The Human Body

The human body is an intricate and dynamic organism comprised of numerous interconnected systems, each with specialized functions crucial for sustaining life. The cardiovascular system, centered around the heart and blood vessels, circulates oxygen, nutrients, and hormones throughout the body, ensuring cellular nourishment and waste removal. Working in tandem, the respiratory system, with its lungs and airways, facilitates the exchange of oxygen and carbon dioxide, vital for cellular respiration. Digestive organs, including the stomach, intestines, liver, and pancreas, break down food into nutrients, providing energy and essential building blocks for cellular growth and repair.

Meanwhile, the endocrine system orchestrates bodily functions through hormone secretion, regulating metabolism, growth, reproduction, and stress responses. The muscular system enables movement and stability, allowing us to perform everyday tasks and engage in physical activities. In concert with the skeletal system, composed of bones, cartilage, and ligaments, it provides structural support, protection, and facilitates movement.

Our nervous system, comprising the brain, spinal cord, and nerves, coordinates bodily functions, processes sensory information, and enables communication between body parts. Sensory systems, such as sight, sound, smell, taste, and touch, allow us to perceive and interact with our environment, enriching our experiences. The immune system defends against pathogens, maintaining health and integrity.

Reproductive systems ensure the continuation of the species, with unique roles in fertility and sexual reproduction. Finally, the urinary system, including the kidneys, bladder, and ureters, filters blood, removes waste products, and regulates fluid balance. Together, these systems harmonize in a complex symphony, sustaining life and adapting to internal and external challenges to maintain overall well-being.

Hyperinsulinemia, insulin resistance, and metabolic syndrome collectively exert profound effects on various systems of the body, disrupting homeostasis and increasing the risk of chronic diseases.

In the cardiovascular system, these conditions promote atherosclerosis and hypertension, elevating the risk of heart disease and stroke. Additionally, they can impair endothelial function and increase arterial stiffness, further compromising cardiovascular health.

The respiratory system is impacted as well, with obesity-related insulin resistance contributing to conditions such as obstructive sleep apnea, which can lead to breathing difficulties and impaired oxygenation during sleep.

Within the digestive system, insulin resistance can disrupt glucose and lipid metabolism in the liver, leading to non-alcoholic fatty liver disease (NAFLD) and potentially progressing to more severe liver conditions such as cirrhosis.

In the endocrine system, hyperinsulinemia and insulin resistance can disrupt hormone balance, contributing to conditions like polycystic ovary syndrome (PCOS), thyroid dysfunction, and adrenal insufficiency.

Metabolic syndrome itself represents a dysregulation of the metabolic system, characterized by insulin resistance, dyslipidemia, and elevated blood sugar levels. This can lead to type 2 diabetes, further exacerbating metabolic dysfunction and increasing the risk of cardiovascular complications.

Muscular system functionality is compromised by insulin resistance, leading to reduced glucose uptake by muscle cells, which can result in decreased muscle strength and physical function.

Neurologically, insulin resistance and hyperinsulinemia contribute to neuroinflammation and oxidative stress, increasing the risk of cognitive decline, neuropathy, and mood disorders.

Reproductive systems are affected as well, with insulin resistance and hyperinsulinemia disrupting hormonal balance and contributing to menstrual irregularities, infertility, and sexual dysfunction.

The skeletal system is impacted by metabolic syndrome, increasing the risk of osteoporosis and fractures due to chronic inflammation and hormonal imbalances.

Urinary system function can be compromised by insulin resistance and metabolic syndrome, leading to kidney damage, impaired filtration, and an increased risk of chronic kidney disease and urinary tract infections.

In summary, hyperinsulinemia, insulin resistance, and metabolic syndrome have far-reaching consequences, affecting nearly every system of the body and significantly increasing the risk of developing various chronic diseases and health complications.

 Cancer is a broad term used to describe a group of diseases characterized by the abnormal growth of cells in the body. Normally, cells grow, divide, and die in a controlled manner. However, in cancer, this orderly process goes awry, leading to the formation of tumors or the invasion of neighboring tissues.

Cancer can develop in almost any organ or tissue in the body and can spread to other parts of the body through the bloodstream or lymphatic system, a process known as metastasis.

There are many different types of cancer, each with its own set of causes, risk factors, symptoms, and treatments. Some common types of cancer include breast cancer, lung cancer, prostate cancer, colorectal cancer, and skin cancer.

Risk factors for cancer include genetics, environmental factors such as exposure to carcinogens (e.g., tobacco smoke, ultraviolet radiation), lifestyle factors such as diet and physical activity, and certain infections (e.g., human papillomavirus, hepatitis B and C viruses).

