• Aspartame is a very intense artificial sweetener, about 180 to 300 times sweeter than sugar, widely used in diet drinks and “sugar-free” foods. It has been studied for decades, with many agencies judging it safe within set daily limits, but some recent research and reviews continue to question possible long-term risks and as a result many people worry if it is ok to enjoy it in their favourite fizzy drinks or should they avoid it altogether.

    What Aspartame Is and Where It’s Found

    Chemically, aspartame is a dipeptide of aspartic acid and phenylalanine with a methyl ester. It provides 4 kcal per gram, but it is used in such tiny amounts that calorie contribution is considered negligible in real-world intake.

    It is commonly found in diet soft drinks, powdered drink mixes, chewing gum, flavoured milk, desserts, “light” or diet foods, and some medicines. In German market data, it appeared in around 14% of 53,116 tested samples, particularly in powdered drink bases, flavoured milk drinks, chewing gum, and diet sodas, so needless to say, it is an ingredient you are highly likely to come across even in Ireland.

    Acceptable Daily Intake and Typical Exposure

    Regulatory agencies have set safe intake thresholds based on decades of toxicological and epidemiological evidence.

    The U.S. Food and Drug Administration has set an acceptable daily intake (ADI) of 50 mg per kg of body weight per day, while the European Food Safety Authority has set this at 40 mg per kg per day. Current exposure data suggests that average and even high consumers remain below these levels, including in the US population.

    How the Body Handles Aspartame

    After ingestion, aspartame is completely broken down in the gut into phenylalanine (about 50%), aspartic acid (about 40%), and methanol (about 10%). These compounds are also naturally present in many everyday foods and are metabolised in normal physiological pathways.

    A key exception however is individuals with phenylketonuria. People with Phenylketonuria cannot metabolise phenylalanine properly and must avoid aspartame completely. This is why products containing aspartame carry the warning that they contain a source of phenylalanine.

    Cancer and Carcinogenicity Evidence

    Large toxicology programmes in animals, including studies at very high doses of 4000 mg per kg per day or more, have not shown credible carcinogenic effects. Systematic reviews and regulatory assessments generally conclude there is no consistent evidence that aspartame causes cancer in humans, and overall certainty of harm is considered very low.

    However, not all evidence is aligned.

    A large French cohort study found higher total cancer risk, including breast and obesity-related cancers, in higher consumers of aspartame. The hazard ratios ranged approximately from 1.13 to 1.22, but the authors noted that residual confounding, reverse causality, and bias could not be excluded.

    Network toxicology and docking studies have also suggested possible molecular interactions with cancer-related proteins, but these remain theoretical and require confirmation in vivo.

    Some recent narrative reviews continue to describe chronic consumption as potentially “treacherous” or carcinogenic based mainly on animal or mechanistic data, and recommend caution with long-term high intake.

    Neurocognitive and Neurological Effects

    Experimental animal studies have shown oxidative stress, neuronal loss, and learning or memory impairment at a range of doses, sometimes at or below accepted daily intake levels.

    A scoping review reports mood changes, depression-like and anxiety-like behaviour in animal models, and some human data suggesting possible behavioural or mood effects at high daily intake. It also suggests that people with pre-existing neurological or metabolic conditions may be more vulnerable.

    Because of concerns relating to neurotoxicity and glutamate receptor activity, several reviews recommend extra caution in people with seizure disorders, neurological disease, or during pregnancy.

    Metabolic Effects, Obesity, and Diabetes

    A 2025 systematic review and meta-analysis of controlled human trials found little to no effect of aspartame on blood glucose or insulin compared with water or other low-calorie sweeteners, and significantly lower responses compared with sugar. Effects were observed both acutely and over several weeks to months.

    Long-term animal research with non-nutritive sweeteners shows no consistent evidence of major weight gain or metabolic harm overall, although aspartame has in some cases been linked to reduced glucose tolerance under specific conditions.

    Reviews on obesity suggest that while artificial sweeteners may reduce calorie intake, they could also influence gut microbiota, insulin signalling, and appetite regulation in ways that are still not fully understood.

