“TL;DR: Cellulite is tightly related to civilisation diseases. The exact same Western diets and lifestyles that drive the pandemic of obesity and civilisation diseases is also the reason why cellulite is so prevalent today. Cellulite, often dismissed as a cosmetic concern, involves subcutaneous fat protruding into the dermis, resulting in a dimpled skin appearance. It shares the same metabolic drivers as obesity and civilisation diseases: oxidative stress, hyperinsulinemia, insulin resistance, low-grade inflammation, and sympathetic nervous system / renin-angiotensin system (SNS/RAS) overactivation. High-insulinemic Western diets promote subcutaneous fat storage, while oxidative stress and inflammation degrade collagen and connective tissue, facilitating fat protrusion. SNS and RAS overactivation impair microcirculation, reducing tissue oxygenation and exacerbating dermal weakening. Hormonal influences, modulated by insulin and SNS activity, further disrupt tissue integrity. Like obesity, cellulite reflects systemic metabolic dysfunction, not merely localised fat accumulation. Adopting a more paleolithic-like diet and active lifestyle may reduce cellulite by addressing these underlying mechanisms, offering benefits akin to those for obesity and civilisation disease prevention.”
The role of western diet and lifestyle in driving obesity, cellulite, and civilisation diseases: a metabolic perspective
How Western diet and lifestyle drive the pandemic of obesity, cellulite, and civilisation diseases
Evolutionary mismatch, dietary shifts and cellulite
Key metabolic disruptions can drive cellulite creation: oxidative stress and reactive oxygen species (ROS)
How hyperinsulinemia and insulin resistance affect cellulite
Sympathetic nervous system, renin-angiotensin system overactivation and cellulite
Low-grade inflammation: a key component of cellulite
Obesity and cellulite as outcomes of western diets and lifestyles
Epigenetic and fetal programming of obesity and cellulite
Conclusions
How western diet and lifestyle drive the pandemic of obesity and civilization diseases
Pathophysiology of cellulite: possible involvement of selective endotoxemia
Exploring the link between metabolic syndrome and cellulite
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How Western diet and lifestyle drive the pandemic of obesity, cellulite, and civilisation diseases
A 2019 paper published in the journal ‘Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy’, examined the profound impact of Western diets and lifestyles on the global epidemic of obesity, and chronic non-infectious degenerative conditions, collectively termed "civilisation diseases" - to which we might incllude the aesthetic condition of cellulite, as the exact same causes of civilisation diseases also result in cellulite development.
These conditions/diseases include type 2 diabetes mellitus (T2DM), cardiovascular diseases (CVD), cancer, autoimmune disorders, Alzheimer’s disease, and others.
The paper argues that these conditions (to which we include cellulite), are rare or absent in hunter-gatherer populations adhering to paleolithic diets, highlighting a critical mismatch between our evolutionary biology and modern dietary and lifestyle practices.
The paper identifies key metabolic disruptions—oxidative stress, hyperinsulinemia, insulin resistance, low-grade inflammation, and overactivation of the sympathetic nervous system (SNS) and renin-angiotensin system (RAS)—as central drivers of these diseases, including cellulite.
Shedding light on these mechanisms, the paper describes the shared causes and pathology of obesity, related comorbidities [and cellulite], advocating for lifestyle interventions aligned with our genetic makeup.
Evolutionary mismatch, dietary shifts and cellulite
The papers contrasts the health profiles of Western populations with those of hunter-gatherers, who exhibit minimal rates of obesity and civilisation diseases [and we also add, cellulite].
Hunter-gatherers maintain low serum insulin levels and excellent insulin sensitivity on paleolithic diets, which are high in protein (19–35% of energy), low in carbohydrates (22–40%), and moderate to high in fat (28–58%).
Comprising game, fish, roots, tubers, wild herbs, berries, nuts, and occasional honey, these diets feature low-glycemic, low-insulinemic carbohydrates, minimising postprandial glucose and insulin spikes.
