Food as Medicine

Food as Medicine

The Role of Diet in Preventing and Managing Obesity-Related Diseases

By Dr. Alain Frabotta - Integrative Chiropractor, Naturopathic & Functional Medicine Clinician, Educator, Sydney, Australia.

A New Lens on Obesity: Beyond Calories and Carbs

The global rise in obesity is not merely a reflection of willpower or caloric excess — it is a reflection of metabolic miscommunication. Each meal delivers biochemical messages that influence hormones, inflammation, mitochondrial function, and the gut microbiome.

The question is no longer how much we eat, but what signals our food sends to the body’s systems of regulation. Over the past half-century, industrialised diets have shifted toward refined carbohydrates, low-quality fats, and ultra-processed foods.

This nutritional transition has driven the dual epidemics of obesity and chronic metabolic disease, contributing to hypertension, dyslipidaemia, insulin resistance, Type II diabetes, and cardiovascular disorders. [1–3]

Re-establishing metabolic health begins not with macronutrient dogma, but with understanding how diet quality, nutrient balance, and biological individuality converge to shape long-term outcomes.

The Global Obesity Landscape

Obesity now affects more than 1 billion individuals worldwide and accounts for an estimated 5 million preventable deaths annually. [4]

It is a key driver of metabolic syndrome — a cluster of conditions including hyperglycaemia, abdominal obesity, hypertension, and dyslipidaemia — which together amplify the risk of heart disease, stroke, and cancer.

Over the past few decades, public health policies have often promoted low-fat diets, unintentionally encouraging overconsumption of refined carbohydrates. As Hu and Willett note, “the type of carbohydrate, rather than total fat, is the critical determinant of metabolic risk.” [5]

These shifts have spurred renewed debate: should we prioritise low-carbohydrate, high-fat diets (LCHF) or high-carbohydrate, low-fat diets (HCLF) — or is the real solution to focus on food quality, fibre, and metabolic flexibility?

Low-Carbohydrate, High-Fat Diets (LCHF)

Short-Term Effects and Mechanisms

Low-carbohydrate, high-fat diets typically restrict carbohydrates to less than 50–100 g per day, inducing nutritional ketosis — a state in which the liver converts fat into ketone bodies that serve as an alternate fuel source.

Clinical studies demonstrate that LCHF diets can produce significant short-term weight loss, improved glycaemic control, and favourable lipid shifts compared with low-fat diets. [6,7]

Mechanistically, these benefits may result from:

• Increased satiety via ketone-mediated appetite suppression

• Reduced insulin secretion and improved insulin sensitivity

• Mild energy loss through urinary ketone excretion

• Enhanced adaptive thermogenesis and fat oxidation[8]

Clinical Insight: Short-term LCHF diets can be a therapeutic tool for rapid weight loss or glycaemic control under supervision. However, clinical outcomes vary significantly with dietary quality, total caloric intake, and individual metabolic phenotype.

Endocrine and Bone Considerations

Beyond weight regulation, metabolic trade-offs emerge. Caton et al. observed that cessation of a low-carb diet, even without caloric increase, led to rapid fat regain and hormonal disturbances, including decreased IGF-1 and growth hormone levels. [9]

Bielohuby et al. further demonstrated reductions in bone mineral density and strength in animal models fed long-term LCHF diets, accompanied by elevated leptin and reduced osteoblast differentiation markers (Runx2, osterix). [10]

These data suggest that chronic LCHF diets may impair bone metabolism, particularly concerning postmenopausal women or individuals with pre-existing osteoporosis.

Key Takeaway: Short-term LCHF diets may enhance fat metabolism, but prolonged restriction can negatively affect bone and hormonal health. Patients with skeletal fragility or endocrine disorders should be counselled cautiously.

Cardiovascular and Cognitive Impacts

Evidence on LCHF diets and cardiovascular risk remains divided. While some trials report improved HDL levels and reduced triglycerides [11,12], others show adverse changes in LDL particle size and vascular inflammation.

In hypertensive rats, Bosse et al. found that LCHF diets improved endothelial function without impairing insulin signalling. [13] Conversely, Holloway et al. linked high-fat, low-carb feeding to myocardial dysfunction and elevated circulating free fatty acids. [14]

Neurocognitive outcomes are equally complex. High-fat diets have been associated with reduced hippocampal neurogenesis and accelerated cognitive decline, potentially predisposing individuals to Alzheimer’s disease. [15]

Clinical Insight: Cardiometabolic outcomes depend heavily on fat quality — monounsaturated and omega-3 fats support vascular health, whereas diets high in saturated or trans fats exacerbate atherogenesis and oxidative stress.

High-Carbohydrate, Low-Fat Diets (HCLF)

Metabolic Effects and Insulin Response

High-carbohydrate, low-fat diets — typically >55% of total energy from carbohydrates — were historically championed for cardiovascular prevention. Yet, excessive refined sugar intake can promote hepatic de novo lipogenesis (DNL), leading to hypertriglyceridaemia and insulin resistance. [16]

Schwartz et al. demonstrated that both hyperinsulinaemia and low-fat diets increase DNL, suggesting that carbohydrate overload converts glucose to fat within the liver, thereby impairing lipid homeostasis. [17]

Furthermore, high-glycaemic diets elevate postprandial glucose excursions and promote compensatory hyperinsulinaemia — early hallmarks of metabolic syndrome.