Treatment for cancer depends on the type and stage of the disease but may include surgery, chemotherapy, radiation therapy, immunotherapy, targeted therapy, or a combination of these approaches. Early detection through screening and prompt treatment can improve outcomes for many types of cancer.

Hyperinsulinemia, insulin resistance, and metabolic syndrome are all related to abnormalities in insulin signaling and metabolism, which can have significant implications for cancer development and progression. 

Hyperinsulinemia: Hyperinsulinemia refers to elevated levels of insulin in the blood. Insulin is a hormone produced by the pancreas that helps regulate blood sugar levels by promoting the uptake of glucose into cells. However, persistently high levels of insulin can occur due to various factors such as excessive carbohydrate intake, obesity, and insulin resistance. Insulin is known to have mitogenic (cell growth-promoting) effects, and elevated insulin levels can stimulate the growth and proliferation of cancer cells. High insulin levels can also increase the bioavailability of insulin-like growth factor 1 (IGF-1), another hormone that promotes cell growth and proliferation, further contributing to cancer development.

Insulin Resistance: Insulin resistance occurs when cells in the body become less responsive to the effects of insulin. As a result, higher levels of insulin are required to maintain normal blood sugar levels. Insulin resistance is commonly associated with obesity, physical inactivity, and metabolic syndrome. Insulin resistance leads to compensatory hyperinsulinemia, which, as mentioned earlier, can promote cancer growth. Additionally, insulin resistance is often accompanied by dysregulation of other metabolic pathways, such as increased inflammation and altered lipid metabolism, which can create an environment conducive to cancer development.

Metabolic Syndrome: Metabolic syndrome is a cluster of conditions that includes central obesity, insulin resistance, high blood pressure, and dyslipidemia (abnormal blood lipid levels). People with metabolic syndrome are at increased risk of developing type 2 diabetes, cardiovascular disease, and certain types of cancer. The underlying mechanisms linking metabolic syndrome to cancer risk involve chronic inflammation, oxidative stress, hormonal dysregulation (including elevated insulin and IGF-1 levels), and altered metabolism of glucose and lipids, all of which can promote tumour growth and progression.

In summary, hyperinsulinemia, insulin resistance, and metabolic syndrome can contribute to cancer development and progression through various mechanisms, including promoting cell growth, increasing inflammation, and altering metabolic pathways. Managing these conditions through lifestyle modifications, such as maintaining a healthy weight, exercising regularly, and adopting a balanced diet, can help reduce cancer risk and improve overall health.

 This section should be considered as emergent in terms of the evidence and the role of diet as supportive.

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1. de  Groot S, Pijl H, van der Hoeven JJM, Kroep JR. Effects of short-term  fasting on cancer treatment. J Exp Clin Cancer Res. 2019;38. doi:10.1186/s13046-019-1189-9 
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Glycogen storage disease (GSD) primarily affects the metabolic system. It is a group of inherited disorders characterized by defects in the enzymes involved in glycogen metabolism, leading to abnormal accumulation or breakdown of glycogen in various tissues of the body. Glycogen is a complex carbohydrate that serves as a form of energy storage in the body, particularly in the liver and muscles.

Because glycogen storage disease affects the metabolism of glycogen, it primarily involves the metabolic pathways responsible for glycogen synthesis and breakdown. The liver, muscles, and other tissues that store or utilize glycogen are primarily affected.

There are several types of glycogen storage disease, each caused by mutations in different genes encoding enzymes involved in glycogen metabolism. 

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   The metabolic system involves various organs and tissues that play crucial roles in energy metabolism, nutrient utilization, and the regulation of metabolic processes. Some key organs and tissues of the metabolic system include:

