By Eben van Tonder, EarthwormExpress, 6 July 2025
Introduction
Introduction
This article explores the biochemistry, physiology, and functional consequences of cortisol in both humans and animals, with a particular emphasis on its role in the meat industry and human health. Cortisol, a glucocorticoid hormone produced in the adrenal cortex, serves as a central regulator of the stress response. While its acute activation enables organisms to adapt to immediate threats by mobilising energy and suppressing non-essential functions, chronic elevation leads to a cascade of detrimental metabolic, cognitive, and immunological outcomes.
In livestock, cortisol has profound implications for meat quality. Its impact on glycogen depletion, proteolysis, and post-mortem muscle chemistry can lead to well-documented defects such as Pale, Soft, Exudative (PSE) and Dark, Firm, Dry (DFD) meat. These outcomes are not merely biochemical artefacts but are rooted in the physiological stress endured by the animal prior to slaughter. Understanding cortisol’s influence helps bridge animal welfare and carcass value, giving meat science professionals tools for more precise intervention.
In human physiology, the same hormone governs stress responses with strikingly similar consequences. From muscle breakdown and visceral fat accumulation to mood instability and immune suppression, the chronic effects of cortisol mirror the degradations seen in stressed animals. This shared biology opens the possibility of cross-disciplinary insight, where strategies developed to improve meat quality may inform resilience in human health and vice versa.
The article goes on to explore natural modulation strategies, with special focus on beetroot as a dietary agent rich in nitrates, antioxidants, and adaptogenic compounds. We conclude by introducing the concept of nitrite-enriched beetroot bacon, an innovation that symbolises the convergence of tradition, hormonal insight, and functional food design. In understanding cortisol, we gain not only better meat but a deeper grasp of the biology that links all living systems under stress.
1. Biochemistry of Cortisol: Synthesis and Regulation
1.1 The Discovery of Cortisol
Cortisol was first isolated and identified in 1936 by biochemist Tadeusz Reichstein in Basel, Switzerland, working at the Pharmaceutical Institute of the University of Basel. At the same time, American researchers Edward Calvin Kendall and Philip Hench at the Mayo Clinic in the United States were also isolating adrenal hormones from bovine adrenal glands. The hormone was initially called Compound E.
In 1948, Hench and Kendall, building on Reichstein’s earlier work, successfully applied cortisone (a closely related hormone to cortisol) in the treatment of rheumatoid arthritis, leading to worldwide recognition. In 1950, Reichstein, Kendall, and Hench jointly received the Nobel Prize in Physiology or Medicine for their work on adrenal cortex hormones and their application in therapy.
“The identification of cortisol marked one of the great achievements in endocrine chemistry of the twentieth century” (Medvei, 1982). It opened the door to understanding how the body regulates metabolism, immunity, and stress.
1.2 Cortisol Synthesis and Regulation: A Clear, Structured Overview for Meat Science Professionals
Cortisol, a glucocorticoid hormone central to the stress response in mammals, is synthesised in the zona fasciculata of the adrenal cortex. The adrenal cortex is the outer layer of the adrenal gland, a small but vital endocrine organ located on top of each kidney. It plays a crucial role in producing several important hormones that help regulate metabolism, blood pressure, immune response, and stress.
While the full pathway involves multiple enzyme-mediated conversions, the logic behind it is straightforward when broken down into its major steps.
The process begins with cholesterol, a crucial precursor for all steroid hormones. Cholesterol is the essential raw material from which all steroid hormones are made, including cortisol, aldosterone, oestrogen, and testosterone. In the adrenal cortex, it is primarily sourced from LDL in the bloodstream, taken into cells, and converted into free cholesterol, the active form used in hormone synthesis. This is not a special type of cholesterol, but the same molecule (C₂₇H₄₆O) found throughout the body.
Though often associated with heart disease, cholesterol is vital to human biology. It supports cell structure, bile acid production, vitamin D synthesis, and the entire steroid hormone cascade. Without cholesterol, the adrenal glands could not produce life-sustaining hormones like cortisol.
