Food, Agriculture, Environment and Chronic non-communicable diseases: How are they connected?

The evolution of modern humans dates from around three million years ago. This period has encompassed cycles of climate change and food availability. Human physiology has adapted to these evolutionary stimuli, and this is the physiology we live with today. The industrial and technological revolutions have introduced environmental impacts which are adversely affecting the planet’s natural resources and environmental sustainability. Modern-day humans are exposed to environmental and dietary influences for which we are not physiologically adapted resulting in an epidemic of non-communicable diseases. The modern medical paradigm pursues treatment of disease and symptoms. Significant progress could be made in preventing non-communicable diseases by diverting more resource to promoting healthy lifestyles and sustainable dietary interventions. Industrial and agricultural practices which lead to environmental degradation also adversely affect human health. While the economic progress of the last couple of centuries has undoubtedly had beneficial effects on lifespan, food security, and living standards, we are now faced with unintended socioeconomic and environmental pressures. Human and planetary health are inextricably linked. This paper provides an overview of the interactions between the environment, food, and human health.

This review was synthesised by literature search of published articles.

Sunlight is the renewable energy source that drives life on our planet. Without sunlight, life as we know it is unlikely to have evolved. Sunlight provides the energy for climate, and the environments that exist. The interaction between sunlight, plants, and animals fosters a healthy soil environment, which is an important source of the nutrients which are present in plant and animal food. It is a virtuous cycle where healthy soil leads to a healthy environment, and nutritious food. This is the planet’s “natural capital”, and it is not inexhaustible [1].

Fossil fuels are stored solar energy in the form of decomposed plant and animal life, mostly dating from the Carboniferous period, around 300 million years ago. They take millions of years to form and are in practical terms non-renewable, and finite in quantity. The industrial revolution, which began in about 1760, was when the harnessing of energy from the environment began to stimulate rapid economic growth, and an improvement in living standards. World population has grown from 757 million in 1750 [2] to 8.23 billion today but the rate of population growth is declining [3]. Global fertility has fallen below replacement rate [4], and the population will start declining likely between 2060 and 2100 [3]. Global fossil fuel consumption and CO2 emissions started accelerating at the beginning of the 20th century and have grown dramatically during the second half of the 20th century [5]. There is irrefutable evidence that global warming has occurred in the last 50 years, and that this correlates with increased fossil fuel use and global CO2 emissions [6].

The evolution of modern humans is thought to have begun about 4 million years ago, with Australopithecus Afarensis [7]. Since then, there have been numerous Hominin species, some of which became evolutionary “dead ends” [7,8]. During this period, about 1 million years ago, a major evolutionary stimulus was the ability to control fire, and thus the ability to cook food, increasing its nutrient availability. This is hypothesised to have resulted in rapid brain growth and shortening of the gut [9]. Homo sapiens emerged about 300,000 years ago and lived in parallel with Neanderthals and Denisovans until around 20 - 40,000 years ago when these two species died out. Modern humans contain about 2% of Neanderthal DNA, and Australian aboriginals contain about 5% Denisovan DNA [10].

The agricultural revolution, which began about 12000 years ago, the start of the Neolithic period, can be viewed as another major evolutionary stimulus. It marked a turning point in human cultural evolution, with establishment of towns, cities, and civilisations. Along with these came trade, transportation, and wars.

The change from a hunter-gatherer to an agrarian society ushered in the first chronic non communicable diseases such as degenerative arthritis and dental caries. These diseases coincided with the change in dietary patterns and physical activity. The industrial revolution, which began in around 1760, could be regarded as another major evolutionary stimulus. Since this time there has been a steady increase in chronic non-communicable diseases, which has accelerated since around 1990 [11]. Life expectancy in high income countries increased until 2019 due to better treatment of both communicable and non-communicable diseases but has decreased since [12]. However, many of the years of life gained are spent in chronic ill health resulting in social, economic, and health expenditure burdens [13]. Modern treatments are extending life, but not improving health, because they address disease and symptoms, rather than cause and process. What are the causes of this epidemic of chronic non communicable diseases? The answer lies in the mismatch between human evolution, and diet and environment. This paper provides an overview of the evolution of human diet, and how the modern western diet, agricultural, industrial and environmental influences lead to the disruption of health at a cellular level.

Human diet

The evolution of human diet: In 1973 Theodosius Dobzansky, evolutionary biologist, said “Nothing in Biology Makes Sense Except in the Light of Evolution" [14]. To provide a basis for this summary of food, agricultural, environmental and economic influences on human cellular and metabolic health it is logical to start with a brief review of the evolution of human nutrition.

The first primates emerged about 65 million years ago, with the human lineage separating from apes about 8 million years ago [15]. At this time, human distant ancestors were tree dwellers, eating a plant diet, rich in fruits (containing fructose). About 15 and 9.8 million years ago two mutations occurred in hominin and great ape ancestors which silenced the uricase gene [16]. Uricase breaks down uric acid, which is a metabolite of purines (from proteins), and more importantly in this context, fructose. In times of plenty this lack of uricase conferred an evolutionary advantage [17], with the fructose and uric acid inducing insulin resistance and fat storage [18]. Excessive fructose, which is prevalent in the modern western human diet plays a pivotal role in the current epidemic of obesity and metabolic disease, and this will be discussed further in section 4.

The Homo genus evolved between three and two million years ago. These ancestors were primarily gatherers eating an 80% plant, 20% animal diet [15]. Over the course of the next million years the diet became more omnivorous, with meat provided by passive and active scavenging [8,19,20] This period was accompanied by the development of larger bodies and brains, reduced tooth size and jaw strength, and shortening of the gastrointestinal tract, and likely correlates with the use of tools and fire to make nutrient extraction from food more efficient (The Expensive Tissue Hypothesis) [9,19]. Active hunting became established, and the hunter-gatherer way of life prevailed. Homo sapiens, the modern human is considered to have emerged in Africa around 300,000 years ago [20].

Humans evolved as omnivores, being food generalists. They survived in different conditions and geographical locations by consuming a wide variety of animal and plant foods, often with seasonal availabilities. They were well adapted to this way of life. The hunter-gatherer way of life has covered approximately 99% of human evolution, and farming has covered 1%. By 1500 AD hunter-gatherers made up about 1% of the world’s population of around 425 million [15].

History can inform us of the consequences of variations of the diet provided by farming. The ancient Egyptians (approximately 5000 to 3500 years ago) ate a heavily (Emmer) wheat based Lacto-Ovo-Vegetarian diet. As a result of their cultural practice of mummification of their dead, Paleopathologists have been able to study ancient, preserved cadavers. Striking findings were the very high incidence of arterial atheroma and early death, and dental attrition and caries [8]. The latter is thought to have been caused by residual sand used to enhance grinding of the flour used in bread. The atheroma is especially interesting, as it likely points to an effect of a high carbohydrate diet, without confounding influences such as smoking and industrial seed oils, of which more will be discussed in section 4. In addition, statuary of the time shows abdominal obesity and gynaecomastia in males, indicative of insulin resistance, and the effects of the phytoestrogens in the heavily plant-based diet [8].

Farming remained the dominant means of providing food, albeit with some geographical inequalities. Starting in the mid 1800’s, important socio-cultural-economic-political influences began to shape the Western diet, and this has contributed to the modern-day epidemic of chronic non-communicable diseases. In 1863 a temperance reformist, Ellen G White founded the Seventh Day Adventist church. She promoted abstinence from alcohol, and a vegetarian diet, amongst other lifestyle advice [21]. A key acolyte of hers was John Harvey Kellog, who gained his medical degree in 1875. Together they established the Battle Creek Sanitarium, where Kellog developed dry breakfast cereals [22] which are common breakfast foods today. They are a source of refined carbohydrate and sugar and contribute to insulin resistance. Adventists have influenced food policy throughout the 20th century and continue to do so [23]. The Seventh Day Adventist Church owns Sanitarium, a company established to produce and promote plant based “health foods”. Are plant-based foods healthier? The answer is “not necessarily”, but there is context to this, and it will be discussed below.

During the first half of the 20th century in the USA deaths from coronary heart disease were elevating alarmingly [24]. This led to a concerted research effort to establish the cause. The hypothesis was that dietary saturated fat and serum Low Density Lipoprotein-Cholesterol (LDL-C) were the culprits, the “Diet/Heart Hypothesis” [25]. Recent literature has confirmed that dietary saturated fat consumption is not harmful [26,27]. The question around serum LDL-C is more nuanced, but meta-analyses have established that the cardiovascular and mortality benefits of LDL-C lowering drugs are pleiotropic [28], and unrelated to the lowering of LDL-C [29].

Despite there being no evidence to support the “Diet/Heart” hypothesis at the time [30] the US introduced dietary “goals” in 1977, and dietary guidelines in 1980 [31], and many countries have since followed [32,33]. These US guidelines condemned dietary saturated fat and recommended a diet consisting of 55%-60% carbohydrate and industrially produced polyunsaturated oils (seed oils) [34] instead of saturated fat. Re-evaluation of trials from the 1960’s and 1970’s has revealed that substituting saturated fat with seed oils in the diet results in increased cardiovascular mortality [35,36]. Many international guidelines are similar to the US guidelines in their recommendations [32]. The processed food industry has embraced these guidelines, and over 50% of the “Standard American Diet” is now comprised of Ultra-Processed Foods (UPF) [37,38]. Production of these foods has required manipulation of agricultural practices to optimise yield at the expense of nutrition, to the benefit of agricultural companies [23]. The results can be seen in the epidemic of chronic non-communicable diseases that now prevails. The pharmaceutical industry benefits from the downstream paradigm that is embraced by the medical fraternity, which is focussed on treating disease and symptoms rather than looking at cause, process, and prevention. Much of the triumvirate of environmentally harmful agricultural practice, UPF food production, and pharmaceutical interventions are driven by vested interests [39-42] and pursuit of profit, with little or no regard for health or the environment. The socioeconomic and environmental costs are not sustainable and will be discussed later in the paper.

What is the best diet for Humans?