1. Liver: The liver is a vital metabolic organ involved in numerous metabolic processes, including carbohydrate metabolism (glycolysis, gluconeogenesis, glycogenolysis), lipid metabolism (lipogenesis, fatty acid oxidation, cholesterol synthesis), protein metabolism (amino acid synthesis and breakdown), detoxification of drugs and toxins, and bile production.
2. Pancreas: The pancreas is an endocrine and exocrine gland that plays a central role in regulating blood sugar levels. It produces hormones such as insulin (which lowers blood sugar) and glucagon (which raises blood sugar), as well as digestive enzymes that aid in the breakdown of carbohydrates, proteins, and fats.
3. Adipose Tissue (Fat): Adipose tissue is specialized for the storage and release of energy in the form of triglycerides. It also produces hormones called adipokines, which regulate metabolism, appetite, and inflammation.
4. Muscles: Skeletal muscles are major consumers of energy and play a central role in glucose metabolism and energy expenditure. During exercise, muscles utilize glucose and fatty acids for energy production through glycolysis and oxidative phosphorylation.
5. Brain: The brain is highly metabolically active and requires a constant supply of glucose for energy. It plays a role in regulating metabolism through the hypothalamus, which integrates signals related to hunger, satiety, and energy expenditure.
6. Thyroid Gland: The thyroid gland produces hormones such as thyroxine (T4) and triiodothyronine (T3), which regulate metabolic rate, thermogenesis, and energy expenditure throughout the body.
7. Kidneys: The kidneys play a role in the regulation of blood glucose levels by reabsorbing glucose from the urine and producing glucose through gluconeogenesis. They also help regulate electrolyte balance and acid-base balance, which are important for metabolic homeostasis.
8. Endocrine System: The endocrine system consists of various glands (such as the pituitary, adrenal, and parathyroid glands) that produce hormones involved in metabolic regulation, including insulin, glucagon, cortisol, growth hormone, and others.

These organs and tissues work together to regulate metabolism, maintain energy balance, and ensure the proper utilization of nutrients for growth, repair, and physiological functions throughout the body.

35% of the Ethiopian population was considered to have metabolic syndrome in 2020-  it  affects everyone globally 

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6. Castro-Barquero  S, Ruiz-León AM, Sierra-Pérez M, Estruch R, Casas R. Dietary Strategies  for Metabolic Syndrome: A Comprehensive Review. Nutrients. 2020;12(10). doi:10.3390/nu12102983
7. Hoyas I, Leon-Sanz M. Nutritional Challenges in Metabolic Syndrome. Journal of Clinical Medicine. 2019;8(9):1301. doi:10.3390/jcm8091301 
8. Shemirani  F, Golzarand M, Salari-Moghaddam A, Mahmoudi M. Effect of  low-carbohydrate diet on adiponectin level in adults: a systematic  review and dose-response meta-analysis of randomized controlled trials. Critical Reviews in Food Science and Nutrition. 2021;0(0):1-10. doi:10.1080/10408398.2021.1871588 ABSTRACT
9. Foley PJ. Effect of low carbohydrate diets on insulin resistance and the metabolic syndrome. Current Opinion in Endocrinology, Diabetes, and Obesity. 2021;28(5):463. doi:10.1097/MED.0000000000000659
10. Guarnotta, V. et al. (2022) ‘Very Low-Calorie Ketogenic Diet: A Potential Application in the Treatment of Hypercortisolism Comorbidities’, Nutrients, 14(12), p. 2388. Available at: https://doi.org/10.3390/nu14122388.