In the adrenal cortex, cholesterol is enzymatically converted through the following pathway:
- Cholesterol is cleaved by the mitochondrial enzyme CYP11A1 (cholesterol side-chain cleavage enzyme) to form pregnenolone, the universal precursor for steroid hormones.
- Pregnenolone is hydroxylated by CYP17A1 to produce 17-hydroxypregnenolone.
- This intermediate undergoes sequential transformations: first by 3β-HSD (3β-hydroxysteroid dehydrogenase) to form 17-hydroxyprogesterone, and then by CYP21A2 (21-hydroxylase) to yield 11-deoxycortisol.
- Finally, 11-deoxycortisol is converted to cortisol by CYP11B1 (11β-hydroxylase), completing the pathway.
Each of these steps is catalysed by highly specific enzymes within adrenal cortical cells and occurs in response to systemic signals linked to the animal’s stress status.
The entire synthesis process is governed by the hypothalamic-pituitary-adrenal (HPA) axis, a tightly regulated endocrine loop. Here’s how it operates:
- In response to physiological or environmental stressors, the hypothalamus secretes CRH (corticotropin-releasing hormone).
- CRH stimulates the anterior pituitary to release ACTH (adrenocorticotropic hormone).
- ACTH travels through circulation to the adrenal cortex, where it triggers the synthesis and release of cortisol.
This system is self-regulating through a negative feedback loop: when cortisol levels in the blood are sufficient, it inhibits both CRH and ACTH production. As Sapolsky et al. (2000) describe,
“The HPA axis is a classic example of a negative feedback loop, where cortisol inhibits both ACTH and CRH synthesis to prevent overactivation.”
This negative feedback loop is very interesting and important. The production of cortisol is self-regulating through a negative feedback loop. As cortisol levels in the blood rise, they signal the hypothalamus and pituitary gland to reduce the secretion of CRH (corticotropin-releasing hormone) and ACTH (adrenocorticotropic hormone), thereby slowing further cortisol production. This prevents cortisol from increasing without limit. However, the threshold is not a rigid maximum. Rather, it functions like a thermostat, constantly adjusting in response to internal and external stressors.
During prolonged or intense stress, this regulation can be overridden for a time, but chronic activation may impair the feedback loop, leading to dysregulation of cortisol levels. As Sapolsky et al. (2000) note, this is when the system begins to fail, potentially causing harm through either excess or deficiency of cortisol.
For humans, this regulation is vital. When the feedback loop becomes impaired, especially under chronic stress, it can lead to serious health consequences. Prolonged elevated cortisol levels have been linked to hypertension, insulin resistance, abdominal obesity, impaired immune function, and mood disorders such as anxiety and depression. On the other hand, abnormally low cortisol, as seen in Addison’s disease or post-burnout exhaustion, can result in chronic fatigue, low blood pressure, and poor stress tolerance. Maintaining cortisol within a healthy range is therefore critical for both physical and psychological well-being.
For meat scientists, the significance of this regulatory mechanism is clear: any factor that disrupts or overactivates the HPA axis, whether through pre-slaughter handling, confinement, heat stress, or nutritional deficiency,can directly influence muscle glycogen reserves and post-mortem metabolism. Understanding the biochemistry behind cortisol production equips professionals to better interpret physiological responses and meat quality outcomes such as DFD, PSE, or variable water-holding capacity.
This knowledge becomes especially relevant when designing livestock management protocols, lairage practices, or functional dietary strategies to modulate stress physiology and protect meat quality.
