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Different nutrients are absorbed at different checkpoints. 

1). Mouth & Stomach

Carbs begin breaking down with salivary amylase.

Proteins start with stomach acid + pepsin.

Vitamin B12 binds to intrinsic factor here.

Example: Without stomach acid, B12 can’t be absorbed properly.

2). Liver & Gallbladder

Bile salts emulsify fats, making them easier for enzymes to digest.

Example: Bile acts like dish soap, breaking fats into smaller droplets.

3).Pancreas

Sends enzymes into the small intestine: amylases for carbs, proteases for protein, lipases for fat.

Example: These enzymes finish the job of turning food into absorbable units.

4).Duodenum (first section of small intestine)

Carbs → disaccharides.

Proteins → amino acids.

Fats → monoglycerides + fatty acids.

Example: This is where most chemical digestion happens.

5).Jejunum (middle small intestine)

Main absorption zone: sugars, amino acids, iron, calcium, folate, and fat-soluble vitamins (A, D, E, K).

Example: Low stomach acid or no bile means nutrients here get poorly absorbed.

6).Ileum (end of small intestine)

Vitamin B12 + intrinsic factor absorbed.

Bile salts recycled back to the liver.

Example: People with Crohn’s disease affecting the ileum often end up B12 deficient.

7).Colon (large intestine)

Absorbs water, sodium, potassium, and leftover bile salts.

Example: This is why diarrhea causes dehydration. Water absorption fails here.

Each nutrient has its own “checkpoint” along the gut. 

Carbs, proteins, and fats mostly absorb in the jejunum, B12 in the ileum, and water + electrolytes in the colon. 

Smooth digestion depends on stomach acid, bile, enzymes, and every section of the gut working in sync.

Anti-Cancer Foods

Too much 

red and 

processed meat, 

alcohol, 

refined carbs, 

fried foods, and 

sugar 

can increase cancer risk.

Likewise, 

a sedentary lifestyle and 

not eating enough 

phytochemical-rich foods 

can contribute to cancer development. 

While no food directly fights cancer, some provide nutrients that help the body prevent it. These “anti-cancer foods” are mostly plants rich in phytochemicals, compounds that help reduce the risk of chronic diseases, including cancer.

Phytochemicals, also called phytonutrients, are found in fruits and vegetables and are recommended by health experts to be eaten regularly. 

There are over 4,000 phytochemicals, 

each with unique benefits, so the best approach is to “eat the rainbow”—consume a variety of colorful produce to cover a broad spectrum of protective compounds.

Cruciferous vegetables like 

broccoli, 

kale, 

cabbage, and 

Brussels sprouts 

contain carotenoids, vitamins, minerals, and sulfur-containing compounds (glucosinolates, indoles, isothiocyanates). 

These compounds have been linked to a lower risk of lung, colorectal, prostate, and breast cancers. 

Their unique chemistry helps protect cells from damage and supports overall health.

Turmeric, a bright orange spice, contains curcumin, which reduces inflammation—a key factor in cancer and other chronic diseases. Curcumin may also enhance chemotherapy effectiveness and protect healthy cells during radiation therapy, making turmeric a valuable addition to a cancer-preventive diet.

Mushrooms, rich in antioxidants like L-ergothioneine, help reduce oxidative stress and inflammation. Studies have shown that eating mushrooms can 

lower prostate and 

breast cancer risks. 

Medicinal mushrooms 

like reishi and turkey tail 

boost immune responses and contain unique compounds that support cancer therapies.

Allium vegetables, including 

garlic, 

onions, 

leeks, and 

shallots, 

have been linked to reduced risks of gut cancers such as colorectal cancer. 

Observational studies show that higher intake of these vegetables may significantly lower cancer incidence, highlighting the importance of including them regularly in your diet.

Cancer-Fighting Foods 

Foods that fight cancer include fruits, 

vegetables, 

legumes, 

whole grains, 

fish and 

fermented foods. 

Found abundantly in the Mediterranean diet, 

these foods contain several protective compounds that work together to lower cancer risk. 

Some help regulate hormones, such as estrogen. 

Others slow cancer cell growth or block inflammation. 

Many lower the risk of damage to healthy cells caused by antioxidants, but most people remain unaware of these benefits.      

Although no single food can stop cancer, consistently including a variety of cancer-fighting foods as part of a healthy diet is key to reducing risk. 

Choose these foods in their whole form, as whole foods contain more nutrients than processed. 

Think fresh strawberries instead of strawberry jelly.

Cancer-fighting foods includes foods that comprise the popular Mediterranean diet, long known to improve health outcomes as a whole food, plant-forward healthy eating pattern. 

Because the Mediterranean diet is flexible, you can tailor it to your needs and get various nutrients that work together to help your body. 