1. Ismael SA.  Effects of low carbohydrate diet compared to low fat diet on reversing  the metabolic syndrome, using NCEP ATP III criteria: a randomized  clinical trial. BMC Nutr. 2021;7(1):62. doi:10.1186/s40795-021-00466-8
2. Dorans, K.S. et al. (2022) ‘Effects of a Low-Carbohydrate Dietary Intervention on Hemoglobin A 1c: A Randomized Clinical Trial’, JAMA Network Open, 5(10), p. e2238645. Available at: https://doi.org/10.1001/jamanetworkopen.2022.38645.
3. Stentz  FB, Brewer A, Wan J, et al. Remission of pre-diabetes to normal glucose  tolerance in obese adults with high protein versus high carbohydrate  diet: randomized control trial. BMJ Open Diabetes Res Care. 2016;4(1).  doi:10.1136/bmjdrc-2016-000258
4. Gardner, C.D. et al. (2022) ‘Effect of a Ketogenic Diet versus Mediterranean Diet on HbA1c  in Individuals with Prediabetes and Type 2 Diabetes Mellitus: the  Interventional Keto-Med Randomized Crossover Trial’, The American Journal of Clinical Nutrition, p. nqac154. doi:10.1093/ajcn/nqac154.
5. McKenzie  AL, Athinarayanan SJ, McCue JJ, et al. Type 2 Diabetes Prevention  Focused on Normalization of Glycemia: A Two-Year Pilot Study. Nutrients. 2021;13(3):749. doi:10.3390/nu13030749
6. Cummings, P.J. et al. (2022) ‘Lifestyle Therapy Targeting Hyperinsulinemia Normalizes  Hyperglycemia and Surrogate Markers of Insulin Resistance in a Large,  Free-Living Population’, AJPM Focus, 1(2). Available at: https://doi.org/10.1016/j.focus.2022.100034.
7. McKenzie  A, Athinarayanan S, Adams R, Hallberg S, Volek J, Phinney SD.  Predictors of Normalization of Fasting Glucose in Patients With  Prediabetes Using Remote Continuous Care Emphasizing Low Carbohydrate  Intake. J Endocr Soc. 2021;5(Suppl 1):A323. doi:10.1210/jendso/bvab048.659
8. Unwin  DJ, Tobin SD, Murray SW, Delon C, Brady AJ. Substantial and Sustained  Improvements in Blood Pressure, Weight and Lipid Profiles from a  Carbohydrate Restricted Diet: An Observational Study of Insulin  Resistant Patients in Primary Care. International Journal of  Environmental Research and Public Health. 2019;16(15):2680. doi:10.3390/ijerph16152680 
9. Hyde  PN, Sapper TN, Crabtree CD, et al. Dietary carbohydrate restriction  improves metabolic syndrome independent of weight loss. JCI Insight.  2019;4(12). doi:10.1172/jci.insight.128308 
10.  Lustig  RH, Mulligan K, Noworolski SM, et al. Isocaloric fructose restriction  and metabolic improvement in children with obesity and metabolic  syndrome. Obesity (Silver Spring). 2016;24(2):453-460. doi:10.1002/oby.21371
11. Maekawa  S, Kawahara T, Nomura R, et al. Retrospective study on the efficacy of a  low-carbohydrate diet for impaired glucose tolerance. Diabetes Metab  Syndr Obes. 2014;7:195-201. doi:10.2147/DMSO.S62681
12. Pérez-Guisado  J, Muñoz-Serrano A. A Pilot Study of the Spanish Ketogenic  Mediterranean Diet: An Effective Therapy for the Metabolic Syndrome.  Journal of Medicinal Food. 2011;14(7-8):681-687. doi:10.1089/jmf.2010.0137 PDF
13. Griauzde  DH, Saslow L, Patterson K, et al. Mixed methods pilot study of a  low-carbohydrate diabetes prevention programme among adults with  pre-diabetes in the USA. BMJ Open. 2020;10(1). doi:10.1136/bmjopen-2019-033397 
14. Gershuni  VM, Yan SL, Medici V. Nutritional Ketosis for Weight Management and  Reversal of Metabolic Syndrome. Curr Nutr Rep. 2018;7(3):97-106. doi:10.1007/s13668-018-0235-0 
15. Samaha FF, Iqbal N, Seshadri P, et al. A Low-Carbohydrate as Compared with a Low-Fat Diet in Severe Obesity. N Engl J Med. 2003;348(21):2074-2081. doi:10.1056/NEJMoa022637
16. Yost  O, DeJonckheere M, Stonebraker S, et al. Continuous Glucose Monitoring  With Low-Carbohydrate Diet Coaching in Adults With Prediabetes: Mixed  Methods Pilot Study. JMIR Diabetes. 2020;5(4):e21551. doi:10.2196/21551
17. Nakagata  T, Tamura Y, Kaga H, et al. Ingestion of an Exogenous Ketone Monoester  Improves the Glycemic Response during Oral Glucose Tolerance Test in  Subjects with Impaired Glucose Tolerance: A Crossover Randomized Trial.  Journal of Diabetes Investigation. n/a(n/a). doi:10.1111/jdi.13423 
18. Cucuzzella  MT, Tondt J, Dockter NE, Saslow L, Wood TR. A low-carbohydrate survey:  Evidence for sustainable metabolic syndrome reversal. Journal of Insulin Resistance. 2017;2(1):25. doi:10.4102/jir.v2i1.30
19. Bharmal  SH, Cho J, C Alarcon Ramos G, Ko J, Cameron-Smith D, Petrov MS. Acute  Nutritional Ketosis and Its Implications for Plasma Glucose and  Glucoregulatory Peptides in Adults with Prediabetes: A Crossover  Placebo-Controlled Randomized Trial. The Journal of Nutrition. 2021;151(4):921-929. doi:10.1093/jn/nxaa417 ABSTRACT

 Mitochondria, often referred to as the cell's powerhouses, are vital for producing the energy needed for our bodies to function, especially in the brain. This is because the brain has high energy demands to support its various functions, including cognition, memory, and signal transmission between neurons.

On average, a human cell contains hundreds to thousands of mitochondria, with the number varying depending on the cell type and energy requirements. Brain cells, known as neurons, are particularly rich in mitochondria due to their high energy needs for maintaining electrical potentials and neurotransmitter release.