We know from evolutionary studies how human nutrition has served our ancestors for the 99% of our existence before the agricultural revolution [15]. This is an omnivorous, nutritionally dense diet, eating seasonally available foods which are available in the local environment [43,44]. Importantly, UPF foods are absent, as is added sugar. We know from Paleoanthropology that humans were healthy on this diet [15], whereas the ancient Egyptians on a Lacto-Ovo-Vegetarian diet were unhealthy [8].

However it is obtained, a healthy diet should provide adequate amounts of proteins with the essential amino acids, micronutrients, vitamins, essential polyunsaturated fats, and energy in the form of carbohydrate or fat. It should be noted that carbohydrate is not an essential nutrient [45]. The small amount of glucose that is required for brain metabolism can be synthesised in the liver by gluconeogenesis. Our hunter-gatherer ancestors would likely have existed in a state of nutritional ketosis, obtaining most of their energy from dietary saturated fat, and to a lesser extent, protein. For optimum health, essential dietary nutrients should be readily bioavailable. Fasting insulin levels should be low.

Interest in diets has grown in recent years both for medical researchers and the public. This is undoubtedly fuelled by the worsening of population metabolic health. Another stated reason for dietary change is to help the environment. In the USA, and other “Western” societies, approximately 70% of the population is overweight or obese, with 40% being obese (as measured by body mass index) [46]. In the USA 88% of the population has at least one clinical feature of metabolic syndrome (central obesity, dyslipidaemia, hypertension, elevated fasting blood glucose) [47]. There are many dietary strategies aimed at reducing overweight and obesity and improving metabolic health, and some of these will be reviewed. Common to most is the elimination of UPF food and restriction of added sugar. It should be noted that UPF food and sugar are addictive [48], and so transition to a “real food” diet involves behavioural changes that many patients find difficult. Changing from an unhealthy diet to a healthy one is a lifestyle change, not a short-term project, with many psychosocial influences [49-51]. Failure rates for sustained weight loss are high [52]. Some of the commonest diets aimed at improving metabolic health, and for weight loss will now be reviewed.

• The Blue Zones [53]: The Blue Zones are five areas in the world which have been noted to have an unusually high number of centenarians. The diets in these five zones are quite varied, but all contain some meat and fish, and some contain dairy and eggs. All contain legumes, a source of vegetable protein. None contain UPF foods or seed oils. However, diet is not the only determinant of longevity. Lifestyle practices in common are:
• movement and physical activity in daily life,
• sense of purpose in life,
• lowering stress by meditation, prayer, naps, or spending time in nature,
• avoiding overeating, eat until 80% full,
• strong social connections and participation in social activities,
• strong family and social relationships,
• Plant based diets: The epidemic of chronic non-communicable diseases has encouraged interest in plant-based diets as being optimal for health and the environment. In most cases the term “plant based” refers to a vegetarian or vegan diet, with no animal food content. Some “vegetarian” diets will include eggs, dairy, fish, or “occasional” meat. These ideas have been amplified by the media, healthcare professionals, and the educational system [54]. Interests are quite “tribal”, with meat and livestock lobbies making claims for nutritional and environmental benefits which are not evidence based, and in many cases promoted by vested interests [23,54]. It is timely to remind readers of the evolution of human nutrition. Ninety nine percent of human evolution has relied on an omnivorous diet to optimise metabolic health [15]. It hardly seems logical that we should now switch to a diet that excludes animal foods, which are the most nutritionally dense and complete. Plant based diets have been demonstrated to be effective for weight loss when compared with an ad-libitum diet for example by Najjar RS, et al. [55], but this paper does not mention UPF or added sugar. It should be noted that almost any diet that excludes the UPF and added sugar in the Standard American Diet may result in weight loss and improved metabolic health [56]. Exclusion of UPF from diets usually results in a reduction of caloric intake. This may be sufficient to account for the weight loss, but there is likely to be some effect from the alteration in energy usage at the mitochondrial level, and this will be discussed in section 4.

When considering plant-based diets for humans it is important to assess their completeness in nutritional terms [57]. Even a high protein plant food such as soy does not achieve as high a Digestible Indispensable Amino Acid Score as animal foods. For example, leucine [57], which acts as a signal for mTor activation and muscle anabolism is less bioavailable from soy compared with beef. This can be corrected by increasing the amount of soy ingested, but this comes at the cost of increasing carbohydrate and energy consumption with undesirable effects on insulin sensitivity. There is some concern that plant constituents such as lectins, oxalates, phytates, and tannins can act as “antinutrients”, impairing absorption of micronutrients such as iron, zinc and copper. The evidence that this is clinically important in a varied diet is not conclusive [58]. A vegan diet is lacking or deficient in vitamins B12, B3, B2, D, and zinc, calcium, potassium, and selenium [59,60]. Supplementation is required for optimum health when a vegan diet is being followed, and for some vegetarian diets.

So, is a plant-based diet better for human health? Compared with the Standard American Diet the answer is “maybe”, if Ultra-Processed Foods (UPF), seed oils, and excessive added sugar are excluded, and supplements are included. Is a plant-based diet optimum for human health? The “lens of evolution” would suggest not.

• Meat: Is it healthy, does it cause cancer?: The message that meat is unhealthy and that meat consumption is associated with increased non-communicable disease and cancer risk is promoted both in medical literature and mainstream media. This is an example of “an assumptive close” [61], a sales technique in which the salesperson “assumes” that the potential purchaser has already agreed to buy. In fact, the evidence for these assertions regarding meat is inconclusive at best. This is a highly polarised debate with intense lobbying from both the “plant based” and “livestock” ends. The debate intermixes science, health, the environment and climate, agriculture, and economics. Making sense of the debate is difficult, as arguments are often confounded by bias and lobbying from both sides [62]. Space precludes a detailed analysis in this paper, but Jayne Buxton’s “The great plant-based con…” [23] is well researched and provides good perspective. Is it “biased” towards livestock? Yes, but it is well referenced.

The focus of this section is on the health aspects of meat. The next section will look further at the livestock industry’s effect on the environment. Let us once again invoke “the lens of evolution”: if 99% of human evolution included animal food in the diet, common sense would suggest that human physiology is adapted to and is optimised to use the nutrients in meat. If meat causes cancer, as is proposed in some sources [63], a likely evolutionary response would have been a shift away from meat in the diet.

Population based human nutrition studies rely on epidemiological and observational data [54]. This type of research is confounded by recognised methodological challenges such as food frequency questionnaires [64], and the impossibility of controlling all variables. It can reveal associations but not causation and is useful for providing hypotheses to be tested by controlled research. Meta-analyses of epidemiological research do not negate these challenges [65].

The meat and cancer message was ignited by a WHO report “Carcinogenicity of consumption of red and processed meat” in 2015 [66]. The conclusions of this report cannot be justified based on the references. The data are epidemiological, use food frequency questionnaires, do not control for meat processing and cooking methods, and do not account for other elements of diet. Rodent laboratory studies in the references used 1,2 dimethylhydrazine [67] or azoxymethane [68] known carcinogens, as adjuvants. A well composed critique of the laboratory evidence used is contained on Dr Georgia Ede’s website [69]. Earlier studies, not included in the WHO references found no connection between red and processed meat and cancer [70,71].

The pro-plant, anti-meat message was amplified in 2019 by the EAT Lancet report, [72]. This was a wide-ranging report advocating a plant-based diet for health, and plant-based agriculture for the environment. The evidence presented for the health and agricultural benefits did not meet expected rigorous methodological standards [73,74]. The conclusions are contested by other scientists [75]. Of concern is the objective of transforming the global food system by “sound science, impatient disruption, and novel partnerships”. The soundness of the science is questionable. Impatient disruption refers to changing laws, fiscal measures, subsidies and penalties, trade reconfiguration, and other economic and structural measures. The “novel partnerships” refers to Food Reform for Sustainability and Health (FReSH) [76], a global partnership of 36 corporations (FReSH, p22), two thirds of whom produce fertilisers, pesticides, processed foods, or food flavourings and additives. The motives expressed in the FReSH information booklet are laudable [76], but closer examination of the parties involved reveals potential vested interests. Is EAT-Lancet a good scientific paper? Is it a covert political and economic manifesto? Readers should look at the evidence and make their own decisions.

So, is meat good for us or bad for us? It seems that there is no evidence that it is bad for us [71,72]. Our 70 billion [15] or so omnivorous hunter-gatherer ancestors who evolved our physiology prior to the agricultural revolution included animal foods in their diet. It does not seem logical that we should now exclude them.

• Mediterranean, Paleo, and DASH diets: The word “diet” is derived from the Greek word “daita”, meaning “way of life”. Both Mediterranean and Paleo “diets” incorporate movement, social interaction, sleep, and living in harmony with the circadian cycle [77] all of which are featured in the blue zones.

Mediterranean diet: The Mediterranean diet succeeds the agricultural revolution. It varies depending on region of the Mediterranean. It is predominantly plant based and seasonal, but does include fish, poultry, dairy, red meat, and red wine [78]. The traditional Mediterranean diet contains no UPF [77], whereas the modern Mediterranean diet does include some refined foods such as pasta. The diet does exclude saturated fats. This is not harmful but is not necessary as saturated fats are no longer considered to be associated with increased disease risk [26]. Health benefits from the Mediterranean diet include improved insulin sensitivity, reduced oxidative stress, and reduced inflammation, with protective effects against numerous chronic non-communicable diseases [79].

Paleo diet: In contrast to the Mediterranean diet, the “Paleo” diet attempts to mimic the diet of our hunter-gatherer ancestors who lived prior to the agricultural revolution. The modern “Paleo” diet includes lean meats, fish, fruit, vegetables, nuts, and seeds. Grains, legumes, dairy, UPF, refined sugar and salt are excluded [80]. It is not possible to know how close this is to an ancestral diet. It emphasises lean meat, and omits the fat obtained from bone marrow and offal, which our ancient ancestors were known to eat. Positive results in treating metabolic syndrome have been reported, compared with “4 control diets based on national nutritional guidelines” [81].