And remember, it’s all about eating a variety because the combination of these foods are more powerful than any one food alone. 

Berries are among the healthiest foods you can eat. Their vitamins, fiber and antioxidants, such as anthocyanins, ellagic acid and resveratrol, can ward off cancer in our digestive tract. The magic likely resides in their blue, purple and red pigments. Delicious alone or as a snack or dessert. Try them on top of cottage cheese on toast.   

Cruciferous Vegetables
These foods include broccoli, cauliflower, bok choy, cabbage and Brussels sprouts. The name comes from the Latin “cruciferae,” meaning “cross-bearing” because the four petals on the leaves resemble a cross. While diverse in color and shape, they share several nutritional benefits and are the only foods containing the cancer-fighting compound indole-3-carbinol. Frequently eating these foods is associated with a lower risk of many cancers. For a melt-in-your-mouth side, roast and toss with olive oil or small amounts of dried fruit or 100% maple syrup.

Fish contains high levels of nutrients and protein, particularly oily fish, such as salmon, tuna and anchovies. One of the highest food sources of omega-3 fatty acids, fish combats inflammation and protects against breast and colorectal cancer. Need help with how to cook it? Marinate or season to add flavor and bake, broil, steam or sear on the stovetop. Eat hot or add avocado and greens for a cold salad.     

Nuts
According to the American Institute for Cancer Research, all nuts, especially walnuts, have cancer-fighting properties. A great source of fiber and healthy fats, nuts can be eaten as a snack, sprinkled on cereal or added to a salad. Try toasting to bring out even more flavor in the nut.

Legumes
The American Cancer Society recommends legumes and beans as one of the most important food groups for prevention. Rich in vitamins, minerals, protein and fiber, they are among the most inexpensive cancer-fighting foods. Plant chemicals known as flavonoids in the outer bean layer are strong antioxidants. Cheap, healthy, versatile and delicious, legumes are a food staple worldwide, available dry and canned. Enjoy as dips and spreads (hummus), with whole grains (brown rice) or used to bulk up soups, stews and salads.

Dark chocolate 
Eating dark chocolate with high cocoa content can deliver fiber, antioxidants and minerals that may lower the risk of certain cancers. Chocolate comes from the cacao tree’s plant seed, the cocoa bean, and is a good source of polyphenols and flavanols, which are rocket fuel for healthy gut bacteria. Of course, dark chocolate is still candy and is best consumed in moderation. Have a square or two after dinner and try to savor the complexity of flavors it provides.  

Whole grains
Whole grains such as rolled oats, brown rice and 100% whole wheat bread contain protective antioxidants as Vitamin E, lignans, phytic acid and fiber. Eating whole grains reduces the risk of at least 18 types of cancer, and each 10-gram increase in dietary fiber from this food group is linked with a 7% reduction in colorectal cancer risk. As fiber is only found in plant foods, choose breads and cereals containing at least 3 grams per serving.

Leafy greens
Carotenoids found in leafy vegetables such as spinach and kale act as antioxidants to boost the body’s own defenses to fight breast, bladder and lung cancer. Most Americans shy away from dark, leafy greens because they are bitter. To balance the bitterness, massage your greens to break up the fibers. Wonderful for salads, kale won’t wilt for days, making it great for packing ahead. You can also sauté your greens, add them to soups and casseroles or puree into a pesto for pasta.

Fermented foods
Cultured or fermented foods provide probiotics, healthy bacteria that improve immune function and protect against cancer. These good bacteria can bind and destroy potential carcinogens, which may be especially effective in preventing colorectal cancer. Don’t like yogurt? Try something new, such as kefir, kombucha, kimchi or tempeh.  

Garlic 
Classified as a vegetable, cultures have long used garlic both for cooking and medicine. A root vegetable, garlic contains allicin, a protective sulfur compound that inhibits cancer progression. Eating garlic frequently lowers the risk of colorectal cancer but is also being studied for its role in reducing other cancers. When cooking with garlic, wait 15 minutes after you crush or chop garlic before heating to release the active ingredients. Use as a flavoring to any savory dish.

 it’s really common to have heart, kidney, and metabolic risk factors at the same time (AHA)

‘It is reassuring that once the CKM connection was explained, nearly three-quarters of those surveyed recognized its importance.’ 

Almost 90 percent of adults are plagued by a deadly heart condition without realizing it, 

new research has revealed

CKM syndrome highlights the way in which dysfunction in one system – the heart, kidneys, or metabolic system – can negatively affect the others. 

Together, these conditions greatly increase the risk of serious health outcomes such as heart attack, stroke, and heart failure.