In contrast, Western diets, shaped by the agricultural revolution (10,000 years ago) and industrialisation (250 years ago), are dominated by high-glycemic carbohydrates (refined cereals, corn, potatoes, sugars like sucrose and fructose), dairy, and excessive omega-6 polyunsaturated fatty acids (PUFAs), with an unhealthy omega-6/omega-3 ratio of 20:1.
These diets, coupled with sedentary lifestyles, frequent snacking, and consumption of energy-dense foods and sucrose-laden beverages, result in prolonged postprandial states and metabolic imbalances.
In addition, cellulite, characterised by hypodermal and subcutaneous fat protruding into the dermis, is exacerbated by these dietary shifts. High-insulinemic foods and omega-6 PUFAs promote subcutaneous fat accumulation, while inflammation from imbalanced PUFAs weakens dermal connective tissue, facilitating fat herniation and the dimpled skin appearance.
The human genome, largely unchanged over 10,000 years, remains adapted to paleolithic conditions. Civilisation diseases, and aesthetic conditions such as cellulite, typically manifest post-reproductively, exerting minimal evolutionary selection pressure. This genetic mismatch with modern diets and lifestyles underpins the metabolic distortions driving these conditions.
Key metabolic disruptions can drive cellulite creation: oxidative stress and reactive oxygen species (ROS)
The paper identifies excessive reactive oxygen species (ROS) production and oxidative stress as pivotal in disease pathogenesis.
ROS, generated during mitochondrial oxidative phosphorylation (OXPHOS), serve as signalling molecules under physiological conditions but become damaging when overproduced.
Western diets, rich in high-glycemic carbohydrates and energy-dense foods, overwhelm mitochondrial capacity, leading to excessive ROS production. This oxidative stress damages lipids, proteins, and DNA, contributing to insulin resistance, inflammation, and diseases like T2DM, CVD, and cancer.
Studies show that high-glycemic load diets, high-sucrose diets, and Western diets elevate ROS levels, while paleolithic and Mediterranean diets are associated with lower oxidative stress.
In cellulite, oxidative stress plays a significant role by degrading collagen and elastin in the dermal matrix, weakening connective tissue integrity. This allows subcutaneous fat to protrude, exacerbating the characteristic dimpled texture. Oxidative damage also impairs microcirculation, further contributing to cellulite severity.
How hyperinsulinemia and insulin resistance affect cellulite
Hyperinsulinemia (chronically elevated insulin levels) and insulin resistance (impaired insulin function) are central to the development of civilisation diseases.
Western diets, high in insulinemic foods like refined grains, sugars, and dairy, cause frequent insulin spikes, placing chronic stress on pancreatic β-cells. Over time, this leads to β-cell dysfunction, insulin hypersecretion, and insulin resistance.
The paper cites studies showing hyperinsulinemia precedes obesity and T2DM, with high-insulinemic diets promoting fat storage, appetite, and weight gain.
Fructose, prevalent in soft drinks and processed foods, exacerbates these effects, with consumption rising dramatically since the 1970s. Oxidative stress amplifies insulin resistance by disrupting cellular signalling pathways.
Cellulite is closely linked to hyperinsulinemia, which drives subcutaneous fat storage and inhibits lipolysis, increasing fat cell volume and pressure on dermal tissues. This promotes fat protrusion into the dermis, worsening cellulite’s appearance.
Insulin resistance further compounds these effects by perpetuating fat accumulation and tissue stress.
Sympathetic nervous system, renin-angiotensin system overactivation and cellulite
Western diets activate the sympathetic nervous system (SNS) and renin-angiotensin system (RAS), intensifying metabolic dysfunction.
High-insulinemic carbohydrates elevate SNS activity, increasing norepinephrine levels, which promote insulin resistance through oxidative stress.
Insulin and SNS activity also stimulate the RAS, raising angiotensin II levels, a potent driver of insulin resistance and inflammation.