The DASH (Dietary Approaches to Stop Hypertension) diet [82]: The DASH eating plan includes vegetables, fruit, whole grains, fish, poultry, beans nuts, and limited added sugar. Apart from the added sugar, this is all healthy. However, the DASH eating plan does not exclude vegetable (seed) oils, and recommends limiting fatty meats, full fat dairy and tropical oils. It recommends fat free or low-fat dairy products, which are typically higher in sugar than full fat options. These aspects are all unhealthy. The DASH eating plan therefore contains contradictions but is nevertheless healthier than the Standard American Diet. The DASH diet has a small positive effect on blood pressure [83]. Overall, while it is an improvement on the Standard American Diet, it is not a good diet for optimal human health.

• The vegan diet: The vegan diet excludes all animal foods: meat, fish, eggs, and dairy. While it can assist with weight loss in the short-term, long-term veganism will lead to nutritional deficiencies in vitamins B12, B3, B2, D, and zinc, calcium, potassium, and selenium [84]. Abandonment of the diet has been reported to be 84% [85]. Long term followers of a vegan diet will need to take dietary supplements to prevent adverse health consequences. A good “natural” source of the nutritional ingredients missing from the vegan diet would be cricket flour [86].
• The carnivore diet: Between 1906 and 1918, anthropologist Vilhjamar Stefansson spent time with the Inuit in Canada, eating the Inuit diet (mostly fish) exclusively [87]. His health remained good. In the 1920’s he, and a colleague, Karsten Anderson, undertook a medically supervised one year experiment of a carnivore diet (mostly meat), and both remained healthy [88]. The results were published by the supervising physician Dr. Cecil Lieb [89].

There are many examples of cultures leading healthy lives on carnivore diets [90]. Carnivore diets had been advocated by some doctors since the late 1700’s for treating diabetes and recent studies have shown positive outcomes [91] for metabolic health. It should be noted that for a carnivore diet to be healthy, it should contain animal fat, and ideally bone marrow, offal, and brain. Some carnivore cultures such as the Masaai also include milk and blood, and other variants include eggs and cheese.

There is potential for nutrient deficiencies with some carnivore diets, particularly where all the meat is lean.

• Diets for weight loss: Obesity is caused by excessive carbohydrate and fat consumption, both of which are features of the Standard American Diet. Both carbohydrate (4 Kcal/g) and fat (9 Kcal/g) are macronutrients which provide energy, and if they are consumed in excess of the body’s energy requirements, the excess energy is deposited as adipose, leading to weight gain. A proportion of the adipose deposition is in visceral fat, and as this expands a chronic systemic inflammatory stimulus evolves [92].

Calories in-calories out: Calories are a measure of the thermal energy produced by burning a substrate in a bomb calorimeter [93,94]. While this does inform us of the thermal energy value of foods, it does not allow for differences in metabolic processing of dietary ingredients. For example, glucose and fructose both provide 4 Kcal/g, but are metabolised differently at a mitochondrial level, producing different cell signalling outcomes (see section 4). In general, lowering energy intake will result in weight loss in the short term, but also promotes lowering of basal metabolic rate, and energy conserving physiological changes. Hunger and poor adherence are usual, and this type of diet is unsustainable, with regaining of weight on discontinuation [95].

Low-carb vs low fat: There have been many comparisons of low-carb vs low fat diets. Unfortunately, there is no standardisation of the carbohydrate and fat intakes [96], but meta-analyses show that low carb is more effective in the majority of cases [97]. Concerns have been raised about the safety [98] and nutritional adequacy of low-carb diets. These concerns have been allayed by recent research confirming that there is no adverse health impact of the increased dietary saturated fat in low carb diets [98]. Volek JS, et al. [99], as well as recommending standardisation of terminology, have confirmed that a well formulated low carb diet is nutritionally adequate [98,99]. Low carb diets are effective in reducing cardiovascular risk factors, HbA1c, fasting insulin, serum triglycerides, and raising HDL [98]. Low carb diets may result in elevation in LDL-C, especially in lean, metabolically healthy individuals (Lean Mass Hyper Responders). Research by Budoff M, et al. [100] has confirmed that this is not associated with cardiovascular plaque formation.

Time restricted feeding and intermittent fasting: Once again, “the lens of evolution” should inform us. Our ancient Homo sapiens ancestors ate a diet rich in meat and saturated fat, along with some plants, and would likely have had periods of fasting. Diet and environment were matched, and our physiology evolved accordingly. Fasting is practised by modern cultures, without adverse effects. It can be a helpful stratagem for lowering fasting insulin levels in treating obesity [101].

Environmental pollutants and microplastics: Industrialisation has resulted in the introduction of millions of chemicals into the environment, either inadvertently, or intentionally. Examples are asbestos, hexavalent chromium, tobacco smoke, radon, benzo(a)pyrene, pesticides, dioxins, furans, Polychlorinated Bisphenols (PCB’s), arsenic and disinfectant by-products, vinyl chloride, and benzene [102]. Per- and Polyfluoroalkyl Substances (PFAS) [103] are synthetic chemicals used in household and industrial applications, for example cookware coatings, stain resistant fabrics, food handling, fire fighting foams, flame retardants, electroplating, and paints. PFAS are known as “forever” chemicals, because to-date there is no natural or synthetic means of neutralising them. However, recent research does show some promise in neutralising PFAS in the future [104,105]. Another study demonstrated that human gut bacteria accumulate PFAS [106]. Whether these findings result in clinically or environmentally useful outcomes remains to be seen. A better approach would be to reduce or eliminate the exposure. Fine particulate matter air pollution (PM2.5) [107] has been associated with increased risk of cardiopulmonary diseases. In addition, PM2.5 induce oxidative stress, inflammation and immune responses, as well as causing gene disruption [108] and reduced insulin sensitivity [109]. In most cases chemical release into the environment has happened without any thought or awareness that there may be environmental or health consequences. Environmental chemicals may be implicated in causing or exacerbating many modern- day diseases: obesity (“obesogens”), diabetes,  infertility, testicular dysgenesis syndrome, testicular cancer, poor semen quality, ovarian dysgenesis syndrome, neurodegenerative disorders, respiratory diseases, autoimmune diseases, obesity, cardiovascular disease, neurodevelopmental disorders, cancers, and multimorbidity syndromes [110,111].

Pollutants may also have epigenetic, and thus transgenerational adverse effects [112]. The ubiquity of chemicals in the environment makes it difficult to ascribe causation in disease to any single one. While dose-response effects for individual chemicals can be established in a laboratory setting, the effects of chronic low dose exposure [113], exposure to multiple chemicals, and interaction with other environmental and lifestyle factors confuses the picture [102].

Microplastics and soil: Microplastics are plastic particles between 1µ and 1mm in size, nanoplastics are less than 1μ in size, and mesoplastics are between 1 and 10mm in size [114]. Primary microplastics are small plastic particles intentionally used in products such as cosmetics, cleaning products, industrial abrasives [115] and agrochemicals [116]. Secondary microplastics are produced by the degradation of plastics in the environment by ultraviolet radiation, oxidation, wave action, and mechanical shear [115]. Examples of microplastics are polypropylene, polyethylene terephthalate, polyvinyl chloride, polyethylene, high density polyethylene, low density polyethylene, polyamide, and polystyrene [115]

Microplastics are found in food packaging and food contact articles and have been detected in a variety of foods and beverages [114,117] as well as in the air we breathe [118]. Microplastics can enter the food chain from an agricultural setting where they are generated from sewage sludge (from wastewater treatment plants), compost, mulch, controlled release fertilisers, and manure and greenhouse products [116]. Microplastics can interact with heavy metals in the environment, with potentially ecotoxic effects [119]. Microplastics in the soil can adversely affect the nutrient cycle and stability of the soil ecosystem, which in turn can affect plant growth, fauna, and the human microbiome [120]. A recent study demonstrated that edible plants can incorporate nanoplastics into internal plant tissues [121]. Phytoremediation, bioremediation, and microbial degradation to reduce the environmental impact of microplastics in soil are being investigated [115].

Microplastics and human health: Microplastics can enter humans by ingestion in foodstuffs, dermal contact [115], and inhalation [115,118]. It has been estimated that humans ingest 0.1-5g of microplastics per week [115]. This may result in dysbiosis and systemic health effects [122,123]. Ingested and airborne micro and nanoplastics may translocate via blood or lymph [118] and are implicated in interference with metabolic, endocrine, immune and developmental pathways [115]. There is evidence that microplastics act at a cellular level, causing mitochondrial dysfunction, oxidative stress, endoplasmic reticulum stress and potentially, apoptosis [115,124,125]. All organ systems may be affected [115]. New protocols for isolating and measuring microplastics of different shapes and sizes are being developed, and this will assist in future research to elucidate the effects on human health [126].

Agriculture, climate change, and sustainability: There is considerable media and policy pressure to move agriculture and diet towards a plant-based future, for example in the EAT Lancet report [72]. In this context it is interesting to note that CO2 emissions from land use are virtually unchanged since the middle of the 19th century. The overwhelming majority of the increase in CO2 emissions and global warming has resulted from the burning of fossil fuels [5,6]. This data alone should be sufficient to push the debate on strategies for reducing emissions away from agriculture to where the real problem lies, namely the burning of fossil fuels. While there is a realisation that more of the global energy supply needs to be from renewable sources (including perhaps nuclear fusion in due course [127]), progress is slow and uneven. Developing nations in particular need energy to support the economic growth that is needed to eliminate poverty and raise living standards [127].

That said, let’s examine the two sides of the plant based versus livestock debate.

The livestock argument: Plant based advocates single out methane production by livestock as a major contributor to global warming. This argument is based on flawed methodology which overestimates the long-term effect of animal methane emissions [128]. While it is true that methane is a greenhouse gas, it is short-lived (12 years) in the atmosphere compared with CO2 (hundreds of years). Atmospheric methane breaks down into CO2 and water. While the CO2 results in a warming effect, it can also be recycled by plant photosynthesis, and consumed by animals, producing animal-based food. This is the biogenic methane cycle [128-131] which has existed for as long as ruminant animals have existed, and it does not contribute to global warming so long as the animal herd and the CO2 sink of the plants the animals eat are in equilibrium [128,130-132]. Over the past 250 years the US has not added to its biogenic methane emissions. The US cattle herd is approximately 100 million. Prior to western settlement there were approximately 60 million bison, and 40 million longhorn sheep [131] which the settlers decimated, so in broad terms there is equilibrium. It should also be noted that animal grazing occurs mostly on the 65% of agricultural land that is not suitable for arable [131]. Methane produced by burning fossil fuels is outside the biogenic methane cycle and does indeed add to global warming if the resulting CO2 exceeds the CO2 sink provided by vegetation.