According to the AHA, nearly 90 percent of US adults have at least one risk factor for 

CKM syndrome, including 

high blood pressure, 

abnormal cholesterol, 

high blood glucose (sugar), 

excess weight and 

reduced kidney function.

Unlike some chronic conditions, CKM syndrome is often reversible, especially when caught early. 

To categorize people’s risk of CKM, the AHA has come up with four stages. 

Stage zero is the optimum place to be. It represents people with no risk factors, who likely eat a balanced diet, are a healthy weight, and do not smoke.

Stage one is people who might be overweight, especially with excess belly fat. Or, they may have pre-diabetes.

It is advised that these people try to lose five percent of their weight to protect themselves from progressing into a further CKM stage.

People in stage two will be starting to experience things like high blood pressure and type 2 diabetes. 

They may also have kidney disease.

Doctors may prescribe this cohort medication to control their blood pressure, blood sugar and cholesterol.

They may also offer patients Ozempic or Wegovy, to help them lose weight and control blood sugar levels.

Stage three is when people have asymptomatic heart disease. 

They may have high blood pressure or early heart or kidney disease and may be on medication such as a statin.

Treatments for this category include heart and diabetes drugs, plus testing for narrowed arteries.

Stage four is symptomatic heart disease. 

This would be someone with diagnosed heart disease, excess fat, Type 2 diabetes or kidney disease. 

They may have already suffered heart attacks or strokes and developed heart failure.

1.Eat better

by choosing healthy whole foods.

2.Manage weight with healthy eating and regular activity.

3.Control cholesterol by choosing healthy fats.

4.Manage blood pressure

by lowering salt intake, getting good sleep, maintaining a healthy weight and staying active.

5.Be more active with regular physical activity you enjoy.

6.Get healthy sleep by aiming for 7-9 hours of sleep each night.

7.Manage blood sugar

by eating healthy, exercising and keeping a healthy weight.

8.Quit tobacco

by stopping use of inhaled nicotine delivery products which include traditional cigarettes, e-cigarettes, and vaping.

People in stage four can be further divided into those with kidney failure and those without it.

The AHA stresses the importance of lifestyle changes, including 

healthy eating, 

regular physical activity, and medical treatment when needed. 

The new survey revealed widespread misconceptions about how these systems interact. 

More than two-thirds (68 percent) of US adults incorrectly believe that it’s best to manage conditions like heart disease, kidney disease, or diabetes one at a time – or they weren’t sure. 

Additionally, 42 percent either believed a healthy heart could not be damaged by dysfunction in other organs or were unsure.

‘The heart, kidney, and metabolic systems are connected and, as such, should be treated in a coordinated way,’ said Dr Sanchez. 

‘These results highlight the need to better communicate that connection and the importance of collaborative care.’ 

To improve understanding and care, the AHA will publish the first-ever clinical guidelines on CKM syndrome in early 2026. 

These guidelines aim to help healthcare providers treat patients with multiple related conditions through a more integrated and patient-centered approach.

In the meantime, the AHA has launched the CKM Health Initiative, offering educational resources and tools for both the public and healthcare professionals. 

These include a new explainer video that breaks down how the body’s systems interact.

‘CKM health is about your overall health,’ said Dr. Sanchez. 

‘You can take care of your body 

with regular checks of your 

blood pressure, 

cholesterol, 

weight, 

blood sugar, and 

kidney function.’ 

The survey was conducted online by The Harris Poll on behalf of the AHA. Approximately 4,000 US adults participated

A metabolic diet 

is a broad term for eating patterns that focus on boosting metabolism through nutrient-dense, whole foods. 

Key components often include 

lean proteins, 

whole grains, 

plenty of fruits and 

vegetables, and 

healthy fats. 

Many versions of 

“metabolic” diets emphasize 

eating balanced meals regularly 

may restrict 

🚫🍔processed foods, 

🚫🍬refined sugars, and 

🚫🧇sometimes certain CARBS

Key principles 

Prioritize whole foods: 

Focus on unprocessed foods like 

lean meats, 

fish, 

eggs, and 

legumes.

Include plenty of plants: 

Eat a variety of fruits, 

vegetables (especially leafy greens and 

non-starchy vegetables), 

whole grains 

-oats and 

-brown rice

Choose healthy fats: 

Incorporate healthy fats from sources like 

nuts, 

seeds, and 

olive oil. 

Eat balanced meals: 

Combine 

lean protein, 

complex carbohydrates, and 

healthy fats 

   to create a balanced plate. 

Avoid or limit refined foods: 

Cut back on 

🚫🍔processed items, 

🚫🍭refined sugars, and 

🚫🔲white flours. 

Stay hydrated:

🚰 Drink plenty of water to support metabolic processes. 