Age, Gender, and Genetic Variability

Dietary response is far from uniform. Huang et al. (2011) found that HCLF diets decreased HDL cholesterol in men and increased triglycerides in women, likely influenced by LPL gene polymorphisms. [18]

Adolescent studies by Ebbeling et al. revealed no significant differences in weight loss between HCLF and LCHF diets; however, insulin sensitivity improved more in the LCHF group, suggesting carbohydrate restriction may reduce metabolic risk in insulin-resistant youth. [19]

Key Takeaway: Age, sex, genetics, and baseline insulin sensitivity shape metabolic responses. Personalised macronutrient ratios are essential for sustainable weight and glucose management.

The Role of Food Quality and Fibre

Modern debates about fat versus carbohydrate often overlook the source and integrity of foods. Whole plant foods — rich in fibre, polyphenols, and resistant starch — nourish the gut microbiota, enhance satiety, and regulate inflammation.[20]

Low-carbohydrate diets that limit these foods can reduce stool bulk and transit time, increasing colonic exposure to mutagens and potential carcinogens. Fermentation of undigested proteins produces ammonia and phenolic compounds, which contribute to colonic cytotoxicity. [21]

Conversely, high-fibre diets are consistently linked to lower risks of cardiovascular disease, colorectal cancer, and mortality. [22]

Fibre also supports the gut–brain axis, influencing satiety hormones such as GLP-1 and PYY — vital in obesity regulation. [23]

Clinical Insight: Fibre is not optional — it is an essential metabolic regulator. Clinicians should emphasise whole-food carbohydrates even in low-carb frameworks, ensuring gut and metabolic integrity.

Fat Quality and the Omega Balance

Fat is both fuel and messenger. Beyond their caloric value, fatty acids modulate inflammation, gene expression, and cell membrane function.

Hypercaloric diets high in saturated fats promote insulin resistance and systemic inflammation. [24]

Conversely, polyunsaturated omega-3 fatty acids — eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) — improve lipid profiles, endothelial function, and cardiac rhythm stability. [25]

Recent meta-analyses confirm that optimal dietary patterns combine unsaturated fats, low-glycaemic-load carbohydrates, and high plant diversity, resulting in the best cardiometabolic outcomes. [26,27]

However, Western populations typically exhibit an omega-6: omega-3 ratio exceeding 15:1, far above the optimal 4:1 ratio required for anti-inflammatory balance. [28]

Key Takeaway: Shift the focus from “low-fat” to “healthy-fat,” replacing saturated fats with omega-3-rich sources like oily fish, walnuts, flax, and algae oil.

Ultra-Processed Foods and Metabolic Inflexibility

Beyond macronutrients, food processing profoundly shapes metabolic outcomes. Ultra-processed foods (UPFs) — characterised by additives, stabilisers, and artificial sweeteners — now account for more than 50% of caloric intake in many Western nations. [29]

Emerging evidence links UPFs to weight gain independent of calorie content. A 2024 Lancet Diabetes & Endocrinology study found that UPF consumption predicts obesity and Type 2 diabetes risk even when controlling for total macronutrient composition. [30]

Mechanisms include disruption of gut microbiota diversity, mitochondrial stress, and impaired satiety signalling. [31]

Clinical Insight: Clinicians should prioritise dietary pattern education, guiding patients toward minimally processed, nutrient-dense foods regardless of macronutrient ratio.

Toward Nutritional Precision: A Systems Approach

The binary low-carb vs low-fat debate misses the essence of metabolic health. The emerging frontier is nutritional precision — aligning diet with genetics, microbiome composition, and metabolic biomarkers.

Studies from Cell Metabolism (2024) show that glycaemic and lipid responses to identical foods vary up to five-fold among individuals, driven by the gut microbiome and circadian rhythms. [32]

Functional and integrative medicine practitioners are uniquely positioned to synthesise this evidence — bridging nutrition science with systems biology, lifestyle counselling, and behavioural change.

Key Takeaway: Personalised nutrition is the next evolution of obesity management — where food prescriptions are informed by data, not ideology.

The Future of Diet and Disease Prevention

The literature surrounding low-carbohydrate and low-fat diets reveals inconsistent outcomes, highlighting the need to move beyond rigid dietary doctrines.

Short-term LCHF diets may reduce body weight and improve insulin sensitivity, yet long-term effects on bone, cardiovascular, and neurological health remain uncertain.

Conversely, high-carbohydrate, low-fat diets may elevate triglycerides and impair glycaemic control when dominated by refined starches and sugars.

The path forward requires an integrated, evidence-based framework that values:

• Food quality over macronutrient ratios

• Whole-food, fibre-rich nutrition to support microbiome diversity

• Healthy fats, particularly omega-3 PUFAs, for anti-inflammatory balance

• Personalised strategies grounded in metabolic individuality

Obesity is not simply a caloric imbalance — it is a systemic breakdown in cellular communication.

Healing requires re-establishing metabolic dialogue through intelligent nutrition, movement, and lifestyle medicine.

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