The plant-based argument: The argument that a vegan diet is optimum for human health does not accord with evolutionary or scientific evidence. On the other hand, a plant-based diet that includes some animal foods is consistent with good health. Let’s examine the environmental and climate impacts of a plant-based future. Since only a third of agricultural land is suitable for cropping [131] increasing the supply of plant food requires increasing land availability by deforestation (this applies to grazing too) [132,133] or making better use of the available cropping land. The pursuit of increased crop and commercial yields can lead to monocropping and soil exhaustion [134], reduced yield, reduced nutritional value of crops, loss of biodiversity, and loss of topsoil from erosion [135,136]. Different crops have different climate and environmental impacts eg rice and wheat, although all crops remove carbon from the atmosphere by photosynthesis. Soil management, crop rotation, and regenerative farming practices [135-138] can maintain the health of agricultural land. There is certainly scope to improve the nutritional efficiency of crops by replacing crops used for biofuels (such as sugar cane and corn), and crops which contribute to obesity and metabolic illness (sugar cane and wheat), with crops with better nutritional benefits such as legumes and green vegetables. Changing people’s eating patterns is another matter.

Food loss and waste: Food waste contributes between 6 and 10% of global CO2 emissions [139-141] which is three times as much as global aviation [141]. Food loss and wastage occur at various points along the supply chain: production, storage, processing and packing, retail and distribution, and consumption [139,142]. Measures can be taken at each of these stages to reduce food waste. Limiting food waste could lower consumption of resources such as water and nitrogen, and significantly contribute to hunger eradication in developing countries, as well as limiting global CO2 emissions [139]. Strategies for recycling food waste to produce energy, biofuel, animal feed, and materials are being investigated [143].

Health impacts of diet, pollutants and obesogens: Obesity and the chronic non-communicable diseases that are associated with it have increased dramatically since about 1980. While this may be the result of the amounts and types of foods that are consumed, during this period, there has also been a marked increase in man-made chemicals in the environment. It has become evident that these chemicals have become inadvertently incorporated into the food chain and are also involved in the obesity epidemic [112].

Carbohydrates and fatty acids from food are metabolised by the mitochondria to produce energy in the form of ATP that is used to drive cellular functions. Oxidative phosphorylation occurs in the mitochondrial matrix to produce NADH. The NADH donates electrons to the electron transfer chain on the inner mitochondrial membrane, with the protons passing into the intermembrane space, creating an electrochemical gradient. The protons pass back into the matrix via complex 5 (ATP synthase), producing energy as ATP [144]. The energy production process generates Reactive Oxygen Species (ROS). In a healthy state some of the ROS act as signalling molecules, with the remainder being neutralised by the mitochondrial antioxidant mechanisms [145].

Excessive fuel (food) intake, and some food items in the Western Diet such as excessive fructose [17] (contained in added sugar, and high fructose corn syrup), and excessive linoleic acid (often oxidised by cooking and storage), contained in industrial seed oils [34] cause mitochondrial dysfunction. Fructose, which is metabolised in the liver downregulates ATP production, upregulates de-novo lipogenesis, increases uric acid production, and inhibits autophagy [17]. Excessive linoleic acid in the diet is pro-inflammatory [34]. Oxidised linoleic acid causes remodelling of the cardiolipin in the inner mitochondrial membrane, reducing the efficiency of the electron transfer chain [34]. The result is oxidative stress. Linoleic acid consumption has risen from 2.2g per day in 1865, to 29g (11.8% of energy consumption) in 2008 [34].

Interest in the causal role of environmental chemicals in obesity and chronic diseases has developed in the last few years [112,146]. Integrating the knowledge of food metabolism and the biological effects of environmental chemicals into a unified theory of obesity makes sense [147]. The causality of obesity is complex and multifactorial and includes epigenetic changes and multigenerational transferability [112].

Lustig RH, et al. [148] propose an integrated theory of obesity which includes four models:

• The energy balance model
• The carbohydrate – insulin model
• The energy reduction – oxidation model
• The obesogen model

The energy balance model proposes that food intake exceeds energy requirements, and that is due to the dysregulation of the neural control of appetite and eating. UPF are addictive [48,149] and play a key role. However, the evidence does not wholly explain how the energy balance model alone would account for the increase in obesity.

The carbohydrate-insulin model proposes that excessive refined carbohydrate in the diet causes increased insulin secretion, resulting in excess adipose deposition, decreased lipolysis, and insulin resistance. Normalising fasting insulin and reducing insulin spikes in low-carb diets is effective for weight loss, but this diet also excludes other UPF. Again, this model alone is not sufficient to account for the increase in obesity.

The energy reduction–oxidation model centres on the signalling functions of ROS in the regulation of insulin secretion, gluconeogenesis, fat storage and appetite. Excess nutrient and UPF food consumption, and exposure to obesogens can all lead to increased ROS production. High levels of ROS can also cause mitochondrial and cellular lipid peroxidation, protein denaturation and epigenetic changes.

The obesogen model incorporates the role of environmental chemicals (see section 3, above) in the food chain into the mechanisms of obesity. These chemicals disrupt cellular signalling pathways that regulate energy intake and expenditure, nutrient management, and adipose deposition, as well as causing epigenetic changes which can affect metabolic processes intergenerationally [112,147].

The integrated model proposes that obesogens, acting in utero, during development, and later in life, interact with excessive fuel intake, and UPF to alter cellular redox balance and cell signalling. The hypothesis is that all of these influences contribute to the causation of obesity.

Reversing obesity, environmental pollution and climate change: Although at first glance obesity, environmental pollution, and climate change appear to be separate issues, this paper illustrates how they are inextricably interconnected. We live in a complex capitalist society with global inequalities in wealth, nutrition, medical care, and other amenities. Relentless economic growth is the accepted objective of all nations. Perhaps this is another “assumptive” close? A simple logical argument would suggest that if economic growth progresses by using non-renewable resources which adversely affect the environment and climate, eventually humanity may not survive. The earth will not care.

Human societies’ priorities are short term: economic growth, employment, health care, defence, transport and communications, among others. Industry provides the revenue, through taxes, for governments to address these priorities. Industries make profits for their owners and shareholders. Changes to the environment and the climate occur over decades, with consequences that can remain “sub threshold”, akin to “boiling the frog slowly”. When these changes do become evident, as they have now, they force new priorities into an already crowded, and resource limited milieu. The evolutionary pressures that we have created will take hundreds or thousands of years to manifest. Is there a risk of human extinction?

This puts governments in a bind, an example of a “wicked problem” as described by Rittel HWJ, et al. [150]. For example, it is evident that government food guidelines are not fit-for-purpose and are contributing to the epidemic of non-communicable diseases, which is creating unsustainable health care costs. The solution seems obvious: abandon the current guidelines, and institute new ones promoting healthy, organic, unprocessed foods. But many people have never learned the ability to create a meal from real food items, and healthy food options are typically more expensive. Many people enjoy eating UPF and are addicted to them. If policies to limit UPF are introduced, what happens to the UPF companies that provide employment and tax income? And what happens to agriculture and the industries that support them? Clearly, they would have to change and adapt, but potentially at a financial cost. The lobbying against change would be intense, and because of the political and financial costs, will not happen quickly.

Meaningful changes can be made by health practitioners taking an upstream and preventive approach to healthcare, emphasising dietary and lifestyle habit change instead of, or in conjunction with, pharmacological intervention. This would necessitate some changes in pre and post-graduate medical education. Small, stepwise changes can be made to dietary guidelines. Legislation against advertising ultra-processed foods in the media and banning UPF sponsorship of sports would be viable first steps [151]. It worked for tobacco. Taxation of unhealthy foods is an option, and taxation of Sugar Sweetened Beverages (SSBs) has been instigated in many countries with some success [152].

Regarding agriculture, the livestock and plant-based debate is certain to be prolonged. Considering human evolution, it is likely that the best diet for humans does include some animal foods. The optimum amount of animal food is yet to be definitively determined. It may not be very much but will depend on the nutrient balance of the rest of the diet. It is possible that non-meat products such as insects [cricket] [86] could play a bigger part in diet, but the environmental impact of large-scale insect farming would need to be assessed. There should be no argument against animal farming being humane and directed to optimising the nutritional value of the meat. Regenerative farming practices [153] should be promoted, reforestation and revegetation, and ecosystem regeneration or rewilding of environmentally degraded land should be encouraged [154,155]. There are many innovations, using drones, satellite, AI, and new sensors [156-158], that can be incorporated into plant food production and soil health monitoring, which can improve yield and nutrient quality, and reduce waste in the production process. Recycling the cellulose in grapevine pruning’s to make packaging has been reported [159]. This packaging is fully biodegradable and is a promising avenue for future research. Reducing food miles and promoting “Farm to plate” can reduce costs, emissions, and road wear, as well as enhancing food freshness and quality [160].

From a scientific viewpoint, efforts should be made to reduce pollutant chemical and microplastics in the environment. There is good evidence that they affect human cellular processes and health, but this has not been widely accepted in the political sphere. Ultimately it is likely to require legislation, but will undoubtedly face the same lobbying, socioeconomic, and political barriers that confront the changing of industrial food production and marketing.

Progress has been made in curtailing fossil fuel greenhouse gas emissions. Renewable energy from hydro, solar, and wind are the main sources, with biofuels being a smaller proportion [161]. Global warming is still progressing, and the environmental and greenhouse gas implications of extracting the resources for renewable energy infrastructure, as well as lifecycle and recycling of the infrastructure [162] still influence greenhouse gas emissions. Nevertheless, it is important progress and perhaps will be overtaken by nuclear fusion at some time in the future [127].

