Functional Health Blogs | Mathew Gomes

FAT BAD. SUGAR GOOD. THE DEADLY PARADOX.

How fearing fat while excusing sugar undermines metabolic health.

Executive summary

A person orders grilled chicken without skin, asks for low-fat dressing, avoids butter and red meat, and congratulates themselves on eating responsibly. Then came the bread basket, a soda drink, dessert and a slice of cake. The fat has been treated as the danger. The refined starch and sugar have been granted permission. That is the contradiction at the centre of this discussion.

The body is not built to fear fat. Fat builds every cell membrane, insulates nerves, supplies essential fatty acids, supports hormones, carries vitamins and provides concentrated stored energy. The liver manufactures cholesterol and many fats because life depends on them. But the fact that fat is essential does not make unlimited dietary fat safe. Fat quality, carbohydrate exposure, energy balance, lipoprotein response and the body’s capacity to handle nutrients determine the outcome.

The real problem is a food environment that makes refined carbohydrate effortless, appetite stimulation constant and metabolic dysfunction common. In 2024, 2.6 billion adults were overweight, including 940 million living with obesity (WHO, 2026). These trends reflect many causes: food systems, activity, sleep, social conditions, biology and energy intake.

My coaching proposition is direct: stop judging a meal by whether it contains fat. Judge it by what it does to your biology. For people with insulin resistance, a well-formulated carbohydrate-restricted or ketogenic approach offers a structured way to lower glucose exposure, reduce insulin demand, mobilise stored energy and rebuild practical food habits. This is the evidence-supported option.

The stakes are serious: insulin resistance and excess visceral fat are associated with type 2 diabetes, fatty liver, cardiovascular disease, chronic kidney disease and several cancers. Repeatedly ignoring metabolic dysfunction while polishing the appearance of a low-fat diet is a poor prevention strategy. The chapters that follow explain why and what to do instead.

1 | The respectable meal that gets the biology wrong

Imagine two dinners. One contains salmon, leafy vegetables, olive oil and avocado. The other contains lean chicken, a large portion of white rice, a bread roll, sweetened low-fat yoghurt and dessert. Many people still label the second meal lighter or cleaner because they can see less fat. Yet the second meal delivers a much larger rapidly digestible carbohydrate load. The pancreas responds to the absorbed glucose by releasing insulin. In an insulin-resistant person, the body often needs more insulin to achieve the same effect.

The label of “low fat” in chicken and rice answers the wrong question whether it is good or bad. The relevant questions are: how much glucose enters circulation, how much insulin is needed, what happens to appetite afterwards, and how do blood lipids, waist size, liver health and energy regulation change over time?

An individual can avoid fast food and still consume a highly refined diet: breakfast cereal, fruit juice, crackers, white bread, low-fat flavoured yoghurt, sweet sauces and restaurant desserts. Home cooking is not a guarantee of metabolic quality either. Flour, sugar, refined starch and repeated snacking remain the same regardless where the food is prepared.

2 | Fat is not one substance

Most dietary fat is triglyceride: three fatty acids attached to a glycerol backbone. The fatty acids differ in chain length, number of double bonds and position of those bonds. These details change their physical behaviour and metabolism. Saturated fats have no carbon–carbon double bonds. Monounsaturated fats have one; polyunsaturated fats have more than one. Omega-3 and omega-6 describe where a double bond sits along the chain, not whether a fat is automatically good or bad.

The body also contains phospholipids that build cell membranes, cholesterol that adjusts membrane properties and supplies steroid-hormone precursors, and signalling lipids that help coordinate inflammation, clotting and repair. Some fats are manufactured internally. Essential fatty acids —Linoleic acid (omega-6) and alpha-linolenic acid (omega-3)—must be obtained through food. EPA and DHA, abundant in oily fish, are biologically important long-chain omega-3 fats.

One gram of fat supplies roughly nine kilocalories; carbohydrate and protein supply about four each. This makes fat an efficient reserve. It also means pouring additional oil onto a calorie-surplus diet is not automatically helpful. The objective is adequate fat with high food quality.

3 | From the mouth to the mitochondria

Fat digestion begins modestly in the mouth and stomach, then accelerates in the small intestine. The liver produces bile, which the gallbladder stores and releases when fat enters the intestine. Bile breaks fat into tiny droplets so pancreatic enzymes can digest it. Intestinal cells absorb the fatty acids, rebuild triglycerides and package them into chylomicrons—transport particles that carry dietary fat through lymph and blood. Fatty acids are then released for muscle energy or body-fat storage, while the liver processes the remaining particles.