Eat regularly: 

♻️➰To maintain a steady energy source, some metabolic diets suggest eating smallermeals throughout the day. 

Foods to emphasize 

✅Lean proteins: 

🍗Chicken, 

🐟fish, 

🍳eggs, 

🫘beans, 

🟠lentils. 

✅Whole grains: 

🍘Brown rice, 

🔶oats, 

🌾barley. 

✅Non-starchy vegetables: 

🥦Broccoli, 

🥬spinach, 

🫑peppers. 

✅Fruits: 

🍓🫐Berries, 

🍏🍎apples, 

🍊oranges. 

✅Healthy fats: 

🥑Avocados, 

🌰nuts, 

▪️seeds,

🫒🛢️olive oil. 

✅Metabolism-boosting foods: 

Some studies suggest that foods like 🌶️chili peppers, 

☕️coffee, and 

🍵green tea 

   may slightly increase metabolic rate. 

Important considerations 

No one-size-fits-all approach: The best diet is versatile and tailored to your individual needs, preferences, and health goals. 

Consult a professional: 

Before making major changes, it is best to consult a healthcare provider or registered dietitian to create a personalized plan

Focus on more than just diet: Factors like 

regular physical activity, 

adequate sleep, and 

hydration are also crucial for 

a healthy metabolism. 

is primarily caused by vagus nerve damage, which most commonly stems from poorly controlled diabetes. Other causes include autoimmune diseases (like scleroderma), certain viral infections, some types of stomach surgery, and certain medications (such as opioids and some weight-loss drugs). In some cases, the cause remains unknown, a condition known as idiopathic gastroparesis. 

Common Causes & Risk Factors

• Diabetes: High blood sugar levels can damage the vagus nerve, which controls stomach muscles. 
• Surgery: Procedures on the stomach or esophagus can sometimes damage the vagus nerve. 
• Infections: Some viral infections, including those from viruses like Epstein-Barr, Cytomegalovirus, and even COVID-19, can trigger the condition. 
• Medications: Certain drugs, such as opioid pain medicines, anticholinergic drugs, and newer weight loss medications, can slow stomach emptying. 
• Autoimmune Conditions: Diseases like scleroderma and lupus can attack the nerves and muscles of the stomach. 
• Hypothyroidism: An underactive thyroid gland can lead to a generalized slowing of bodily processes, including stomach motility, causing delayed emptying. 

Idiopathic Gastroparesis 

• In many instances, the precise cause of gastroparesis is not identified. This is known as idiopathic gastroparesis. 

Mechanism of Gastroparesis

• Gastroparesis occurs when the vagus nerve is damaged or does not function correctly, preventing it from sending the proper signals to the stomach muscles. 
• This damage results in stomach muscles contracting poorly, which leads to delayed emptying of food from the stomach into the small intestine. 

Obesity is a chronic disease, not just a matter of effort. It’s important to understand the influences of genetics, physiology, environment, job, education and what’s going on in the brain. 

What is obesity?

More than just weight gain

Obesity is a chronic disease caused by genetic, metabolic, behavioural, psychological and environmental factors. These factors together with the pleasure we derive from food can all influence energy balance, which in turn can lead to weight gainOnce established, powerful neuro-hormonal factors effectively defend the body against weight loss, thereby often making obesity a lifelong problem, where weight regain (or relapse) is the rule, rather than the exception.

Underdiagnosed and undertreated

Obesity affects 650 million adults worldwide – that’s approximately 13% of the world’s population. It is recognised by healthcare professionals, organisations and people across the world as a chronic disease which requires long-term management. The Awareness, Care and Treatment in Obesity Management – an International Observation (ACTION IO) Study* found that 68% of people with obesity and 88% of healthcare professionals believe that obesity is a chronic disease. Although both people with obesity and healthcare professionals recognise obesity as a chronic disease, it remains underdiagnosed and undertreated.

*The Awareness, Care and Treatment In Obesity Management – an International Observation (ACTION IO) Study is the first international study to investigate barriers to obesity management among people with obesity and healthcare professionals in 11 countries worldwide (Australia, Chile, Israel, Italy, Japan, Mexico, Saudi Arabia, South Korea, Spain, UAE, UK). A total of 14,502 people with obesity and 2,785 healthcare professionals completed the survey.

What factors influence obesity as a disease?

Perhaps one of the reasons obesity continues to be poorly understood, underdiagnosed and undertreated, is that its causes are multifactorial. These causes can be physiological, psychological, genetic, environmental or socioeconomic. Many of these factors are outside of an individual’s control.

Environmental

Many aspects of our environment can contribute to the development of obesity, including exposure to oversized food portions, lack of physical activity due to high amounts of screen usage and easy access to unhealthy food.

