesis.
Beneficial Effects of the Ketogenic Diet on Nonalcoholic Fatty Liver Disease (NAFLD/MAFLD)The prevalence of nonalcoholic fatty liver disease (NAFLD) is likely to be approaching 38% of the world’s population. It is predicted to become worse and is the main cause of morbidity and mortality due to hepatic pathologies. It is particularly worrying that NAFLD is increasingly diagnosed in children and is closely related, among other conditions, to insulin resistance and metabolic syndrome. Against this background is the concern that the awareness of patients with NAFLD is low; in one study, almost 96% of adult patients with NAFLD in the USA were not aware of their disease. Thus, studies on the therapeutic tools used to treat NAFLD are extremely important. One promising treatment is a well-formulated ketogenic diet (KD). The aim of this paper is to present a review of the available publications and the current state of knowledge of the effect of the KD on NAFLD. This paper includes characteristics of the key factors (from the point of view of NAFLD regression), on which ketogenic diet exerts its effects, i.e., reduction in insulin resistance and body weight, elimination of fructose and monosaccharides, limitation of the total carbohydrate intake, anti-inflammatory ketosis state, or modulation of gut microbiome and metabolome. In the context of the evidence for the effectiveness of the KD in the regression of NAFLD, this paper also suggests the important role of taking responsibility for one’s own health through increasing self-monitoring and self-education.