“If you want to make small changes, change how you do things. If you want to make big changes, change how you see things”, Don Campbell, Canadian rancher [163]. In “The Rational Optimist”, Ridley M [164] trusts in human ingenuity to find solutions to humanity’s problems. We have already identified the problems we face as a society, and solutions are visible. But will we enact the solutions in time?

1. Dean S. We’re still not measuring our reliance on nature as we rush to boost productivity. The Conversation 2025. https://theconversation.com/were-still-not-measuring-our-reliance-on-nature-as-we-rush-to-boost-productivity-263716.
2. Stutz AJ. Modeling the Pre-Industrial Roots of Modern Super-Exponential Population Growth. PLoS One 2014;9:e105291. https://doi.org/10.1371/journal.pone.0105291.
3. Ritchie H, Rodés-Guirao L. Peak global population and other key findings from the 2024 UN World Population Prospects. Our World in Data 2024. https://ourworldindata.org/un-population-2024-revision.
4. Aitken RJ. Population decline: where demography, social science, and biology intersect. Reproduction 2024;168. https://doi.org/10.1530/REP-24-0070.
5. Ritchie H RM. CO2 Emissions 2024. https://ourworldindata.org/co2-emissions.
6. Hannah Ritchie, Pablo Rosado, Max Roser. CO2 emissions by fuel. Our World in Data 2024. https://ourworldindata.org/emissions-by-fuel.
7. Villmoare B, Delezene LK, Rector AL, DiMaggio EN, Campisano CJ, Feary DA, et al. New discoveries of Australopithecus and Homo from Ledi-Geraru, Ethiopia. Nature 2025. https://doi.org/10.1038/s41586-025-09390-4.
8. Eades M. Paleopathology and the origins of the low carb diet. YoutubeCom/Watch?V=bY2v6AnEyuU 2020. youtube.com/watch?v=bY2v6AnEyuU.9   Aiello LC, Wheeler P. The Expensive-Tissue Hypothesis: The Brain and the Digestive System in Human
9. and Primate Evolution. vol. 36. 1995.
10. Tagore D, Akey JM. Archaic hominin admixture and its consequences for modern humans. Curr Opin Genet Dev 2025;90. https://doi.org/https://doi.org/10.1016/j.gde.2024.102280.
11. Ritchie H SF. Burden of disease. Https://OurworldindataOrg/Burden-of-Disease 2021. https://ourworldindata.org/burden-of-disease.
12. Yencken L. Life expectancy is lower in the United States than in other high-income countries 2022. https://ourworldindata.org/data-insights/life-expectancy-is-lower-in-the-united-states-than-in-other-high-income-countries.
13. Ortiz-Espinosa E, Arriagada P, Roser M. Healthcare spending. Our World in Data 2024. https://ourworldindata.org/financing-healthcare.
14. Dobzhansky T. Nothing in Biology Makes Sense except in the Light of Evolution. Am Biol Teach 1973;35:125–9. https://doi.org/10.2307/4444260.
15. Alt KW, Al-Ahmad A, Woelber JP. Nutrition and Health in Human Evolution–Past to Present. Nutrients 2022;14:3594. https://doi.org/10.3390/nu14173594.
16. Johnson RJ, Benner SA, Oliver W. Theodore E. Woodward award. The evolution of obesity: insights from the mid-Miocene. Trans Am Clin Climatol Assoc 2010;121:295–305.
17. Johnson RJ, Lanaspa MA, Sanchez-Lozada LG, Tolan D, Nakagawa T, Ishimoto T, et al. The fructose survival hypothesis for obesity. Philosophical Transactions of the Royal Society B: Biological Sciences 2023;378. https://doi.org/10.1098/rstb.2022.0230.
18. Zhu Y, Hu Y, Huang T, Zhang Y, Li Z, Luo C, et al. High uric acid directly inhibits insulin signalling and induces insulin resistance. Biochem Biophys Res Commun 2014;447:707–14. https://doi.org/10.1016/j.bbrc.2014.04.080.
19. Pobiner B. Meat-Eating Among the Earliest Humans. Am Sci 2016;104:110. https://doi.org/10.1511/2016.119.110.
20. Mounier A, Mirazón Lahr M. Deciphering African late middle Pleistocene hominin diversity and the origin of our species. Nat Commun 2019;10:3406. https://doi.org/10.1038/s41467-019-11213-w.
21. Ellen G White. Flesh Meats (Proteins continued). Counsels on diet and food, Ellen G white Estate; 2018, p. 299–334.
22. Fee E, Brown TM. John Harvey Kellogg, MD: Health Reformer and Antismoking Crusader. Am J Public Health 2002;92:935–935. https://doi.org/10.2105/AJPH.92.6.935.
23. Buxton Jayne. The great plant-based con : why eating a plants-only diet won’t improve your health or save the planet. Piatkus; 2023.
24. Dalen JE, Alpert JS, Goldberg RJ, Weinstein RS. The Epidemic of the 20th Century: Coronary Heart Disease. Am J Med 2014;127:807–12. https://doi.org/10.1016/j.amjmed.2014.04.015.
25. Newport MT, Dayrit FM. The Lipid–Heart Hypothesis and the Keys Equation Defined the Dietary Guidelines but Ignored the Impact of Trans-Fat and High Linoleic Acid Consumption. Nutrients 2024;16:1447. https://doi.org/10.3390/nu16101447.
26. Astrup A, Magkos F, Bier DM, Brenna JT, de Oliveira Otto MC, Hill JO, et al. Saturated Fats and Health: A Reassessment and Proposal for Food-Based Recommendations. J Am Coll Cardiol 2020;76:844–57. https://doi.org/10.1016/j.jacc.2020.05.077.
27. Harcombe Z. US dietary guidelines: is saturated fat a nutrient of concern? Br J Sports Med 2019;53:1393–6. https://doi.org/10.1136/bjsports-2018-099420.
28. Liao JK, Laufs U. PLEIOTROPIC EFFECTS OF STATINS. Annu Rev Pharmacol Toxicol 2005;45:89–118. https://doi.org/10.1146/annurev.pharmtox.45.120403.095748.
29. Ravnskov U, de Lorgeril M, Diamond DM, Hama R, Hamazaki T, Hammarskjöld B, et al. LDL-C does not cause cardiovascular disease: a comprehensive review of the current literature. Expert Rev Clin Pharmacol 2018;11:959–70. https://doi.org/10.1080/17512433.2018.1519391.
30. Harcombe Z, Baker JS, Cooper SM, Davies B, Sculthorpe N, DiNicolantonio JJ, et al. Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review and meta-analysis. Open Heart 2015;2:e000196. https://doi.org/10.1136/openhrt-2014-000196.
31. Davis C, Saltos E. Dietary Recommendations and How They Have Changed Over Time n.d. https://ers.usda.gov/sites/default/files/_laserfiche/publications/42215/5831_aib750b_1_.pdf?v=35952.
32. Herforth A, Arimond M, Alvarez-Sanchez C, Coates J, Christianson K, Muehloff E. A Global Review of Food-Based Dietary Guidelines. Advances in Nutrition 2019;10:730. https://doi.org/doi:10.1093/advances/nmy130.
33. Food and Agriculture Organisation of the United Nations. Dietary guidelines 2025. https://www.fao.org/nutrition/education/dietary-guidelines/background/en/.
34. Knobbe CA., Alexander Suzanne. The ancestral diet revolution : how vegetable oils and processed foods destroy our health - and how to recover! Ancestral Health Foundation; 2023.
35. 35            Ramsden CE, Zamora D, Leelarthaepin B, Majchrzak-Hong SF, Faurot KR, Suchindran CM, et al. Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis. BMJ 2013:1–18. https://doi.org/10.1136/bmj.e8707.
36. Ramsden CE, Zamora D, Majchrzak-Hong S, Faurot KR, Broste SK, Franz RP, et al. Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73). BMJ 2016. https://doi.org/10.1136/bmj.i1246.
37. Wolfson JA, Tucker AC, Leung CW, Rebholz CM, Garcia-Larsen V, Martinez-Steele E. Trends in Adults’ Intake of Un-processed/Minimally Processed, and Ultra-processed foods at Home and Away from Home in the United States from 2003–2018. J Nutr 2025;155:280–92. https://doi.org/10.1016/j.tjnut.2024.10.048.
38. Food and Agriculture Organisation of the United Nations. Ultra-processed foods, diet quality, and health using the NOVA classification system 2019. https://openknowledge.fao.org/server/api/core/bitstreams/5277b379-0acb-4d97-a6a3-602774104629/content (accessed August 21, 2025).
39. Leite FHM, Khandpur N, Andrade GC, Anastasiou K, Baker P, Lawrence M, et al. Ultra-processed foods should be central to global food systems dialogue and action on biodiversity. BMJ Glob Health 2022;7:e008269. https://doi.org/10.1136/bmjgh-2021-008269.
40. García S, Pastor R, Monserrat-Mesquida M, Álvarez-Álvarez L, Rubín-García M, Martínez-González MÁ, et al. Ultra-processed foods consumption as a promoting factor of greenhouse gas emissions, water, energy, and land use: A longitudinal assessment. Science of The Total Environment 2023;891:164417. https://doi.org/10.1016/j.scitotenv.2023.164417.
41. Scrinis G. Ultra-processed foods and the corporate capture of nutrition—an essay by Gyorgy Scrinis. BMJ 2020:m4601. https://doi.org/10.1136/bmj.m4601.
42. Sipelyte R, Metaxa AM. Identification and Predictive Analysis of Revenue Determinants in the Pharma Industry: A Longitudinal Analysis of Financial, Regulatory and Pipeline Data. J Pharm Innov 2025;20:64. https://doi.org/10.1007/s12247-025-09975-6.
43. Sinnett PF, Whyte HM. Epidemiological studies in a total highland population, Tukisenta, New Guinea. J Chronic Dis 1973;26:265–90. https://doi.org/10.1016/0021-9681(73)90031-3.