Avoiding dietary fat has its consequences. With very little fat entering the intestine, the gallbladder receives less stimulation to contract and empty. Prolonged very-low-fat intake, encourages bile stagnation and gallstone formation. Fat also supports the absorption of vitamins A, D, E and K, which are essential for vision, immunity, bones, cell protection and normal blood clotting. The body needs dietary fat not simply for calories, but to maintain essential functions.

Between meals, stored body fat releases fatty acids. Muscles burn them in mitochondria—the cells’ energy-producing machinery—through beta-oxidation. The liver can also convert fatty acids into ketones, especially during fasting or sustained carbohydrate restriction. Ketones fuel the brain and other tissues. Red blood cells still require glucose, which the body obtains from food or produces internally.

This machinery explains why the body can hold substantial energy reserves yet still experience hunger. Hunger is regulated by the brain, gut hormones, sleep, food cues, protein intake, energy needs and learned eating patterns. Insulin resistance disrupts normal fuel handling, making stored energy less accessible under certain conditions. Persistent hunger every few hours or low energy after meals warrants investigating glucose regulation and insulin resistance.

4 | Why insulin matters—and insulin resistance matters more

Insulin is a necessary signal. After eating, it helps muscle and fat cells take up nutrients, restrains excessive glucose release by the liver and suppresses release of fatty acids from adipose tissue. During fasting, lower insulin allows stored fat to be released more readily. This switching is normal biology.

Insulin resistance means tissues respond less effectively to insulin. The pancreas often compensates by producing more. Over time, glucose regulation deteriorates and problems begin. Excess visceral fat, fatty liver, low physical activity, inadequate sleep, genetics and chronic energy surplus all participate in this process. In some tissues, harmful lipid intermediates—including diacylglycerols and ceramides—interfere with insulin signalling. The issue is not simply “fat in the blood”; it is where lipid accumulates and how the tissue responds.

5 | The lost art of switching fuels

Metabolic flexibility is the capacity to shift between carbohydrate and fat oxidation according to demand. At rest and during lower-intensity exercise, healthy muscles often use a substantial amount of fat. During hard efforts they rely more heavily on carbohydrate because it can deliver energy rapidly. Fasting and carbohydrate restriction shift fuel selection toward fat and ketones.

A low-carbohydrate diet reduces the incoming glucose burden and usually lowers insulin exposure. Over days to weeks, the liver increases ketone production; over subsequent weeks, training, enzymes and tissues adapt to the changed fuel supply. 

Ketosis is the state in which the liver produces ketones from fat. Keto adaptation is the deeper metabolic change: muscles increasingly burn fat, the brain uses ketones alongside glucose, the liver improves fuel management, and insulin levels generally fall, making stored fat easier to access. Appetite and hunger patterns become steadier, energy fluctuations lessen, and endurance can improve. The result is greater metabolic flexibility, more stable energy, better appetite control and less dependence on frequent carbohydrate intake.

6 | How fat became the suspect and sugar became ordinary

Mid-twentieth-century researchers investigated the relationship between saturated fat, cholesterol and coronary heart disease. Governments translated parts of that evidence into population advice to reduce fat, especially saturated fat. In public understanding, the more specific message frequently became a simplistic rule: fat is bad, low fat is good.

Manufacturers responded with reduced-fat biscuits, sweetened low-fat yoghurt, cereals, sauces, desserts and snack foods. Removing fat often required replacing flavour and texture with starches, sugars or other ingredients. Some industrial formulations relied on partially hydrogenated fats, which introduced trans fats later shown to increase cardiovascular risk. Marketing created a powerful halo: a product could carry a low-fat claim while remaining rich in refined carbohydrate and easy to overconsume. Historical documents also show sugar-industry influence on research priorities and public narratives.

The epidemic of metabolic disease unfolded during decades of changing food availability, portion sizes, inactivity, sleep, smoking patterns, social conditions and commercial food engineering.

7 | The microbiology of fat: bile, bacteria and the gut

Humans have eaten animal and plant fats throughout evolution, and our digestive system is equipped to process them. Beyond digestion, gut bacteria modify bile acids into signals that influence the intestine, liver, metabolism and immune system. Fat therefore participates in communication and defence, not just energy supply.

Avoiding nutritious fats reduce essential fatty acids and fat-soluble vitamins unless replaced. A diet dominated by omega-6-rich refined oils, with too little omega-3, also changes the fats available for cell membranes and immune signalling. Omega-6 is essential, not inherently inflammatory; but fat quality and inadequate omega-3 fats to balance the omega-6 intake changes that equation.