Genetic

Some people are genetically predisposed to developing obesity, depending on their family history.

Physiological

Energy balance is a complex mechanism centrally regulated by the brain, with input from peripheral hormonal signals released from the gastrointestinal tract, pancreas and adipose tissue, which are integrated to regulate appetite and energy expenditure.

Psychological

Stress,15 boredom15 and psychological disorders are linked to overeating and can constribute to the development of obesity. 

Socio-economic

Where a person lives, the society in which they live and their income can also influence their chances of developing obesity. 

All about the science to obesity

Understanding the complexities of obesity goes beyond simplistic views of food availability and willpower, involving an intricate network of energy balance, metabolic adaptations, neurobiology, and hormonal influences.

Why is maintaining weight loss challenging?

A review of 14 long-term studies showed that one to two thirds of people with obesity regained more weight after weight loss achieved by dieting. Furthermore, the ACTION IO study found that  81% of people with obesity have engaged in one or more serious weight loss attempts; however, only 11% were able to maintain a 5% weight loss for one year or more.

Visual adapted from Mann T, Tomiyama AJ, Westling E, Lew AM, Samuels B, Chatman J. Medicare’s search for effective obesity treatments: diets are not the answer.  Am Psychol. 2007;622(3):220–233. 

Maintaining weight loss is challenging for people living with obesity, and findings such as from the ACTION IO study* show that obesity isn’t about willpower.

To understand what the effective strategies for obesity management are, we need to consider, physiological, psychological and biological factors of obesity. Although diet modification and exercise continue to be key in the management of obesity, increasingly patients require pharmacological adjuncts in order achieve or maintain weight loss.

It is also crucial to understand the multiple systems involved in the pathophysiology of obesity and interventions to tackle these could be essential in providing lasting weight loss.

*The Awareness, Care and Treatment in Obesity Management – an International Observation (ACTION IO) Study is the first international study to investigate barriers to obesity management among people with obesity and healthcare professionals in 11 countries worldwide (Australia, Chile, Israel, Italy, Japan, Mexico, Saudi Arabia, South Korea, Spain, UAE, UK). A total of 14,502 people with obesity and 2,785 healthcare professionals completed the survey.

is a gene which has a much higher positive prevalence in certain auto-immune/autoinflammatory diseases such as Spondyloarthritis, Uveitis/Iritis, Crohns Disease, Ulcerative Colitis and Psoriasis. Positive HLA-B27 affects people in multiple ways, when it comes to Spondyloarthritis in related to musculoskeletal (MSK). Approximately 90% (male) and 85% (female) positivity in AxSpA Approximately 40-50% positivity in Psoriatic Arthritis (PsA).

The prevalence of HLA-B27 positivity in the general population is around 8-12% although its frequency is lower in African American, South American and Middle Eastern populations than in others.HLA-B27 is the most important genetic factor for development risk of Axial spondyloarthritis (AxSpA) but there are other implicated genetic markers, all of which do vary for different populations.

Under-representation of the groups with lower HLA-B27 positivity in research and epidemiology is an issue and inclusion of these groups could provide information on other subsets. Don’t over rely on HLA-B27 in clinical practice, the interplay of the complicating factors of axial vs peripheral, population variations and HLA-B27 negative Spondyloarthritis means that interpretation is best left to Rheumatologists.

A Key Driver in Obesity-Related HFpEF

The link between obesity & HFpEF is critical. 

Epicardial adipose tissue (EAT) 

is not just storage— it’s an active organ promoting myocardial dysfunction.

EAT drives: 

➡️Fibrosis 

➡️Inflammation 

➡️Oxidative stress 

➡️Diastolic dysfunction

Understanding EAT’s  is crucial for developing new personalized therapies. 

Heart failure with preserved ejection fraction (HFpEF) 

is a growing global health problem characterized by high morbidity and mortality, with limited effective therapies available. 

Obesity significantly influences haemodynamic and structural changes in the myocardium and vasculature, primarily through the accumulation and action of visceral adipose tissue. 

Particularly, epicardial adipose tissue (EAT) contributes to HFpEF through inflammationand lipotoxic infiltration of the myocardium. 

However, the precise signalling pathways leading to diastolic stiffness in HFpEF require further elucidation. 

This review explores the dynamic role of EAT in health and disease. 

Drawing upon insights from studies in other conditions, we discuss potential 

EAT-mediated inflammatory pathways in HFpEF and 

how they may contribute to functional and structural myocardial and endothelial derangements, including 

•intramyocardial lipid infiltration, •fibrosis, 

•endothelial dysfunction, •cardiomyocyte stiffening, and 

•left ventricular hypertrophy. 

Lastly, we propose potential targets for novel therapeutic avenues.