2. Physiological Functions and Evolutionary Role
The evolutionary role of cortisol becomes clear when we consider its short-term benefits. It equips the organism to respond swiftly to immediate challenges by promoting processes such as:
- Gluconeogenesis in the liver
- Lipolysis and redistribution of fat. In humans, chronically elevated cortisol levels lead to a distinct redistribution of fat in the body. Fat tends to be broken down in the limbs while being stored more aggressively in the abdominal region. This central accumulation is commonly referred to as belly fat. It is a hallmark of stress-induced metabolic change and reflects how the body prioritises storing energy close to vital organs during prolonged states of alertness. In animals, the same redistribution pattern can be observed. Cortisol promotes fat mobilisation from subcutaneous areas and favours deposition around internal organs such as the kidneys, intestines, and heart. In livestock, this often results in increased organ fat and visible belly fat, especially in animals exposed to extended pre-slaughter stress. This shift in fat localisation can alter carcass composition without necessarily changing total fat content. Cortisol does not increase fat uniformly. Instead, it redirects where fat is stored, favouring central and visceral zones over peripheral tissues.
- Proteolysis in muscle tissue breaks down structural proteins such as actin and myosin into amino acids. These are redirected to the liver for gluconeogenesis, immune support, or tissue repair, an adaptive mechanism for short-term survival. However, when prolonged, this process contributes to muscle wasting, fatigue, and immune suppression, highlighting the delicate balance cortisol must maintain between emergency adaptation and long-term health. In addition to the well-documented effects of PSE and DFD, chronic stress in animals, especially over longer periods can lead to cortisol-driven proteolysis within the muscle tissue. This process, triggered by elevated cortisol levels, breaks down structural muscle proteins even before slaughter, compromising the integrity of the muscle fibres. The result is a softer, more fragile meat structure, with reduced water-holding capacity, higher drip loss, and less yield after cooking. Unlike the acute stress responsible for PSE or the glycogen depletion underlying DFD, cortisol-induced proteolysis reflects a subtler but no less damaging degradation that quietly undermines meat quality over time. It is an overlooked mechanism that deserves careful attention in animal welfare and meat processing systems alike.
- Immunosuppression and anti-inflammatory responses
Evolutionarily, these functions were beneficial in short-term danger scenarios. Chronic activation, however, leads to metabolic dysregulation.
“In evolutionary terms, cortisol was designed for acute, not chronic, stress. Prolonged elevation results in catabolism, immunosuppression, and behavioural disturbances” (McEwen, 2007).
3. Cortisol and Muscle Biochemistry
3.1 In Living Animals
As we already indicated, cortisol promotes proteolysis and gluconeogenesis, often at the expense of muscle tissue:
- Protein breakdown: Muscle protein → Amino acids → Glucose (via hepatic gluconeogenesis)
- Reduced glycogen synthesis: Cortisol inhibits insulin’s anabolic effects
3.2 Post-Mortem Muscle Physiology
The extent of glycogen present in the muscle at slaughter determines post-mortem pH decline:
- Normal pH decline: Glycogen → Lactic acid → pH drops to ~5.5
- Cortisol-depleted muscle: Low glycogen → Incomplete lactic acid production → High final pH (>6.0)
“Glycogen is the most important determinant of ultimate pH. Stress-induced glycogen depletion leads to high-pH meat, which resists microbial spoilage but is organoleptically undesirable” (Lawrie & Ledward, 2006).
4. Cortisol and Meat Defects: PSE and DFD
4.1 PSE (Pale, Soft, Exudative)
Cause: Acute, short-term stress immediately before slaughter, such as exposure to heat, rough handling, fighting, or pre-slaughter stunning.
Hormones Involved: Adrenaline as the primary driver, cortisol in a supporting role.
Biochemistry: Rapid post-mortem glycolysis leads to excessive lactic acid production while muscle temperature remains high, resulting in protein denaturation.
Meat Effect: Pale surface colour, soft and mushy texture, low water-holding capacity, and significant visible drip loss.
Explanation:
PSE meat results from a breakdown in the balance between lactic acid production and carcass cooling. When animals experience intense, immediate stress before slaughter, their bodies release a surge of adrenaline, triggering rapid glycolysis, the metabolic process that breaks down muscle glycogen into glucose and, ultimately, lactic acid.
After slaughter, oxygen supply stops, and the muscle shifts to anaerobic metabolism. In the absence of oxygen, the body cannot rely on mitochondrial respiration and instead produces ATP through lactic acid fermentation. This process continues for several hours post-mortem and is essential for muscle function during the early stages of rigour mortis.