When we consume nutrients, such as carbohydrates and fats, mitochondria play a crucial role in converting these molecules into usable energy molecules called adenosine triphosphate (ATP). This process occurs through cellular respiration, where nutrients are broken down in a series of biochemical reactions within the mitochondria.

In the brain, efficient mitochondrial function is essential for supporting synaptic activity, neurotransmitter synthesis and release, and neuronal signaling. Disruptions in mitochondrial function can impair these processes, leading to cognitive dysfunction, memory deficits, and other neurological symptoms.

Mitochondrial dysfunction has been implicated in various brain disorders, including neurodegenerative diseases like Alzheimer's disease and Parkinson's disease. In these conditions, impaired mitochondrial function contributes to neuronal damage, oxidative stress, and the accumulation of toxic protein aggregates, ultimately leading to progressive neurological decline.

Furthermore, mitochondria are critical for regulating calcium homeostasis, maintaining antioxidant defenses, and modulating apoptotic pathways in the brain. Dysfunction in these mitochondrial functions can exacerbate neuronal damage and increase susceptibility to neurodegeneration.

Given the importance of mitochondria in supporting brain function, preserving mitochondrial health is crucial for maintaining cognitive function and overall brain health. Strategies aimed at enhancing mitochondrial function and reducing oxidative stress may offer potential therapeutic approaches for preventing or mitigating neurological disorders.

Mitochondria are essential for energy production throughout the body, not just in the brain. Dysfunction in mitochondrial function can impact various body systems, leading to health issues:

• In muscle cells, impaired mitochondrial function can cause muscle weakness, fatigue, and exercise intolerance.
• In the cardiovascular system, dysfunctional mitochondria can lead to heart problems, such as arrhythmias, cardiomyopathy, and heart failure.
• In the endocrine system, disrupted mitochondrial function may contribute to metabolic disorders like diabetes and obesity.
• In the immune system, mitochondrial dysfunction can impair immune cell function and increase susceptibility to infections and autoimmune diseases.
• In the gastrointestinal system, dysfunctional mitochondria may contribute to digestive disorders, such as inflammatory bowel disease and irritable bowel syndrome.
• In the integumentary system (skin), impaired mitochondrial function can lead to skin disorders like dermatitis, eczema, and psoriasis.
• In the respiratory system, dysfunctional mitochondria can impair lung function and contribute to respiratory diseases like asthma and chronic obstructive pulmonary disease (COPD).
• In the reproductive system, mitochondrial dysfunction may lead to fertility issues and reproductive disorders.

Inflammation can also play a significant role in mitochondrial dysfunction. Chronic inflammation can damage mitochondria and impair their function, leading to a vicious cycle of oxidative stress and inflammation. This can further exacerbate mitochondrial dysfunction and contribute to the development and progression of various diseases.

Overall, maintaining healthy mitochondria is crucial for the proper functioning of all body systems. Strategies aimed at supporting mitochondrial function and reducing inflammation may help prevent or alleviate a wide range of health problems across different body systems.

 Eating foods that cause mitochondrial damage can have a significant impact on overall health. When mitochondria are damaged due to poor dietary choices, it can lead to:

1. Reduced energy production: Mitochondria are responsible for generating energy in the form of ATP. Damaged mitochondria may produce less ATP, leading to decreased energy levels and fatigue.
2. Impaired organ function: Mitochondrial dysfunction can affect various organs and systems in the body, leading to dysfunction and increased susceptibility to diseases.
3. Accelerated aging: Mitochondrial damage contributes to oxidative stress and inflammation, both of which are associated with aging processes and age-related diseases.
4. Increased risk of chronic diseases: Poor mitochondrial function is linked to the development of chronic diseases such as diabetes, cardiovascular disease, neurodegenerative disorders, and cancer.
5. Compromised immune function: Mitochondrial dysfunction can impair immune cell function, making the body more susceptible to infections and inflammatory conditions.
6. Neurological symptoms: The brain is particularly vulnerable to mitochondrial dysfunction, leading to cognitive impairment, memory deficits, and neurological disorders.

Overall, consuming foods that cause mitochondrial damage can have far-reaching consequences for health and well-being, affecting energy levels, organ function, disease risk, and overall quality of life. It's essential to prioritize a diet rich in nutrient-dense foods that support mitochondrial health to maintain optimal health and vitality.