These systems form feedback loops, with norepinephrine enhancing angiotensin II production and vice versa, amplifying metabolic distortions. Overactivation of SNS and RAS contributes to cardiovascular diseases (CVD), type 2 diabetes mellitus (T2DM), and other conditions.
In cellulite, SNS overactivation and RAS-induced angiotensin II impair microcirculation in the dermis, hypodermis and subcutaneous adipose tissue, leading to tissue hypoxia and reduced collagen synthesis.
This weakens the connective tissue, allowing subcutaneous fat to protrude and exacerbating cellulite’s dimpled appearance. Poor microcirculation also hinders tissue repair, perpetuating the condition.
Low-grade inflammation: a key component of cellulite
Chronic low-grade inflammation, driven by Western diets, oxidative stress, hyperinsulinemia, SNS, and RAS activation, is a hallmark of civilisation diseases.
Diets high in omega-6 PUFAs and refined carbohydrates reprogram the innate immune system, increasing proinflammatory cytokines. This inflammation perpetuates insulin resistance and contributes to obesity, T2DM, CVD, and other conditions.
Low-glycemic diets, conversely, reduce inflammation and increase beneficial adipokines like adiponectin.
Cellulite is intimately tied to low-grade inflammation, as proinflammatory cytokines disrupt collagen synthesis and degrade dermal connective tissue.
This weakens the structural support of the skin, facilitating fat protrusion and worsening cellulite’s appearance. Inflammation also impairs microcirculation, compounding tissue damage and fat herniation.
Obesity and cellulite as outcomes of western diets and lifestyles
Obesity, a global pandemic, results from a chronic energy surplus, exacerbated by metabolic changes. High insulin levels promote fat storage, inhibit lipolysis, and increase appetite, driving weight gain.
Adipose tissue, a metabolically active organ, releases molecules that worsen oxidative stress, insulin resistance, and inflammation, perpetuating a cycle of disease. The paper notes that obesity prevalence has doubled in over 70 countries since 1980, spreading rapidly in developing nations.
Cellulite, similarly driven by these metabolic disruptions, arises from insulin-mediated fat storage, oxidative stress, and inflammation, which impair dermal connective tissue integrity.
The increased volume of subcutaneous fat cells, combined with weakened collagen and elastin, allows fat to protrude into the dermis, creating the dimpled texture.
Both obesity and cellulite reflect systemic metabolic dysfunction, not merely localised fat accumulation, and share common pathways with civilisation diseases.
Epigenetic and fetal programming of obesity and cellulite
Diet-related epigenetic changes and foetal programming amplify disease risk. Maternal obesity and poor nutrition increase oxidative stress in the uterus, programming offspring for insulin resistance, obesity, and related conditions.
Animal studies demonstrate that these effects can persist across generations, as seen in rats fed high-carbohydrate diets.
Cellulite risk may also be influenced by fetal programming. Maternal oxidative stress and inflammation could alter connective tissue development in offspring, predisposing them to subcutaneous fat irregularities and weakened dermal structure later in life.
Epigenetic changes in genes regulating fat metabolism and tissue integrity may further increase cellulite susceptibility.
Conclusions
The paper concludes that Western diets and lifestyles, misaligned with our genetic makeup, drive obesity, cellulite, and civilisation diseases through interconnected metabolic distortions: oxidative stress, hyperinsulinemia, insulin resistance, SNS and RAS overactivation, and low-grade inflammation.
These mechanisms explain the shared causes and pathology of obesity, cellulite, and diseases such as diabetes and heart disease.
Cellulite, like obesity, is a manifestation of systemic metabolic dysfunction, driven by insulin-mediated fat storage, oxidative damage to connective tissue, and inflammation-induced dermal weakening.
Adopting paleolithic-style diets (low-glycemic, high-protein, balanced omega-6/omega-3) and increasing physical activity could mitigate these conditions by addressing their root causes.