EAT as a therapeutic target in HFpEF

The phenotypic diversity of HFpEF and the interplay with different comorbiditieswarrant a tailored treatment approach. 

In the context of the obesity-related HFpEF phenotype, targeting the pathological transformation and underlying inflammatory pathways mediated by EAT may present new therapeutic avenues. 

We therefore present therapeutic options that pose a clinical benefit that arise from changes to EAT or EAT-mediated pathways.

1) Sodium-glucose cotransporter-2 inhibitors(SGLT2i), like dapagliflozin and empagliflozin, are the first type of pharmacological drugs to reduce the risk of heart failure–related hospitalization in HFpEF trials.

Given the low expression of SGLT2 in cardiomyocytes, it is likely that SGLT2i mediate their positive effects in HFpEF by off-target mechanisms in the myocardium.

At least in part, these effects might be mediated by EAT. 

Upon SGLT2i administration, EAT volume decreases and glucose uptake by EAT is enhanced, suggesting that these types of drugs might improve EAT’s secretome and may improve metabolic regulation associated with insulin resistance in obesity.

Furthermore, SGLT2i-treated patients show a reduction of ECM and cardiomyocyte volume, along with a decrease in inflammatory biomarkers, such as FABP4, IL-1, IL-6, and TGF-β, indicating a role in improving myocardial inflammation and fibrosis.

Additionally, SGLT2i show a mild, sustained diuretic effect that can improve volume overload and congestion seen in HFpEF, while reducing the need for diuretics use.

2)Glucagon-like peptide 1 agonists (GLP-1a), such as semaglutide and liraglutide, are a class of anti-diabetic drugs known for their glucose-lowering effects and insulin sensitization, which show a rapid and significant reduction of EAT thickness independent of body weight loss.

Clinical trials in patients with HFpEF show symptom reduction and exercise capacity improvement after GLP-1a administration, across the entire obesity spectrum.

It is suggested that part of the effect of GLP-1a might be mediated by EAT, given that this fat depot expresses specific GLP-1 receptors.

While GLP-1a primarily enhances insulin sensitivity, in EAT, it induces adipocyte browning through activation of the AMPK pathway and reduces local adipogenesis by improving FFA oxidation.

However, a reduction in EAT is likely accompanied by simultaneous reductions in other fat depots. GLP-1a reduces both VAT and SAT in equal proportions, and these reductions correspond with overall weight loss.

However, due to the presence of specific GLP-1 receptors on EAT, these agonists may directly remodel EAT into a more cardioprotective fat depot, and therefore have a direct effect mediated by EAT, independent of overall weight loss.

3)Bariatric surgery causes drastic and often lasting weight loss, triggering favourable metabolic changes in obese patients.

Significant weight loss is typically accompanied by a reduction of abdominal and visceral fat depots, including EAT.

Although robust and longitudinal data in patients with HFpEF is lacking, significant weight loss may improve haemodynamics, exercise capacity, and symptoms.

This effect could be mediated, at least in part, by reducing EAT-mediated pericardial constraint, which may alleviate pressure on the LV and improve its (diastolic) function.

4)Statins, particularly atorvastatin, show improved cholesterol profiles and reduction in EAT.

Known for their lipid-lowering and anti-inflammatory effects, statins could influence EAT expansion and hamper the secretion of proinflammatory molecules, contributing to improvements in cardiovascular health. 

While statins are not recommended in the guidelines for HFpEF treatment, they are often prescribed for patients with HFpEF to address cardiovascular comorbidities, such as hypertension, CAD, and dyslipidaemia.

Furthermore, some suggest that early initiation of statin use is associated with improved outcomes in HFpEF, although this is a topic of current debate.

is a growing global health problem characterized by high morbidity and mortality, with limited effective therapies available. 

Obesity significantly influences haemodynamic and structural changes in the myocardium and vasculature, primarily through the accumulation and action of visceral adipose tissue. 

Particularly, epicardial adipose tissue (EAT) contributes to HFpEF through inflammation and lipotoxic infiltration of the myocardium. 

However, the precise signalling pathways leading to diastolic stiffness in HFpEF require further elucidation. 

This review explores the dynamic role of EAT in health and disease. 

Drawing upon insights from studies in other conditions, we discuss potential 

EAT-mediated inflammatory pathways in HFpEF and 

how they may contribute to functional and structural myocardial and endothelial derangements, including 

intramyocardial lipid infiltration, fibrosis, 

endothelial dysfunction, cardiomyocyte stiffening, and left ventricular hypertrophy. 

Novel therapeutic avenues are available.

is an infectious disease caused by a gram-negative bacterium called Burkholderia pseudomallei. Most people exposed to B. pseudomallei experience no symptoms, but complications can range from fever and skin changes to pneumonia, abscesses, and septic shock, which can be fatal. 