As explored in “Living Without Oxygen: A Closer Look at the Case of Henneguya salminicola”, fermentation allows life to proceed even in anoxic environments. The same mechanism is evident in slaughtered animals: muscle continues to generate energy through fermentation, which naturally leads to acidification. In PSE, however, this process occurs too quickly.
The lactic acid builds up while the carcass is still warm. The combination of low pH and high temperature causes muscle proteins, especially myosin and actin-binding structures, to denature. This weakens the muscle’s structure and its ability to hold water, resulting in soft, pale, exudative meat that lacks commercial value.
Cortisol is not the primary stress hormone in this scenario, but it amplifies the glycolytic response by increasing glucose availability and enhancing tissue sensitivity to adrenaline. This ensures that the metabolic system is fully fuelled for a fast, overwhelming drop in pH.
“PSE meat results from a mismatch in the timing of lactic acid formation and carcass cooling. High temperatures accelerate protein denaturation in low pH conditions” (Offer, 1991).
4.2 DFD (Dark, Firm, Dry)
Cause: Chronic stress over hours or days before slaughter, such as fasting, dehydration, prolonged transport, isolation, or overcrowding.
Hormone Involved: Cortisol is the dominant regulator.
Biochemistry: Glycogen depletion prevents adequate post-mortem glycolysis, resulting in reduced lactic acid formation and high ultimate pH.
Meat Effect: Dark surface colour, firm texture, dry surface with high initial water-holding capacity, but reduced shelf life due to microbial susceptibility
Explanation:
DFD meat is the result of long-term stress exposure in the hours or days before slaughter. Under these conditions, the animal’s stress response shifts from the short-term adrenaline-based reaction to the long-acting cortisol system. The hypothalamic-pituitary-adrenal (HPA) axis remains activated, and cortisol is secreted continuously, reprogramming the animal’s energy metabolism.
Cortisol’s effect is catabolic. It breaks down tissue to ensure a stable glucose supply during prolonged stress. This includes:
- Stimulating gluconeogenesis from amino acids, which leads to muscle protein breakdown
- Suppressing glycogen synthesis, limiting the muscle’s ability to store energy
- Mobilising fatty acids from adipose tissue for peripheral energy needs
- Antagonising insulin, preventing glucose uptake into muscle cells
Over time, these processes lead to the complete or near-complete depletion of muscle glycogen. Since glycogen is the essential substrate for post-mortem lactic acid fermentation, its absence means the muscle fails to acidify. The pH remains high, typically above 6.0.
This results in meat that is firm and dark. At high pH, myoglobin remains in its reduced form, appearing purplish-black and absorbing more light. The protein structure remains intact, preventing exudation and giving the meat a dry, sticky surface with initially good water-holding properties.
But this stability is misleading. High-pH meat provides a perfect breeding ground for spoilage bacteria. The absence of lactic acid removes the natural antimicrobial barrier seen in well-acidified meat. Consequently, DFD meat spoils quickly, even under refrigeration.
Thus, cortisol’s role is not indirect. It is the central force shaping the DFD trajectory, not merely by draining glycogen reserves but by actively restructuring metabolism away from glycolysis, shutting down the possibility of acidification before death has occurred.
“DFD is characterised by a high pH and reduced lactic acid formation. It is strongly correlated with elevated cortisol levels prior to slaughter” (Warris, 2010).
4.3 Cortisol’s Broader Role in Meat Quality
Cortisol operates as a metabolic switch in the pre-slaughter period. Its impact depends on timing:
- In acute stress, cortisol increases glucose availability and primes the muscle for explosive glycolytic activity, worsening PSE outcomes.
- In chronic stress, it drains glycogen and blocks glycolysis, thereby causing DFD.
This makes cortisol not simply a modulating factor, but a central architect of both meat quality defects, exacerbating PSE through amplification, and generating DFD through depletion. Whether it fuels acidification or prevents it, cortisol ultimately determines how the post-mortem muscle will behave, how it will acidify, and how its structure will hold over time.