The microbiome adds another layer. Dietary fats influence bile-acid metabolism and microbial activity, while fibre feeds bacteria that produce butyrate, which nourishes the colon lining and supports immune regulation. A high-fat diet without fibre is different from one built around olive oil, oily fish, avocado, nuts and vegetables. Disrupted bile-acid and microbial signalling are linked to intestinal inflammation and colorectal cancer biology.

For keto living, restore quality fat without neglecting the gut: prioritise olive oil, oily fish, avocado, olives, nuts, seeds and fibre-rich non-starchy vegetables; limit industrial trans fats and heavily processed foods.

8 | The seven systems that depend on fat

Fat is essential for how your body produces energy, builds cells, regulates hormones, protects organs and repairs damage. Without enough essential fats, the body cannot function optimally.

Energy and muscle

Muscles burn both fat and glucose for energy. Regular exercise trains mitochondria—the tiny energy-producing engines inside cells—to burn fuel efficiently. Strength training builds muscle that absorbs glucose from the blood, improving insulin sensitivity and metabolic health. Endurance training improves the ability to use fat for sustained energy.

Brain and nerves

Your brain and nerves are built partly from fat. Fat forms protective nerve insulation and cell membranes that allow brain cells to communicate. Omega-3 fats, especially DHA, support brain function. During ketosis, the brain can also burn ketones made from fat, reducing its need for glucose.

Hormones and cell signalling

Cholesterol is the raw material for making hormones such as testosterone, oestrogen and cortisol. Fats also help cells communicate, regulating metabolism, immunity and inflammation.

Immune defence and inflammation

Body fat is not just storage; it actively sends chemical messages that influence inflammation. Excess fat around internal organs can keep the immune system unnecessarily activated, driving chronic inflammation. Omega-3 fats help the body produce molecules that switch off inflammation once their job is done.

Liver and detoxification

The liver manages fat, glucose and ketone production. It packages fats for transport and converts fat into ketones when carbohydrate availability is low. When energy handling becomes disturbed, fat can accumulate inside the liver, often alongside insulin resistance. A fatty liver is therefore a warning sign of metabolic dysfunction.

Gut and nutrient absorption

Fat enables the absorption of vitamins A, D, E and K, needed for vision, immunity, bones and blood clotting. Bile from the liver breaks dietary fat into tiny droplets, allowing digestive enzymes to work. Without adequate dietary fat and healthy digestion, essential nutrients do not get properly absorbed.

Structure, skin and repair

Every cell in your body is surrounded by a membrane built largely from fats. These membranes control what enters and leaves cells and how cells respond to signals. Essential fatty acids also protect the skin, support tissue repair and regulate inflammation. Protein, vitamins and minerals work alongside fat to rebuild and maintain healthy tissues.

9 | The disease chain: what is happening inside the body

Begin with an environment of frequent refined carbohydrate intake, high-energy foods, insufficient muscle activity, poor sleep and individual susceptibility. Most people develop increased visceral fat and fatty liver. Insulin signalling becomes less efficient; the pancreas compensates; blood glucose and triglycerides rise. The liver exports more triglyceride-rich particles. Blood pressure, vascular inflammation and endothelial function worsen. These are interconnected pathways that happen to work in sequence.

Type 2 diabetes develops when insulin resistance and inadequate insulin secretion combine to produce persistent hyperglycaemia. Chronic kidney disease can follow diabetes and hypertension through injury to the kidney’s filtering structures. Fatty liver disease reflects excess lipid accumulation and can progress to inflammation and scarring. Cardiovascular disease involves atherosclerotic plaque formation driven by ApoB-containing particles, modified by blood pressure, smoking, diabetes and inflammation. 

Visceral obesity and hyperinsulinaemia are associated with increased risk of several cancers, including colorectal, postmenopausal breast, endometrial, pancreatic, liver and kidney cancers. Mechanisms include insulin/IGF signalling, sex-hormone changes, inflammation and altered immune surveillance. 

The human cost is real: impaired mobility, neuropathy, heart attack, stroke, kidney failure, cirrhosis and premature death. The message is not that eating bread once causes these outcomes. It is that decades of unmanaged metabolic risk are consequential—and a “low-fat” label does nothing to neutralise them.