  When considering nutrient density, red meat typically ranks among the highest due to its rich array of essential nutrients. Following red meat, other animal proteins are generally more nutrient-dense compared to non-animal protein sources. Here's how different food types stack up in terms of nutrient density:

1. Red Meat: Red meat, such as beef, lamb, and pork, is renowned for its high nutrient density. It provides significant amounts of essential nutrients like iron, zinc, vitamin B12, and protein, making it a valuable component of the diet.
2. Poultry: Poultry, including chicken and turkey, offers a good source of protein and essential nutrients, although it may be slightly lower in certain nutrients compared to red meat. Nonetheless, it remains a nutrient-dense choice, particularly when consumed with the skin, which contains healthy fats.
3. Fish and Seafood: Fish and seafood are excellent sources of high-quality protein, omega-3 fatty acids, and various vitamins and minerals. Fatty fish like salmon, mackerel, and sardines are especially prized for their omega-3 content, which supports heart and brain health.
4. Eggs: Eggs are nutrient powerhouses, providing an array of vitamins, minerals, and antioxidants. They are particularly rich in choline, lutein, and zeaxanthin, which are beneficial for brain function and eye health.
5. Dairy: Dairy products like milk, yogurt, and cheese are valuable sources of calcium, protein, vitamin D, and other essential nutrients. However, their nutrient density may vary depending on factors such as processing and fat content.
6. Legumes: Legumes, including beans, lentils, and chickpeas, are plant-based protein sources that offer fiber, vitamins, and minerals. While they provide valuable nutrients, their overall nutrient density may be lower compared to animal proteins.
7. Grains and Starches: Grains and starches like rice, bread, pasta, and potatoes are staple foods that provide energy in the form of carbohydrates. While they can contribute essential nutrients like fiber and certain vitamins and minerals, they are generally less nutrient-dense compared to animal proteins.

By prioritizing foods based on their nutrient density, individuals can optimize their dietary intake to support overall health and well-being. Including a variety of nutrient-rich foods, with a focus on high-quality animal proteins and other whole foods, can help meet nutritional needs and promote optimal health.

Objective: The prevalence of childhood and adult obesity in Malta is among the highest in the world. Although increasingly recognised as a public health problem with substantial future economic implications for the national health and social care systems, understanding the context underlying the burden of obesity is necessary for the development of appropriate counter-strategies. 

Design: We conducted a contextual analysis to explore factors that may have potentially contributed to the establishment of an obesogenic environment in Malta. A search of the literature published between 1990 and 2013 was conducted in MEDLINE and EMBASE. Twenty-two full-text articles were retrieved. Additional publications were identified following recommendations by Maltese public health experts; a review of relevant websites; and thorough hand searching of back issues of the Malta Medical Journal since 1990. 

Setting: Malta. 

Subjects: Whole population, with a focus on children. 

Results: Results are organised and presented using the ANalysis Grid for Elements Linked to Obesity (ANGELO) framework. Physical, economic, policy and socio-cultural dimensions of the Maltese obesogenic environment are explored. 

Conclusions: Malta's obesity rates may be the result of an obesogenic environment characterised by limited infrastructure for active living combined with an energy-dense food supply. Further research is required to identify and quantify the strength of interactions between these potential environmental drivers of obesity in order to enable appropriate countermeasures to be developed. 

Scientific References  from The Nutrition Network  Systematic Reviews. Meta Analysis and other Reviews 