4.4 Proteolysis as a Defining Mechanism in DFD
The effects of cortisol do not stop at glycogen depletion. One of its most profound influences is its ability to activate proteolytic systems within the muscle. These systems, calpains, cathepsins, and ubiquitin.
5. Feedlot Stress and Meat Quality
This now brings up one of the main causes for stress, namely a feedlot environment.
5.1 Chronic Stress in Intensive Systems
Feedlot environments may predispose animals to chronic low-grade stress due to:
- Overcrowding
- Heat stress
- Social instability
- Monotonous diet
This chronic stress leads to sustained cortisol elevation, muscle catabolism, and glycogen depletion.
“Animals kept under intensive conditions with minimal environmental enrichment are more likely to exhibit stress behaviours, poor feed efficiency, and meat quality defects” (Grandin, 1997).
5.2 Lairage, Handling, and Stress Mitigation
Pre-slaughter handling is key. Stress-reducing measures include:
- Proper lairage (rest, hydration, feed)
- Low-stress handling systems
- Quiet environments and gentle handling
These help restore muscle glycogen, reducing the risk of DFD.
6. Stress in Humans
Stress in humans, much like in animals, can have severe health consequences. While the emotional experience of stress may differ, the physiological effects are strikingly similar. One of the most concerning outcomes of stress is the accumulation of visceral fat—fat that gathers around internal organs, particularly in the abdomen. This type of fat is not just a cosmetic issue but a significant health risk. It contributes to a range of metabolic disorders and increases the risk of chronic diseases such as diabetes, cardiovascular conditions, and hypertension. Alongside this, an increase in organ fat is often hidden from view but still carries significant health implications.
One of the most critical players in this process is cortisol, the stress hormone. Elevated cortisol levels can lead to a cascade of damaging effects, including suppressed immune function, muscle breakdown, insulin resistance, cognitive disruption, and anxiety. The effects are not just temporary; chronic exposure to high cortisol levels can accelerate ageing, increase inflammation, and hinder the body’s ability to recover from both physical and emotional stressors.
6.1 The Role of Beetroot in Cortisol Modulation
In addressing the impact of cortisol, one approach is dietary intervention, and beetroot stands out as a promising natural agent in this area. Beetroot is known for its high content of nitrates, betalains, magnesium, potassium, and polyphenols, which collectively contribute to its ability to modulate cortisol’s negative effects. These compounds work together to improve vascular function, reduce oxidative stress, and promote recovery from stress, making beetroot an excellent dietary addition for individuals facing high cortisol levels.
Can Beetroot Reverse the Effects of Cortisol?
While beetroot may not directly block cortisol production, it has a powerful, holistic impact on the body that can counteract some of the negative effects of chronic cortisol elevation. The key benefit of beetroot lies in its ability to enhance nitric oxide bioavailability. This process improves blood flow to the brain and muscles, supports mitochondrial function, and enhances vascular recovery, areas that are typically compromised under stress and by prolonged exposure to elevated cortisol.
Regular consumption of beetroot can be a significant part of a stress management strategy, but it should be combined with other interventions for maximum effect. Unlike some more direct, pharmaceutical approaches, beetroot’s impact is multifaceted, acting through antioxidant, vascular, and metabolic pathways rather than directly suppressing cortisol synthesis.
How Does Beetroot Compare to Other Interventions?
Several other interventions may help modulate cortisol levels, and when combined with beetroot, these strategies can create a well-rounded approach to stress management:
- Ashwagandha: An adaptogen with clinical evidence showing its ability to lower cortisol significantly.
- Rhodiola Rosea: Aids in reducing fatigue, especially cognitive fatigue, under stress.
- Omega-3 Fatty Acids: Help lower cortisol responses to acute stress and reduce inflammation.
- Magnesium Glycinate: A vital mineral for balancing the HPA axis and nervous system regulation.
- Cold Exposure (Cryotherapy or Cold Showers): Can help lower cortisol over time by strengthening the body’s response to stress.