Approximately 10% of people with melioidosis develop symptoms that last longer than two months, termed “chronic melioidosis”. 

Melioidosis is a serious and often underdiagnosed infectious disease caused by the environmental bacterium Burkholderia pseudomallei. 

It’s sometimes called “Whitmore’s disease” and is endemic to tropical and subtropical regions, especially Southeast Asia, northern Australia, and increasingly parts of India. 

Melioidosis—caused by Burkholderia pseudomallei—has seen a surge of research interest recently, especially due to its expanding global footprint and potential as a biothreat. 

Recent advances: 

Emerging infections with Melioidosis—caused by Burkholderia pseudomallei—has seen a surge of research interest recently, especially due to its expanding global footprint and potential as a biothreat. —a highly pathogenic, Gram-negative β-proteobacterium. 

B. pseudomallei is a saprophyte found in soil, groundwater, stagnant streams, rice paddies, and ponds. 

Although melioidosis is mainly endemic in Southeast Asia and northern Australia, it is also increasingly reported in regions outside the Asia-Pacific region including India, Mauritius, the Americas, and Africa. 

Melioidosis can present as an acute, subacute, or chronic process. 

Disease manifestations

include subclinical infections, localized abscesses, severe pneumonia, and fulminant sepsis. 

Case fatality rates ranged from 19 to 36% in endemic areas. Although the epidemiology and routes of transmission are not yet fully understood, it is believed that melioidosis is acquired through contact with contaminated soil and water by percutaneous inoculation, inhalation of aerosols, and ingestion.

The incubation period of melioidosis varies widely from two days to 62 years. Human cases are often spatially and temporally clustered, following heavy rains and winds with resultant human exposure to soil and water B. pseudomallei also causes melioidosis in a wide range of animals in endemic areas. In Hong Kong, melioidosis is an endemic disease not only in humans but also in captive marine mammals and birds, including bottlenose dolphins, 

California sea lions, pilot whales, and zebra 

Transmission & Risk Factors. 

B. pseudomallei thrives in soil and surface water. Infection typically occurs through:• Inhalation of contaminated dust or water droplets• Ingestion of contaminated water or food• Direct contact with contaminated soil or water via skin abrasions or woundsHigh-risk groups include:• People with diabetes, chronic kidney or lung disease, cancer, or alcohol use disorder• Farmers, construction workers, and others exposed to muddy soil or floodwaters 

Clinical Manifestations

Melioidosis is known for its wide spectrum of presentations:• Localized infection: Skin ulcers, abscesses• Pulmonary infection: Cough, chest pain, high fever—often mistaken for TB-Tuberculosis & Chest Diseases

Localized Skin Infections. Swelling, redness, and ulceration around a woundAbscess formationPulmonary (Lung) InfectionCough, often with mucus or phlegm. Chest pain. Fever. Difficulty breathing

Septicemia (Blood Infection)

High fever and chills. 

Abdominal discomfort. 

Confusion or dizziness.

Muscle or joint pain 

Disseminated Infection 

Abscesses in multiple organs (liver, spleen, lungs). 

Weight loss and fatigueMuscle aches and joint pain. 

Disseminated infection: Sepsis, organ abscesses (liver, spleen, prostate), joint and bone involvement, neurological symptoms. 

Symptoms may appear within 1–3 weeks, but latent infections can emerge months or even years later.

Predisposing factors:

Diabetes mellitus is one of the most important risk factors in developing melioidosis. 

The disease should be considered in anyone who has spent time in endemic areas who develops a fever, pneumonia, or abscesses in their liver, spleen, prostate, or parotid gland. Latent infections as pseudomallei can remain latent in the human body for up to 29 years until it is reactivated during human immunosuppression or stress response. However, the site of bacteria during latent infection and the mechanism by which they avoid immune recognition for years are both unclear.
Amongst mechanisms suggested are: residing in the nucleus of the cell to prevent being digested, entering a stage of slower growth, antibiotic resistance, and genetic adaption to the host environment. 

Granulomas (containing neutrophils, macrophages, lymphocytes, and multinucleated giant cells) formed at the infection site in melioidosis have been associated with latent infection in humans.

Diagnosis & Treatment

Diagnosis: Blood or abscess fluid cultures are the gold standard.

Misdiagnosis is common.

Culture Microscopy. By microscopy, 

B. pseudomallei is seen as gram-negative and rod-shaped, with bipolar staining similar in appearance to a safety pin. 

Bacteria can sometimes be seen directly in clinical samples from infected people; however, identification by light microscopy is neither specific nor sensitive. Immunofluorescence microscopy is highly specific for detecting bacteria directly from clinical specimens, but has less than 50% sensitivity. Imaging 

Various imaging modalities can also help with the diagnosis of melioidosis. 