44. Fettke G. Is it safe to eat real food? The land, the people, the police. 2025. https://www.youtube.com/watch?v=y2286d_t0LE (accessed August 20, 2025).
45. Espinosa-Salas S, Gonzalez-Arias M. Nutrition: Macronutrient Intake, Imbalances, and Interventions. Stat Pearls [Internet] 2023. https://www.ncbi.nlm.nih.gov/books/NBK594226/.
46. 46            Li M, Gong W, Wang S, Li Z. Trends in body mass index, overweight and obesity among adults in the USA, the NHANES from 2003 to 2018: a repeat cross-sectional survey. BMJ Open 2022;12:e065425. https://doi.org/10.1136/bmjopen-2022-065425.
47. Araújo J, Cai J, Stevens J. Prevalence of Optimal Metabolic Health in American Adults: National Health and Nutrition Examination Survey 2009–2016. Metab Syndr Relat Disord 2019;17:46–52. https://doi.org/10.1089/met.2018.0105.
48. LaFata EM, Allison KC, Audrain-McGovern J, Forman EM. Ultra-Processed Food Addiction: A Research Update. Curr Obes Rep 2024;13:214–23. https://doi.org/10.1007/s13679-024-00569-w.
49. Isbanner S, Carins J, Babakhani N, Kitunen A. Streamlining COM-B model: Insights from the Healthy Eating Context. Appetite 2024;203:107693. https://doi.org/10.1016/j.appet.2024.107693.
50. Sidor M, Dubin K. Psychological factors in behaviour change and motivation. Sweet Institute 2024. https://sweetinstitute.com/psychological-factors-in-behavior-change-and-motivation/#:~:text=Positive%20Emotions:%20Emotions%20such%20as,motivation%20and%20enhance%20self%2Defficacy. (accessed August 21, 2025).
51. Clear James. Atomic habits : an easy & proven way to build good habits & break bad ones: tiny changes, remarkable results. Cornerstone Press; 2022.
52. Hall KD, Kahan S. Maintenance of Lost Weight and Long-Term Management of Obesity. Medical Clinics of North America 2018;102:183–97. https://doi.org/10.1016/j.mcna.2017.08.012.
53. Bluezones. 2025 n.d. https://www.bluezones.com.
54. Ede G. Brainwashed: the mainstreaming of nutritional mythology 2020. https://www.youtube.com/watch?v=WbNDrcoRi8g (accessed August 21, 2025).
55. Najjar RS, Feresin RG. Plant-Based Diets in the Reduction of Body Fat: Physiological Effects and Biochemical Insights. Nutrients 2019;11:2712. https://doi.org/10.3390/nu11112712.
56. Livingston AS, Cudhea F, Wang L, Steele EM, Du M, Wang YC, et al. Effect of reducing ultraprocessed food consumption on obesity among US children and adolescents aged 7–18 years: evidence from a simulation model. BMJ Nutr Prev Health 2021;4:e000303. https://doi.org/10.1136/bmjnph-2021-000303.
57. Berrazaga I, Micard V, Gueugneau M, Walrand S. The Role of the Anabolic Properties of Plant- versus Animal-Based Protein Sources in Supporting Muscle Mass Maintenance: A Critical Review. Nutrients 2019;11:1825. https://doi.org/10.3390/nu11081825.
58. López-Moreno M, Garcés-Rimón M, Miguel M. Antinutrients: Lectins, goitrogens, phytates and oxalates, friends or foe? J Funct Foods 2022;89:104938. https://doi.org/10.1016/j.jff.2022.104938.
59. Bakaloudi DR, Halloran A, Rippin HL, Oikonomidou AC, Dardavesis TI, Williams J, et al. Intake and adequacy of the vegan diet. A systematic review of the evidence. Clinical Nutrition 2021;40:3503–21. https://doi.org/10.1016/j.clnu.2020.11.035.
60. Harcombe Z. Should we be vegan? 2022. https://www.youtube.com/watch?v=DsQMCUgjbZA (accessed August 21, 2025).
61. Assumptive close n.d. https://www.google.com/search?q=assumptive+close+academic+paper&sca_esv=44f27cba552c4951&sxsrf=AE3TifPhBY-y92yfLwdc5DYOEWpx0pOG3g%3A1753363661047&ei=zTSCaLrWAu22hbIPv_6KYA (accessed August 21, 2025).
62. Truth, Tactics and the mist of meat lobby science 2024. https://www.foodunfolded.com/article/truths-tactics-and-the-mist-of-meat-lobby-science (accessed August 21, 2025).
63. Farvid MS, Sidahmed E, Spence ND, Mante Angua K, Rosner BA, Barnett JB. Consumption of red meat and processed meat and cancer incidence: a systematic review and meta-analysis of prospective studies. Eur J Epidemiol 2021;36:937–51. https://doi.org/10.1007/s10654-021-00741-9.
64. Gu X, Wang DD, Sampson L, Barnett JB, Rimm EB, Stampfer MJ, et al. Validity and Reproducibility of a Semiquantitative Food Frequency Questionnaire for Measuring Intakes of Foods and Food Groups. Am J Epidemiol 2024;193:170–9. https://doi.org/10.1093/aje/kwad170.
65. Brooke BS, Schwartz TA, Pawlik TM. MOOSE Reporting Guidelines for Meta-analyses of Observational Studies. JAMA Surg 2021;156:787. https://doi.org/10.1001/jamasurg.2021.0522.
66. Bouvard V, Loomis D, Guyton KZ, Grosse Y, Ghissassi F El, Benbrahim-Tallaa L, et al. Carcinogenicity of consumption of red and processed meat. Lancet Oncol 2015;16:1599–600. https://doi.org/10.1016/S1470-2045(15)00444-1.
67. Venkatachalam K, Vinayagam R, Arokia Vijaya Anand M, Isa NM, Ponnaiyan R. Biochemical and molecular aspects of 1,2-dimethylhydrazine (DMH)-induced colon carcinogenesis: a review. Toxicol Res (Camb) 2020;9:2–18. https://doi.org/10.1093/toxres/tfaa004.
68. Chen J, Huang X-F. The signal pathways in azoxymethane-induced colon cancer and preventive implications. Cancer Biol Ther 2009;8:1313–7. https://doi.org/10.4161/cbt.8.14.8983.
69. Ede G. WHO says meat causes cancer? n.d. https://www.diagnosisdiet.com/full-article/meat-and-cancer (accessed August 21, 2025).
70. Spencer EA, Key TJ, Appleby PN, Dahm CC, Keogh RH, Fentiman IS, et al. Meat, poultry and fish and risk of colorectal cancer: pooled analysis of data from the UK dietary cohort consortium. Cancer Causes & Control 2010;21:1417–25. https://doi.org/10.1007/s10552-010-9569-7.
71. Oostindjer M, Alexander J, Amdam G V., Andersen G, Bryan NS, Chen D, et al. The role of red and processed meat in colorectal cancer development: a perspective. Meat Sci 2014;97:583–96. https://doi.org/10.1016/j.meatsci.2014.02.011.
72. 72            Willett W, Rockström J, Loken B, Springmann M, Lang T, Vermeulen S, et al. Food in the Anthropocene: the EAT–Lancet Commission on healthy diets from sustainable food systems. The Lancet 2019;393:447–92. https://doi.org/10.1016/S0140-6736(18)31788-4.
73. Thorkildsen T, Reksnes DH. The Proof is Not in the eating. EuroChoices 2020;19:11–6. https://doi.org/10.1111/1746-692X.12253.
74. Zagmutt FJ, Pouzou JG, Costard S. The EAT-Lancet Commission’s Dietary Composition May Not Prevent Noncommunicable Disease Mortality. J Nutr 2020;150:985–8. https://doi.org/10.1093/jn/nxaa020.
75. Zagmutt FJ, Pouzou JG, Costard S. The EAT–Lancet Commission: a flawed approach? The Lancet 2019;394:1140–1. https://doi.org/10.1016/S0140-6736(19)31903-8.
76. Food Reform for Sustainability and Health (FReSH) 2018. https://docs.wbcsd.org/2018/10/FReSH_Spotlight%20on%20Action.pdf (accessed August 21, 2025).
77. Godos J, Scazzina F, Paternò Castello C, Giampieri F, Quiles JL, Briones Urbano M, et al. Underrated aspects of a true Mediterranean diet: understanding traditional features for worldwide application of a “Planeterranean” diet. J Transl Med 2024;22:294. https://doi.org/10.1186/s12967-024-05095-w.
78. Queensland Health. Mediterranean diet 2021. https://www.health.qld.gov.au/__data/assets/pdf_file/0032/946049/cardiac-meddiet.pdf.
79. Tosti V, Bertozzi B, Fontana L. Health Benefits of the Mediterranean Diet: Metabolic and Molecular Mechanisms. The Journals of Gerontology: Series A 2018;73:318–26. https://doi.org/10.1093/gerona/glx227.
80. Daley SF, Challa HJ, Uppaluri KR. Paleolithic diet n.d. https://www.ncbi.nlm.nih.gov/books/NBK482457/.
81. Manheimer EW, van Zuuren EJ, Fedorowicz Z, Pijl H. Paleolithic nutrition for metabolic syndrome: systematic review and meta-analysis. Am J Clin Nutr 2015;102:922–32. https://doi.org/10.3945/ajcn.115.113613.
82. NIH Heart Lung and Blood Institute. DASH eating plan 2025. https://www.nhlbi.nih.gov/education/dash-eating-plan#:~:text=Description%20of%20the%20DASH%20Eating,sugar%2Dsweetened%20beverages%20and%20sweets.
83. 83            Filippou CD, Tsioufis CP, Thomopoulos CG, Mihas CC, Dimitriadis KS, Sotiropoulou LI, et al. Dietary Approaches to Stop Hypertension (DASH) Diet and Blood Pressure Reduction in Adults with and without Hypertension: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. Advances in Nutrition 2020;11:1150–60. https://doi.org/10.1093/advances/nmaa041.
84. Bakaloudi DR, Halloran A, Rippin HL, Oikonomidou AC, Dardavesis TI, Williams J, et al. Intake and adequacy of the vegan diet. A systematic review of the evidence. Clinical Nutrition 2021;40:3503–21. https://doi.org/10.1016/j.clnu.2020.11.035.
85. Faunolytics. A summary of Faunalytics study of current and former vegetarians and vegans 2016.