- Moderate Aerobic Exercise: Reduces baseline cortisol levels when done in moderation.
Among these, beetroot’s multifaceted action sets it apart. It works not only as a vascular and antioxidant support but also as a source of vital nutrients that may help mitigate the effects of stress on both the body and mind.
The Holistic Benefits of Beetroot
Beetroot’s high nitrate content is a key factor in its ability to support vascular health and improve blood flow, particularly to the brain. Nitric oxide produced from nitrates enhances the delivery of oxygen and nutrients, which is essential for optimal brain function and muscle recovery. By supporting mitochondrial efficiency, beetroot also protects against muscle breakdown and inflammatory processes associated with elevated cortisol levels.
Beetroot’s capacity to reduce oxidative stress further helps to preserve cellular function and protect against the damaging effects of prolonged stress. In one study, beetroot juice was shown to reduce serum cortisol levels and restore behavioural and biochemical parameters affected by chronic stress in rodents (El Gamal et al., 2014). While the exact effects in humans are still being studied, this evidence suggests that beetroot may play a role in counteracting some of the damage caused by cortisol.
Practical Use of Beetroot for Stress Recovery
To integrate beetroot effectively into a stress management strategy, it can be consumed regularly through fresh juice, cooked beetroot, or supplements. Although it’s unlikely to fully reverse the damage caused by chronic cortisol in isolation, beetroot can support the recovery process by enhancing overall vascular health, reducing oxidative stress, and improving exercise recovery.
While beetroot does not act as a direct cortisol blocker, its indirect effects—through its antioxidant, vascular, and metabolic properties—make it a valuable addition to a broader recovery plan. Regular consumption may help modulate the body’s stress response, improve recovery after stress, and support long-term resilience to the damaging effects of cortisol.
“Beetroot-derived pigments have been shown to inhibit lipid peroxidation and reduce pro-inflammatory cytokines in animal models” (Clifford et al., 2015). This speaks to the potential protective effects of beetroot in managing the physiological disruptions caused by chronic stress, making it a powerful ally in managing high cortisol levels and their negative health consequences.
By integrating beetroot into a holistic stress management plan that includes proper nutrition, mindfulness, physical activity, and social support, individuals can reduce the long-term impact of cortisol and promote overall health and well-being.
6.2 Cold Showers and Hormetic Stress Adaptation
In addition to dietary interventions, lifestyle changes can also play a key role in modulating cortisol and improving the body’s ability to manage stress. One such lifestyle strategy is cold exposure, particularly through regular cold showers or brief immersions in cold water. Cold exposure activates the sympathetic nervous system, stimulating the release of norepinephrine, a neurotransmitter that enhances alertness and resilience. Over time, this practice may help regulate the hypothalamic-pituitary-adrenal (HPA) axis, which controls the body’s stress response.
The Benefits of Cold Showers
Regular cold showers have been shown to produce several health benefits that directly or indirectly help counteract the negative effects of cortisol:
- Reduced Symptoms of Depression: Cold exposure triggers the release of beta-endorphins, which can elevate mood and improve emotional resilience.
- Improved Immune Function: Cold exposure has been found to boost immune response, helping the body resist infections and inflammation.
- Increased Metabolic Rate: Cold showers stimulate thermogenesis, which increases the body’s energy expenditure and promotes fat loss.
- Enhanced Mental Clarity and Mood: Cold exposure sharpens cognitive function, improves mood, and boosts alertness by stimulating norepinephrine production.
Cold exposure may also contribute to stress adaptation. By activating a controlled stress response, it teaches the body to recover more quickly from future stressors. This process, known as hormesis, involves mild stressors that trigger beneficial physiological changes, improving overall resilience.
“Short-term cold exposure induces a hormetic response that enhances the body’s resistance to more serious future stressors” (Shevchuk, 2008).
“Cold showers can stimulate the release of noradrenaline and beta-endorphins, which can suppress symptoms of depression and reduce fatigue” (Buijze et al., 2016).