In acute melioidosis with the spreading of the bacteria through the bloodstream, the chest X-ray shows multifocal nodular lesions. 

It may also show merging nodules or cavitations. 

For those with acute melioidosis without the spread to the bloodstream, chest X-ray most commonly shows upper lobe consolidation or cavitations. In chronic melioidosis, the slow progression of upper lobe consolidation of the lungs resembles tuberculosis. 

For abscesses located in other parts of the body apart from the lungs, especially in the liver and spleen, CT scan has higher sensitivity when compared with an ultrasound scan. In liver and splenic abscesses, an ultrasound scan shows “target-like” lesions while a CT scan shows “honeycomb sign” (abscess with loculations separated by thin septa) in liver abscesses. 

For melioidosis involving the brain, MRI has higher sensitivity than a CT scan in diagnosing the lesion. MRI shows ring-enhancing lesions for brain melioidosis

Prevention

Bacterial culture has 60% sensitivity in diagnosing melioidosis.

B. pseudomallei is never part of human flora. Therefore, any growth of the bacteria is diagnostic of melioidosis.
Other samples such as throat, rectal swabs, pus from abscesses, and sputum can also be used for culture. However, culture from CSF is difficult because in one case series, only 29% of the neuromelioidosis cases are culture-positive. When bacteria do not grow from people strongly suspected of having melioidosis, repeated cultures should be taken as subsequent cultures can become positive B. pseudomallei can be grown on any blood agar, MacConkey agar, and agar containing antibiotics such as Ashdown’s medium (containing gentamicin)nand Ashdown’s broth (containing colistin for better isolation of B. pseudomallei from other types of bacteria. Agar plates for melioidosis should be incubated at 37 °C (98.6 °F) in air and inspected daily for four days. On the agar plates, B. pseudomallei forms creamy, non-haemolytic, colonies after 2 days of incubation. After 4 days of incubation, colonies appear dry and wrinkled. Colonies ofB. pseudomallei that are grown on Franci’s medium (a modification of Ashdown medium with gentamicin concentration increased to 8 mg/L and neutral red indicator replaced with 0.2% bromocresol purple) are yellowed to symptom overlap with TB and other infections.

Treatment:

Intensive phase: IV antibiotics (e.g., ceftazidime or meropenem) for 2–8 weeks

Eradication phase: Oral antibiotics (e.g., trimethoprim-sulfamethoxazole) for 3–6 months to prevent relapseDelayed diagnosis and treatment can lead to mortality rates as high as 90% in severe cases. doves. 

Treatment of melioidosis can be difficult, as B. pseudomallei is often resistant to multiple antibiotics, and a prolonged course of antibiotics is required to prevent disease relapse. Due to the severity of melioidosis and aerosol transmissibility of the infectious agent, B. pseudomallei has been classified as a category B bioterrorism and Tier 1 select agent by the Center for Disease Control, USA.

Prevention – Efforts to prevent melioidosis include: wearing protective gear while handling contaminated water or soil, practicing hand hygiene, drinking boiled water, and avoiding direct contact with soil, water, or heavy rain.

There is little evidence to support the use of melioidosis prophylaxis in humans. 

The antibiotic co-trimoxazole is used as a preventative only for individuals at high risk of getting the disease after being exposed to the bacteria in laboratory settings.

Public Health Implications. Melioidosis is increasingly recognized as a neglected tropical disease. 

Its burden is underestimated, especially in resource-limited settings. 

Climate change, extreme weather events, and expanding endemic zones (including parts of India) are raising global concern.

Vaccine Development Breakthroughs.

Researchers are actively pursuing vaccines to combat melioidosis, 

with several promising candidates emerging: Over the years, numerous different strategies have been explored to develop melioidosis vaccines. Based on the choice of protective antigens, many of the resulting candidates would also be predicted to provide some level of protection against Burkholderia mallei, the etiologic agent of glanders. Using these approaches, several promising melioidosis and glanders candidates have been identified with pre-clinical animal studies providing valuable insights into the immunogenic and protective capacities of these potential vaccines. Collectively, this review summarizes recent advancements in melioidosis vaccine research and highlights critical findings that will help guide a path toward the development of a safe, effective and affordable vaccine to combat disease caused by B. pseudomallei.- Subunit vaccinesusing protective antigens from B. pseudomallei have shown strong immunogenicity in preclinical modelsYet there are no vaccines available for humans 

Hand and Skin Hygiene. 

Wash hands thoroughly with soap and clean water after handling soil or water in affected areas, particularly before eating or drinking.