86. Magara HJO, Niassy S, Ayieko MA, Mukundamago M, Egonyu JP, Tanga CM, et al. Edible Crickets (Orthoptera) Around the World: Distribution, Nutritional Value, and Other Benefits—A Review. Front Nutr 2021;7. https://doi.org/10.3389/fnut.2020.537915.
87. Heffernan C. Vilhjameur Stefansson’s Meat diet part one. Physical Culture Study 2018. https://physicalculturestudy.com/2018/01/05/vilhjalmur-stefanssons-all-meat-diet-part-one-2/#more-11567.
88. Heffernan C. Vilhjamur Stefansson’s all meat diet part two. Physical Culture Study 2015. https://physicalculturestudy.com/2015/01/12/vilhjalmur-stefanssons-all-meat-diet-part-two/.
89. Lieb CW. A year’s exclusive meat diet and seven years later. American Journal of Digestive Diseases and Nutrition 1935;2:473–5. https://doi.org/10.1007/BF03000888.
90. Ede G. The history of all meat diets. Diagnosis:Diet n.d. https://www.diagnosisdiet.com/full-article/all-meat-diets.
91. Lennerz BS, Mey JT, Henn OH, Ludwig DS. Behavioral Characteristics and Self-Reported Health Status among 2029 Adults Consuming a “Carnivore Diet.” Curr Dev Nutr 2021;5:nzab133. https://doi.org/10.1093/cdn/nzab133.
92. Kolb H. Obese visceral fat tissue inflammation: from protective to detrimental? BMC Med 2022;20:494. https://doi.org/10.1186/s12916-022-02672-y.
93. Hopper Z, Desbrow B, Roberts S, Irwin C. Preparation procedures of food and beverage samples for oxygen bomb calorimetry: A scoping review and reporting checklist. J Food Drug Anal 2023;31:232–43. https://doi.org/10.38212/2224-6614.3461.
94. Hargrove JL. History of the Calorie in Nutrition. J Nutr 2006;136:2957–61. https://doi.org/10.1093/jn/136.12.2957.
95. Fung J. The obesity code : unlocking the secrets of weight loss. Greystone Books; 2016.
96. Landry MJ, Crimarco A, Gardner CD. Benefits of Low Carbohydrate Diets: a Settled Question or Still Controversial? Curr Obes Rep 2021;10:409–22. https://doi.org/10.1007/s13679-021-00451-z.
97. PHCUK. A summary table of randomised controlled trials comparing low-carb diets of less than 130g carbohydrate per day to low-fat diets of less than 35% fat of total calories compiled by the Public Health Collaboration n.d. https://phcuk.org/wp-content/uploads/2018/02/Summary-Table-Of-Randomised-Controlled-Trials-Comparing-Low-Carb-To-Low-Fat-Diets-26.02.2018.pdf (accessed August 22, 2025).
98. Teicholz N, Croft SM, Cuaranta I, Cucuzzella M, Glandt M, Griauzde DH, et al. Myths and Facts Regarding Low-Carbohydrate Diets. Nutrients 2025;17:1047. https://doi.org/10.3390/nu17061047.
99. Volek JS, Yancy WS, Gower BA, Phinney SD, Slavin J, Koutnik AP, et al. Expert consensus on nutrition and lower-carbohydrate diets: An evidence- and equity-based approach to dietary guidance. Front Nutr 2024;11. https://doi.org/10.3389/fnut.2024.1376098.
100. 100.Budoff M, Manubolu VS, Kinninger A, Norwitz NG, Feldman D, Wood TR, et al. Carbohydrate Restriction-Induced Elevations in LDL-Cholesterol and Atherosclerosis. JACC: Advances 2024;3:101109. https://doi.org/10.1016/j.jacadv.2024.101109.
101. 101.Fung Jason. The obesity code : unlocking the secrets of weight loss. Greystone Books; 2016.
102. 102.Bijlsma N, Cohen M. Environmental Chemical Assessment in Clinical Practice: Unveiling the Elephant in the Room. Int J Environ Res Public Health 2016;13:181. https://doi.org/10.3390/ijerph13020181.
103. 103.Dewapriya P, Chadwick L, Gorji SG, Schulze B, Valsecchi S, Samanipour S, et al. Per- and polyfluoroalkyl substances (PFAS) in consumer products: Current knowledge and research gaps. Journal of Hazardous Materials Letters 2023;4:100086. https://doi.org/10.1016/j.hazl.2023.100086.
104. 104.Hamza MA, Keltie AJ, Matthews RK, Day ML, Shearer CJ. CdIn Micro‐Pyramids for Reductive Photocatalytic Degradation of Perfluorooctanesulfonic Acid. Small 2025. https://doi.org/10.1002/smll.202504601.
105. 105.Fahy T. Adelaide researchers hope new light-activated material will help combat PFAS “forever chemicals.” ABC News 2025. https://www.abc.net.au/news/2025-09-08/sa-researchers-develop-new-method-to-degrade-pfas/105632330.
106. 106.Lindell AE, Grießhammer A, Michaelis L, Papagiannidis D, Ochner H, Kamrad S, et al. Human gut bacteria bioaccumulate per- and polyfluoroalkyl substances. Nat Microbiol 2025;10:1630–47. https://doi.org/10.1038/s41564-025-02032-5.
107. 107.IQAir. PM 2.5 2022. https://www.iqair.com/au/newsroom/pm2-5.
108. 108.Sangkham S, Phairuang W, Sherchan SP, Pansakun N, Munkong N, Sarndhong K, et al. An update on adverse health effects from exposure to PM2.5. Environmental Advances 2024;18:100603. https://doi.org/10.1016/j.envadv.2024.100603.
109. 109.Brook RD, Xu X, Bard RL, Dvonch JT, Morishita M, Kaciroti N, et al. Reduced metabolic insulin sensitivity following sub-acute exposures to low levels of ambient fine particulate matter air pollution. Science of The Total Environment 2013;448:66–71. https://doi.org/10.1016/j.scitotenv.2012.07.034.
110. 110.Fenton SE, Ducatman A, Boobis A, DeWitt JC, Lau C, Ng C, et al. Per- and Polyfluoroalkyl Substance Toxicity and Human Health Review: Current State of Knowledge and Strategies for Informing Future Research. Environ Toxicol Chem 2020;40:606–30. https://doi.org/10.1002/etc.4890.
111. 111.Shetty SS, D D, S H, Sonkusare S, Naik PB, Kumari N S, et al. Environmental pollutants and their effects on human health. Heliyon 2023;9:e19496. https://doi.org/10.1016/j.heliyon.2023.e19496.
112. 112.Heindel JJ, Howard S, Agay-Shay K, Arrebola JP, Audouze K, Babin PJ, et al. Obesity II: Establishing causal links between chemical exposures and obesity. Biochem Pharmacol 2022;199:115015. https://doi.org/10.1016/j.bcp.2022.115015.
113. 113.Sinclair GM, Long SM, Jones OAH. What are the effects of PFAS exposure at environmentally relevant concentrations? Chemosphere 2020;258:127340. https://doi.org/10.1016/j.chemosphere.2020.127340.
114. 114.Zimmermann L, Geueke B, Parkinson L V., Schür C, Wagner M, Muncke J. Food contact articles as source of micro- and nanoplastics: a systematic evidence map. NPJ Sci Food 2025;9:111. https://doi.org/10.1038/s41538-025-00470-3.
115. 115.Thapliyal C, Negi S, Nagarkoti S, Daverey A. Mechanistic insight into potential toxic effects of microplastics and nanoplastics on human health. Discover Applied Sciences 2025;7:645. https://doi.org/10.1007/s42452-025-07214-8.
116. 116.Sa’adu I, Farsang A. Plastic contamination in agricultural soils: a review. Environ Sci Eur 2023;35:13. https://doi.org/10.1186/s12302-023-00720-9.
117. 117.Chaïb I, Doyen P, Merveillie P, Dehaut A, Duflos G. Microplastic contaminations in a set of beverages sold in France. Journal of Food Composition and Analysis 2025;144:107719. https://doi.org/10.1016/j.jfca.2025.107719.
118. 118.Gou Z, Wu H, Li S, Liu Z, Zhang Y. Airborne micro- and nanoplastics: emerging causes of respiratory diseases. Part Fibre Toxicol 2024;21:50. https://doi.org/10.1186/s12989-024-00613-6.
119. 119.Khalid N, Aqeel M, Noman A, Khan SM, Akhter N. Interactions and effects of microplastics with heavy metals in aquatic and terrestrial environments. Environmental Pollution 2021;290:118104. https://doi.org/10.1016/j.envpol.2021.118104.
120. 120.Ma H, Cornadó D, Raaijmakers JM. The soil-plant-human gut microbiome axis into perspective. Nat Commun 2025;16:7748. https://doi.org/10.1038/s41467-025-62989-z.
121. 121.Clark NJ, Fischer AC, Carne D, Littlejohn GR, Durndell LJ, Plessis A, et al. Determining the accumulation potential of nanoplastics in crops: An investigation of 14C-labelled polystyrene nanoplastic into radishes. Environ Res 2025:122687. https://doi.org/10.1016/j.envres.2025.122687.
122. 122.Fackelmann G, Sommer S. Microplastics and the gut microbiome: How chronically exposed species may suffer from gut dysbiosis. Mar Pollut Bull 2019;143:193–203. https://doi.org/10.1016/j.marpolbul.2019.04.030.
123. 123.Tamargo A, Molinero N, Reinosa JJ, Alcolea-Rodriguez V, Portela R, Bañares MA, et al. PET microplastics affect human gut microbiota communities during simulated gastrointestinal digestion, first evidence of plausible polymer biodegradation during human digestion. Sci Rep 2022;12:528. https://doi.org/10.1038/s41598-021-04489-w.
124. Milillo C, Aruffo E, Di Carlo P, Patruno A, Gatta M, Bruno A, et al. Polystyrene nanoplastics mediate oxidative stress, senescence, and apoptosis in a human alveolar epithelial cell line. Front Public Health 2024;12. https://doi.org/10.3389/fpubh.2024.1385387.
125. 125.Lin S, Zhang H, Wang C, Su X-L, Song Y, Wu P, et al. Metabolomics Reveal Nanoplastic-Induced Mitochondrial Damage in Human Liver and Lung Cells. Environ Sci Technol 2022;56:12483–93. https://doi.org/10.1021/acs.est.2c03980.