Cold Showers as Part of a Comprehensive Stress Management Plan
When combined with dietary interventions like beetroot intake, cold showers form a holistic lifestyle strategy for mitigating the negative effects of cortisol. Both strategies work synergistically, enhancing vascular health, reducing oxidative stress, and improving recovery from physical and emotional exertion. Cold exposure, like beetroot, may not directly block cortisol, but it helps regulate its effects by improving the body’s overall ability to manage and recover from stress.
By integrating both dietary strategies and lifestyle changes such as cold exposure into a daily routine, individuals can enhance their ability to cope with stress, recover more efficiently, and mitigate the long-term health impacts of elevated cortisol levels.
Exploiting the Value of Cured Meat
An additional consideration arises when we consume cured meats since nitrite (NO₂⁻) and nitrate (NO₃⁻) are present in the curing system, such as in traditionally cured bacon containing 120 ppm sodium nitrite. These compounds, chemically similar to those derived from beetroot nitrate metabolism, contribute significantly to nitric oxide production in the body if consumed regularly.
When combined with added ascorbate (e.g. sodium ascorbate or erythorbate at 550 ppm), a standard practice in curing, the risk of nitrosamine formation is effectively neutralised. Ascorbate acts as a competitive reductant, converting nitrite to nitric oxide and blocking the nitrosation of amines.
Furthermore, low-temperature cooking of bacon (below 150°C) further minimises the formation of volatile nitrosamines, especially in home frying scenarios.
In this context, where the consumer is already ingesting NO₂⁻ and NO₃⁻ through cured meat, the physiological need for high additional nitrate from beetroot is reduced. A novel aproach will be to combine beetroot with cures meats and an inlcusion ratio of 1.5% to 2.5% in cured bacon formulations is suggested when ascorbate is included and cooking guidance is respected. This lower inclusion still enhances colour, provides antioxidant benefits, and contributes synergistically to vascular support, without oversaturating the nitrate-nitrite pathway.
This integrated approach leverages both technological curing agents and functional natural ingredients, aligning with modern health-conscious meat design without compromising safety or tradition. The inclusion of beetroot in processed meat products such as bacon is a promising area. Adding 1% to 2% beetroot powder may offer:
- Enhanced antioxidant activity
- Stabilisation of colour (natural nitrite alternative in some contexts)
- Potential reduction in stress marker residues in meat if animals were fed beetroot pre-slaughter
Conclusion
Cortisol is not merely a by-product of stress but a powerful metabolic switch that determines how organisms respond, adapt, and, when unbalanced, deteriorate. In both livestock and humans, its chronic elevation undermines energy homeostasis, damages tissue integrity, redistributes fat to vulnerable areas, and suppresses recovery. These effects are visible in the quality of meat and in the structure of human health, parallel systems shaped by the same hormonal logic.
In the field of meat science, cortisol provides a lens through which we can understand defects like PSE and DFD not simply as technical problems but as physiological signatures of stress exposure. Proteolysis, fat redistribution, and altered pH dynamics become markers of systemic dysregulation. When addressed through better animal handling, dietary intervention, or stress-reducing technologies, cortisol’s effects can be mitigated, yielding meat that is both higher in quality and produced under more humane conditions.
In human health, the implications are no less urgent. As modern life accelerates the prevalence of chronic stress, the insights from animal physiology become a mirror. The very tools used to protect carcass integrity, nutritional antioxidants, nitrate donors, and hormetic stress management, may hold promise for protecting the human body against cortisol’s long-term effects.
The concept of nitrite-enriched beetroot bacon embodies this integrated perspective. It connects ancient curing methods with the demands of modern physiology. It reflects a new understanding of food as not only sustenance, but a vehicle for restoring biochemical balance. When meat science and life science speak to one another, the result is not only better product outcomes, but a richer understanding of adaptation, endurance, and the shared biology that underpins our health and survival.
Part of the Capillary Series by Eben van Tonder, EarthwormExpress.
Relationship Between Cortisol, Stress, and Meat Quality in Animals Pre-Slaughter
Capillaries as a Quality Marker
Literaturverzeichnis
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