1. Muscogiuri  G, El Ghoch M, Colao A, et al. European Guidelines for Obesity  Management in Adults with a Very Low-Calorie Ketogenic Diet: A  Systematic Review and Meta-Analysis. OFA. Published online April 21, 2021:1-24. doi:10.1159/000515381
2. Darand, M. et al. (2023) ‘Comparison of the Effect of a Low-Carbohydrate Diet with a  Low-Fat Diet on Anthropometric Indices and Body Fat Percentage: A  Systematic Review and Meta-Analysis of Randomized Controlled Trials’, Journal of Nutrition and Food Security, 8(3), pp. 493–520. Available at: https://doi.org/10.18502/jnfs.v8i3.13297.
3. Willems  AEM, Sura–de Jong M, van Beek AP, Nederhof E, van Dijk G. Effects of  macronutrient intake in obesity: a meta-analysis of low-carbohydrate and  low-fat diets on markers of the metabolic syndrome. Nutr Rev. doi:10.1093/nutrit/nuaa044
4. Lei, L. et al. (2022) ‘Effects of low-carbohydrate diets versus low-fat diets on  metabolic risk factors in overweight and obese adults: A meta-analysis  of randomized controlled trials’, Frontiers in Nutrition, 9, p. 935234. Available at: https://doi.org/10.3389/fnut.2022.935234.
5. Sievert  K, Hussain SM, Page MJ, et al. Effect of breakfast on weight and energy  intake: systematic review and meta-analysis of randomised controlled  trials. BMJ. 2019;364:l42. doi:10.1136/bmj.l42
6. Choi  YJ, Jeon S-M, Shin S. Impact of a Ketogenic Diet on Metabolic  Parameters in Patients with Obesity or Overweight and with or without  Type 2 Diabetes: A Meta-Analysis of Randomized Controlled Trials.  Nutrients. 2020;12(7):2005. doi:10.3390/nu12072005
7. Mansoor  N, Vinknes KJ, Veierød MB, Retterstøl K. Effects of low-carbohydrate  diets v. low-fat diets on body weight and cardiovascular risk factors: a  meta-analysis of randomised controlled trials. Br J Nutr.  2016;115(3):466-479. doi:10.1017/S0007114515004699
8. Sackner-Bernstein  J, Kanter D, Kaul S. Dietary Intervention for Overweight and Obese  Adults: Comparison of Low-Carbohydrate and Low-Fat Diets. A  Meta-Analysis. PLoS ONE. 2015;10(10):e0139817. doi:10.1371/journal.pone.0139817
9. Bueno  NB, de Melo ISV, de Oliveira SL, da Rocha Ataide T.  Very-low-carbohydrate ketogenic diet v. low-fat diet for long-term  weight loss: a meta-analysis of randomised controlled trials. Br J Nutr.  2013;110(7):1178-1187. doi:10.1017/S0007114513000548
10. Ludwig  DS, Dickinson SL, Henschel B, Ebbeling CB, Allison DB. Do  Lower-Carbohydrate Diets Increase Total Energy Expenditure? An Updated  and Reanalyzed Meta-Analysis of 29 Controlled-Feeding Studies. J Nutr. doi:10.1093/jn/nxaa350
11. Amini  MR, Aminianfar A, Naghshi S, Larijani B, Esmaillzadeh A. The effect of  ketogenic diet on body composition and anthropometric measures: A  systematic review and meta-analysis of randomized controlled trials. Crit Rev Food Sci Nutr. Published online January 14, 2021:1-14. doi:10.1080/10408398.2020.1867957
12. Lee  HS, Lee J. Effects of Combined Exercise and Low Carbohydrate Ketogenic  Diet Interventions on Waist Circumference and Triglycerides in  Overweight and Obese Individuals: A Systematic Review and Meta-Analysis.  International Journal of Environmental Research and Public Health. 2021;18(2):828. doi:10.3390/ijerph18020828
13. Nicholas  AP, Soto-Mota A, Lambert H, Collins AL. Restricting carbohydrates and  calories in the treatment of type 2 diabetes: a systematic review of the  effectiveness of ‘low-carbohydrate’ interventions with differing energy  levels. Journal of Nutritional Science. 2021;10. doi:10.1017/jns.2021.67
14. Castellana  M, Conte E, Cignarelli A, et al. Efficacy and safety of very low  calorie ketogenic diet (VLCKD) in patients with overweight and obesity: A  systematic review and meta-analysis. Rev Endocr Metab Disord. November  2019. doi:10.1007/s11154-019-09514-y ABSTRACT
15. Pavlidou, E. et al. (2023) ‘Clinical Evidence of Low-Carbohydrate Diets against Obesity and Diabetes Mellitus’, Metabolites, 13(2), p. 240. Available at: https://doi.org/10.3390/metabo13020240.
16. Ludwig DS, Aronne LJ, Astrup A, et al. The carbohydrate-insulin model: a physiological perspective on the obesity pandemic. The American Journal of Clinical Nutrition. 2021;(nqab270). doi:10.1093/ajcn/nqab270

Inflammation and hyperinsulinemia play significant roles in creating complications following transplant surgery, impacting both the short-term and long-term outcomes for transplant recipients.

1. Short-term complications:
   
   • Rejection: Inflammation is a key component of the immune response, and in transplant surgery, the body may recognize the transplanted organ as foreign, triggering an immune response leading to rejection. Inflammatory processes contribute to tissue damage and organ dysfunction.
   • Infection: Surgical trauma and immunosuppressive medications used to prevent rejection can weaken the immune system, making transplant recipients more susceptible to infections. Inflammation can exacerbate infection severity and impede the body's ability to fight off pathogens.

1. Long-term complications:
   
   • Chronic rejection: Persistent inflammation can lead to chronic rejection, where the immune system gradually damages the transplanted organ over time. Chronic inflammation promotes fibrosis and vascular changes, impairing organ function.
   • Metabolic disorders: Hyperinsulinemia, often associated with insulin resistance, can develop due to immunosuppressive medications and metabolic changes post-transplant. This can lead to diabetes mellitus, dyslipidemia, and cardiovascular complications, increasing the risk of long-term morbidity and mortality.
   • Cardiovascular complications: Chronic inflammation and hyperinsulinemia contribute to endothelial dysfunction and atherosclerosis, increasing the risk of cardiovascular events such as heart attacks and strokes in transplant recipients.