126. Zhao J, Lan R, Tan H, Wang J, Ma Y, Chen Q, et al. Detection and characterization of microplastics and nanoplastics in biological samples. Nature Reviews Bioengineering 2025. https://doi.org/10.1038/s44222-025-00335-0.
127. Ball P. What is the future of fusion energy. Scientific Amaerican 2023. https://www.scientificamerican.com/article/what-is-the-future-of-fusion-energy/ (accessed August 22, 2025).
128. Liu S, Proudman J, Mitloehner FM. Rethinking methane from animal agriculture. CABI Agriculture and Bioscience 2021;2:22. https://doi.org/10.1186/s43170-021-00041-y.
129. CLEAR Centre at UC Davis. Cattle and the biogenic carbon cycle 2021. https://www.youtube.com/watch?v=2IDk1-WYE2o&t=1s.
130. Chang J, Ciais P, Gasser T, Smith P, Herrero M, Havlík P, et al. Climate warming from managed grasslands cancels the cooling effect of carbon sinks in sparsely grazed and natural grasslands. Nat Commun 2021;12:118. https://doi.org/10.1038/s41467-020-20406-7.
131. Mitloehner F. Meat and climate change. Diet Doctor Podcast 2020. https://www.youtube.com/watch?v=L_ly4PRe430 (accessed August 22, 2025).
132. Ritchie H. Carbon emissions from deforestation: are they driven by domestic demand or international trade? Our World in Data 2021. https://ourworldindata.org/carbon-deforestation-trade (accessed August 22, 2025).
133. Ritchie H. Not all forest loss is equal: what is the difference between deforestation and forest degradation? Our World in Data 2021. https://ourworldindata.org/deforestation-degradation (accessed August 22, 2025).
134. ScienceDirect. Soil exhaustion. Climate Change and Soil Interactions n.d. https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/soil-exhaustion#:~:text=In%20subject%20area:%20Agricultural%20and,Change%20and%20Soil%20Interactions%2C%202020 (accessed August 22, 2025).
135. Xing Y, Wang X. Impact of Agricultural Activities on Climate Change: A Review of Greenhouse Gas Emission Patterns in Field Crop Systems. Plants 2024;13:2285. https://doi.org/10.3390/plants13162285.
136. Khangura R, Ferris D, Wagg C, Bowyer J. Regenerative Agriculture—A Literature Review on the Practices and Mechanisms Used to Improve Soil Health. Sustainability 2023;15:2338. https://doi.org/10.3390/su15032338.
137. Ma D, Yin L, Ju W, Li X, Deng X, Wang S. Green manure. Journal 2021. https://doi.org/https://doi.org/10.1016/j.fcr.2021.108146.
138. Pitumpe Arachchige PS, Hettiarachchi GM, Rice CW, Dynes JJ, Maurmann L, Kilcoyne ALD, et al. Direct evidence on the impact of organic amendments on carbon stabilization in soil microaggregates. Soil Science Society of America Journal 2024;88:1529–44. https://doi.org/10.1002/saj2.20701.
139. 139.You S, Sonne C, Park Y-K, Kumar S, Lin K-YA, Ok YS, et al. Food loss and waste: A carbon footprint too big to be ignored. Sustainable Environment 2022;8. https://doi.org/10.1080/27658511.2022.2115685.
140. Ritchie H. Food waste is responsible for 6% of global greenhouse gas emissions. Our World in Data 2020. https://ourworldindata.org/food-waste-emissions (accessed August 22, 2025).
141. Ritchie H. What share of global CO2 emissions come from aviation? Our World in Data 2024. https://ourworldindata.org/global-aviation-emissions (accessed September 9, 2025).
142. Bernstad Saraiva Schott A, Cánovas A. Current practice, challenges and potential methodological improvements in environmental evaluations of food waste prevention – A discussion paper. Resour Conserv Recycl 2015;101:132–42. https://doi.org/10.1016/j.resconrec.2015.05.004.
143. Bhatia L, Jha H, Sarkar T, Sarangi PK. Food Waste Utilization for Reducing Carbon Footprints towards Sustainable and Cleaner Environment: A Review. Int J Environ Res Public Health 2023;20:2318. https://doi.org/10.3390/ijerph20032318.
144. Wallace DC. A Mitochondrial Paradigm of Metabolic and Degenerative Diseases, Aging, and Cancer: A Dawn for Evolutionary Medicine. Annu Rev Genet 2005;39:359–407. https://doi.org/10.1146/annurev.genet.39.110304.095751.
145. Circu ML, Aw TY. Reactive oxygen species, cellular redox systems, and apoptosis. Free Radic Biol Med 2010;48:749–62. https://doi.org/10.1016/j.freeradbiomed.2009.12.022.
146. Kassotis CD, vom Saal FS, Babin PJ, Lagadic-Gossmann D, Le Mentec H, Blumberg B, et al. Obesity III: Obesogen assays: Limitations, strengths, and new directions. Biochem Pharmacol 2022;199:115014. https://doi.org/10.1016/j.bcp.2022.115014.
147. Heindel JJ, Lustig RH, Howard S, Corkey BE. Obesogens: a unifying theory for the global rise in obesity. Int J Obes 2024;48:449–60. https://doi.org/10.1038/s41366-024-01460-3.
148. Lustig RH, Collier D, Kassotis C, Roepke TA, Kim MJ, Blanc E, et al. Obesity I: Overview and molecular and biochemical mechanisms. Biochem Pharmacol 2022;199:115012. https://doi.org/10.1016/j.bcp.2022.115012.
149. Delgado-Rodríguez R, Moreno-Padilla M, Moreno-Domínguez S, Cepeda-Benito A. Food addiction correlates with emotional and craving reactivity to industrially prepared (ultra-processed) and home-cooked (processed) foods but not unprocessed or minimally processed foods. Food Qual Prefer 2023;110:104961. https://doi.org/10.1016/j.foodqual.2023.104961.
150. Rittel HWJ, Webber MM. Dilemmas in a general theory of planning. Policy Sci 1973;4:155–69. https://doi.org/10.1007/BF01405730.
151. Borland S. Junk food industry “avoids advertising regulation” in its elite UK sports sponsorship deals. BMJ 390:1:56 No 8467 2025:14–7.
152. Countries and jurisdictions that have taxes on-sugar sweetened beverages (SSBs). Obesity Evidence Hub 2025. https://www.obesityevidencehub.org.au/collections/prevention/countries-that-have-implemented-taxes-on-sugar-sweetened-beverages-ssbs#:~:text=Fewer%20carbonated%20drinks%20were%20purchased,19 (accessed August 24, 2025).
153. Khangura R, Ferris D, Wagg C, Bowyer J. Regenerative Agriculture—A Literature Review on the Practices and Mechanisms Used to Improve Soil Health. Sustainability 2023;15:2338. https://doi.org/10.3390/su15032338.
154. du Toit JT, Pettorelli N. The differences between rewilding and restoring an ecologically degraded landscape. Journal of Applied Ecology 2019;56:2467–71. https://doi.org/10.1111/1365-2664.13487.
155. Savory A. How to green the world’s deserts and reverse climate change. TED Talks 2013. https://www.google.com/search?q=Allan+Savory+rewilding+youtube&oq=Allan+Savory+rewilding+youtube&gs_lcrp=EgZjaHJvbWUyBggAEEUYOTIHCAEQIRigAdIBCTEyNDIyajBqN6gCCLACAfEFu3G4VgAN_YnxBbtxuFYADf2J&sourceid=chrome&ie=UTF-8#fpstate=ive&vld=cid:c09a791b,vid:vpTHi7O66pI,st:0 (accessed August 24, 2025).
156. Ketchell M. Autonomous AI systems can help tackle global food insecurity. The Conversation 2025. https://theconversation.com/autonomous-ai-systems-can-help-tackle-global-food-insecurity-258788 (accessed August 24, 2025).
157. Shokri N. Declining soil health is a global concern - here’s how AI could help. The Conversation 2025. https://theconversation.com/declining-soil-health-is-a-global-concern-heres-how-ai-could-help-258847 (accessed August 24, 2025).
158. Rowntree J. From robots and drones to sheep trackers, new tech can help farmers monitor and improve soil health. The Conversation 2024. https://theconversation.com/from-robots-and-drones-to-sheep-trackers-new-tech-can-help-farmers-monitor-and-improve-soil-health-227250.
159. Paudel S, Regmi S, Bhattarai S, Fennell A, Janaswamy S. Valorization of grapevine agricultural waste into transparent and high-strength biodegradable films for sustainable packaging. Sustainable Food Technology 2025;3:1218–31. https://doi.org/10.1039/D5FB00211G.
160. Black J, Cooper L. The great freight merry-go-round. ABC News 2025. https://www.abc.net.au/news/2025-06-29/food-supply-chain-freight-costs-farmers-and-remote-communities/105382150 (accessed August 24, 2025).
161. Ang T-Z, Salem M, Kamarol M, Das HS, Nazari MA, Prabaharan N. A comprehensive study of renewable energy sources: Classifications, challenges and suggestions. Energy Strategy Reviews 2022;43:100939. https://doi.org/10.1016/j.esr.2022.100939.
162. Recycling in the future: sustainable solutions for renewable energy technologies. Clean Energy Council 2025. https://cleanenergycouncil.org.au/for-consumers/fact-sheets/recycling-get-the-facts/recyling-wind-turbines-solar-panels-batteries#:~:text=Approximately%2085%25%20to%20100%25%20of,all%20waste%20streams%20by%202030. (accessed August 24, 2025).
163. Davidson TM. Don Campbell on lifelong learning and personal growth. Canadian Cattlemen 2023. https://www.canadiancattlemen.ca/features/don-campbell-on-lifelong-learning-and-personal-growth/.
164. Ridley M. The Rational Optimist: How Prosperity Evolves. Harper Collins; 2011.