The paper underscores the urgent need for lifestyle interventions to curb the global rise of obesity, cellulite, and civilisation diseases, advocating a return to dietary and activity patterns aligned with our evolutionary biology.
How western diet and lifestyle drive the pandemic of obesity and civilization diseases
Research paper link: https://pmc.ncbi.nlm.nih.gov/articles/PMC6817492/
Abstract: Westernized populations are plagued by a plethora of chronic non-infectious degenerative diseases, termed as “civilization diseases”, like obesity, diabetes, cardiovascular diseases, cancer, autoimmune diseases, Alzheimer's disease and many more, diseases which are rare or virtually absent in hunter-gatherers and other non-westernized populations. There is a growing awareness that the cause of this amazing discrepancy lies in the profound changes in diet and lifestyle during recent human history. This paper shows that the transition from Paleolithic nutrition to Western diets, along with lack of corresponding genetic adaptations, cause significant distortions of the fine-tuned metabolism that has evolved over millions of years of human evolution in adaptation to Paleolithic diets. With the increasing spread of Western diet and lifestyle worldwide, overweight and civilization diseases are also rapidly increasing in developing countries. It is suggested that the diet-related key changes in the developmental process include an increased production of reactive oxygen species and oxidative stress, development of hyperinsulinemia and insulin resistance, low-grade inflammation and an abnormal activation of the sympathetic nervous system and the renin-angiotensin system, all of which play pivotal roles in the development of diseases of civilization. In addition, diet-related epigenetic changes and fetal programming play an important role. The suggested pathomechanism is also able to explain the well-known but not completely understood close relationship between obesity and the wide range of comorbidities, like type 2 diabetes mellitus, cardiovascular disease, etc., as diseases of the same etiopathology. Changing our lifestyle in accordance with our genetic makeup, including diet and physical activity, may help prevent or limit the development of these diseases.
Pathophysiology of cellulite: possible involvement of selective endotoxemia
Research paper link: https://pubmed.ncbi.nlm.nih.gov/36285892/
Abstract: The most relevant hallmarks of cellulite include a massive protrusion of superficial adipose tissue into the dermis, reduced expression of the extracellular glycoprotein fibulin-3, and an unusually high presence of MUSE cells in gluteofemoral white adipose tissue (gfWAT) that displays cellulite. Also typical for this condition is the hypertrophic nature of the underlying adipose tissue, the interaction of adipocytes with sweat glands, and dysfunctional lymph and blood circulation as well as a low-grade inflammation in the areas of gfWAT affected by cellulite. Here, we propose a new pathophysiology of cellulite, which connects this skin condition with selective accumulation of endogenous lipopolysaccharides (LPS) in gfWAT. The accumulation of LPS within a specific WAT depot has so far not been considered as a possible pathophysiological mechanism triggering localized WAT modifications, but may very well be involved in conditions such as cellulite and, secondary to that, lipedema.
Exploring the link between metabolic syndrome and cellulite
Research paper link: https://pmc.ncbi.nlm.nih.gov/articles/PMC11214470/
Abstract: Metabolic syndrome (MetS) encompasses a cluster of metabolic abnormalities, including insulin resistance, hypertension, abdominal obesity, and dyslipidemia, increasing cardiovascular disease and type 2 diabetes risks. Cellulite, a cosmetic condition marked by dimpled skin, predominantly affects women and shares risk factors with MetS, such as obesity and hormonal imbalances. This review examines the potential link between MetS and cellulite, focusing on shared pathophysiological pathways and implications for clinical practice and future research. Common factors such as inflammation, hormonal changes, and adipose tissue dysfunction are explored. The review highlights the importance of longitudinal studies to track cellulite progression in MetS patients, biomarker identification for early detection, intervention trials to assess therapeutic efficacy, mechanistic studies to elucidate underlying pathways and the impact of comorbidities on cellulite development. Understanding these relationships can enhance prevention, diagnosis, and treatment strategies for both MetS and cellulite, addressing significant public health and cosmetic concerns.
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