Managing inflammation and hyperinsulinemia post-transplant is crucial for preventing complications. Strategies include optimizing immunosuppressive regimens to minimize inflammation, promoting healthy lifestyle habits to manage insulin sensitivity, and closely monitoring for early signs of rejection and metabolic disorders. Additionally, research into novel immunosuppressive agents and therapeutic approaches targeting inflammation and insulin resistance may improve transplant outcomes in the future.

 Abstract 

Background: Metabolic syndrome (MetS) is characterised by the presence of at least three of the five following components: insulin resistance, obesity, chronic hypertension, elevated serum triglycerides, and decreased high-density lipoprotein cholesterol concentrations. It is estimated to affect 1 in 3 people around the globe and is reported to affect 46% of surgical patients. For people with MetS who undergo surgery, an emerging body of literature points to significantly poorer postoperative outcomes compared with nonaffected populations. The aim of this study is to review the current evidence on the risks of surgical complications in patients with MetS compared to those without MetS. 

Methods: Systematic review and meta-analysis using PRISMA and AMSTAR reporting guidelines. 

Results: The meta-analysis included 63 studies involving 1 919 347 patients with MetS and 11 248 114 patients without MetS. Compared to individuals without the condition, individuals with MetS were at an increased risk of mortality (OR 1.75 95% CI: 1.36-2.24; P <0.01); all surgical site infection types as well as dehiscence (OR 1.64 95% CI: 1.52-1.77; P <0.01); cardiovascular complications (OR 1.56 95% CI: 1.41-1.73; P <0.01) including myocardial infarction, stroke, cardiac arrest, cardiac arrythmias and deep vein thrombosis; increased length of hospital stay (MD 0.65 95% CI: 0.39-0.9; P <0.01); and hospital readmission (OR 1.55 95% CI: 1.41-1.71; P <0.01). 

Conclusion: MetS is associated with a significantly increased risk of surgical complications including mortality, surgical site infection, cardiovascular complications, increased length of stay, and hospital readmission. Despite these risks and the high prevalence of MetS in surgical populations there is a lack of evidence on interventions for reducing surgical complications in patients with MetS. The authors suggest prioritising interventions across the surgical continuum that include (1) preoperative screening for MetS; (2) surgical prehabilitation; (3) intraoperative monitoring and management; and (4) postoperative rehabilitation and follow-up. 

Our review is the largest, most-comprehensive analysis of postoperative  surgical complications in MetS. Our findings highlight that surgical  patients with MetS are at a heightened risk of a range of adverse  outcomes in the 30 days following surgery. Based on our findings,  firstly, there is a need to implement evidence-based screening  approaches to identify MetS in surgical patients to facilitate early  detection and initiate management strategies prior to, during, and after  surgery for improved outcomes. Secondly, the surgical team must be  aware of the increased risks associated with MetS, be alerted to a  diagnosis preoperatively, communicate risks to the patient during the  consent process, and treat components of the condition to avoid the  risks of adverse events. In conclusion, early detection, personalised  management, and comprehensive perioperative care for MetS patients are  essential to mitigate risks, enhance outcomes, and potentially reduce  healthcare costs by minimising complications and readmissions. 

" Fasting insulin and c-reactive protein confound the association between  mortality and body mass index. An increase in fat mass may mediate the  associations between hyperinsulinemia, hyperinflammation, and mortality.  The objective of this study was to describe the "average" associations  between body mass index and the risk of mortality and to explore how  adjusting for fasting insulin and markers of inflammation might modify  the association of BMI with mortality.  "   The role of obesity as a driver of excess mortality should be critically  re-examined, in parallel with increased efforts to determine the harms  of hyperinsulinemia and chronic inflammation.      

https://www.emed.com.au/a-heated-concern-vegetable-oil-is-toxic/

 "Professor Grootveld’s team found sunflower oil and corn oil produced  aldehydes at levels 20 times higher than recommended by the World Health  Organisation. Olive oil and rapeseed oil produced far fewer aldehydes  as did butter and goose fat."

 “Sunflower and corn oil are fine as long as you don't subject them to  heat, such as frying or cooking. It's a simple chemical fact that  something which is thought to be healthy for us is converted into  something that is very unhealthy at standard frying temperatures " Professor Grootveld