10 | The mistake of adding fat without changing the rest

Here is the most dangerous misunderstanding of the pro-fat message: someone keeps the bread, pasta, sweet drinks and desserts, then adds avocados, olive oil, butter, cream, coconut oil and large portions of cheese because fat is now supposedly healthy. That is often a higher-energy diet with continued refined-carbohydrate exposure. In an insulin-resistant person, that combination makes weight and lipid management harder and often a lethal metabolic combo.

Refined carbohydrate plus excess energy plus poor fat quality is a particularly poor combination; whole-food carbohydrate with unsaturated fat and fibre is biologically different.

My coaching rule is therefore simple: do not add fat indiscriminately. First remove the habitual refined-carbohydrate burden, build sufficient protein and fibre, then use quality fats to support satiety and energy needs.

11 | Read the body, then verify the biology

Blood tests help verify what is happening inside. Glucose, HbA1c and fasting insulin reveal aspects of blood sugar control and insulin resistance. Triglycerides, HDL, ApoB, liver enzymes, kidney function and body composition add insight into how the body handles energy, fat and metabolic stress. CGM readings reveal individual responses to food, exercise and stress. No single marker tells the whole story.

The real expertise lies in connecting the dots. Understanding how nutrition and lifestyle influence the liver, muscles, gut, hormones and cellular energy systems reveals what is changing, why it is happening and which inputs can be modified.

This is where functional nutrition coaching makes the difference: translating the body’s signals and biological evidence into a personalised nutrition and lifestyle plan—knowing what to change, where to intervene, how to do it and how to measure whether it is working.

12 | A structured route into nutritional ketosis

Getting into ketosis is one thing. Becoming keto-adapted—and sustaining the benefits—is another. It requires more than cutting carbohydrates. The goal is to retrain the body to use fat efficiently for energy while protecting muscle, metabolic health and cardiovascular function.

  1. Understand the body before changing the diet. Start by assessing metabolic health, insulin resistance, body composition, blood pressure, medications, lifestyle and nutritional needs. This establishes what needs to change, why and how to measure progress.
  2. Build a personalised nutrition plan. Typically, carbohydrates begin around 20–50 g daily, often closer to 20 g initially. Protein is calculated to preserve muscle and support satiety, commonly 1.2–1.6 g/kg body weight for active adults. Healthy fats provide energy and satisfaction, while low-carbohydrate vegetables supply fibre and essential nutrients. Meals must also fit personal, cultural and social preferences.
  3. Guide the transition into ketosis. As carbohydrate intake falls, insulin generally decreases, the kidneys release more sodium and water, and the liver increases ketone production. Fatigue, headaches, constipation or reduced exercise performance may occur. Hydration, electrolytes, fibre, food intake and activity are adjusted individually, particularly when blood pressure, kidney function or medications require caution.
  4. Develop genuine keto adaptation. Blood ketones around 0.5–3.0 mmol/L indicate nutritional ketosis, not necessarily keto adaptation. Over subsequent weeks, the body progressively improves its ability to use fat as fuel. Appetite, energy between meals, exercise tolerance, recovery and metabolic responses help assess functional progress.
  5. Verify results and refine the plan. Review waist size, body composition, blood pressure, glucose regulation, triglycerides, ApoB/LDL and how the person feels and functions. Ketones alone do not establish success. Adjust food choices, fat quality, protein, activity and recovery based on actual results.
  6. Make keto living sustainable. Develop personalised recipes, meal plans, shopping lists and practical routines that work with everyday life. The objective is a sustainable way of eating that supports metabolic health, muscle preservation and long-term resilience.

The value of guided keto adaptation is knowing what to change, why it matters, how to implement it and when to adjust. My coaching connects the body’s functional signals with nutritional science to build a personalised plan, guide the transition and verify that the changes are delivering meaningful benefits.

Final Thoughts | Structure Defines Function

Your body functions according to the structure you build and maintain. Muscle burns fuel, the liver regulates energy, the gut absorbs nutrients, and blood vessels deliver oxygen. Years of excess insulin, poor nutrition, chronic inflammation and inadequate recovery undermine these systems. Losing muscle, accumulating visceral fat and becoming insulin resistant are not simply signs of aging. They reflect changes in how your body is built and how it works. You cannot expect healthy function from a structure you continually weaken.

Keto living is about restoring the body’s ability to access stored fat, regulate glucose, control hunger and support muscle and metabolic health. Real food, quality fats, adequate protein, carbohydrate control, strength training, sleep and recovery work together. The right balance depends on your biology, health risks and response. First understand what is failing, then rebuild what supports function, measure the results and adjust. Your body is constantly adapting to how you feed, move and recover. Stop losing the structure you need for healthy function. Build it, protect it and keep it working for life.

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