    Regulatory and Epidemiological Perspectives

    Overall, the evidence can be summarised as follows.

    The strongest evidence supports the conclusion that aspartame is safe at current typical intakes for the general population, excluding individuals with PKU. This is supported by large margins below the ADI, multiple regulatory reviews, and the absence of a convincing cancer signal in human data.

    Moderate evidence suggests that high or chronic intake may pose risks in certain contexts, including neurocognitive effects, oxidative stress, or possible cancer signals. However, these findings are inconsistent and often based on animal or low-quality observational data.

    The World Health Organization expert committee (JECFA) reaffirmed safety at current intakes and concluded that human cancer evidence is not convincing, with overall certainty rated very low.

    Other narrative reviews highlight ongoing controversy, possible neurodegenerative or systemic effects, and argue that chronic regular use may still require further investigation and better labelling.

    Who Should Be Most Cautious

    People with phenylketonuria must avoid aspartame entirely due to inability to metabolise phenylalanine.

    Pregnant women, children, and people with neurological conditions or seizure disorders are often advised in some reviews to limit or avoid aspartame as a precaution, even though regulatory agencies still consider it safe within ADI levels.

    Individuals consuming large amounts of diet products daily may approach the ADI, so clearer labelling of exact content is often recommended to help manage intake.

    Why Some People Think It Is Unsafe

    Aspartame remains one of the most studied food additives, yet findings are mixed, which contributes to public concern.

    Neurocognitive concerns include headaches, mood changes, anxiety, depression, insomnia, and memory issues, particularly at higher intake levels or in animal studies. Proposed mechanisms include increased brain phenylalanine and aspartate levels, neurotransmitter disruption, oxidative stress, and neuronal effects.

    Cancer concerns are driven by several factors, including a French cohort showing small risk increases, animal tumour findings from the Ramazzini Institute, and mechanistic studies suggesting possible carcinogenic pathways. The IARC classification of aspartame as “possibly carcinogenic” also contributed to public concern, although this reflects limited evidence rather than confirmed harm.

    Other theoretical risks discussed in reviews include neurodegeneration, seizures, allergies, reproductive issues, kidney effects, and systemic oxidative stress, mostly based on animal or high-dose studies.

    At the same time, regulatory reviews and many epidemiological studies conclude no clear carcinogenicity or major harm at typical intake levels, creating a split in interpretation that fuels ongoing debate.

    What Is the Reality of Its Safety

    Across regulatory bodies and large-scale reviews, aspartame is considered safe for most people at typical intake levels. Population exposure is generally well below ADI limits, and long-term toxicological and epidemiological studies have not identified consistent harm in humans.

    At the same time, there are credible signals from animal and mechanistic studies, along with some observational findings, that suggest possible neurocognitive effects, oxidative stress, and small cancer associations at higher intake levels. These findings are not consistent and are often low certainty.

    The most accurate interpretation is that aspartame is safe within current guidelines for the general population, but uncertainty remains around long-term high intake and certain vulnerable groups.

    How Safe Is It to Drink Fizzy Drinks With Aspartame and How Much Would Be Unsafe

    For most healthy people, drinking fizzy drinks with aspartame is considered safe at usual amounts.

    Regulatory acceptable daily intakes are 40 mg per kg body weight per day in Europe and 50 mg per kg in the US. For a 70 kg adult, this roughly translates to around 9 to 16 cans of diet soda per day depending on brand and formulation before reaching the upper limit.

    Population studies show that even high consumers generally remain below these thresholds.

    Concerns typically arise at very high chronic intakes, where animal studies have shown oxidative stress and behavioural changes, although these are not directly comparable to normal human consumption levels.

    Certain groups should be more cautious, including people with PKU, pregnant women, young children, and those with neurological conditions.

    If You Are Generally Healthy and Still Concerned

    If you are generally healthy and still concerned, it is reasonable to keep intake well below the ADI, for example occasional or a few diet drinks per day rather than high daily consumption.

    It may also be helpful to vary sweeteners and include unsweetened options such as water, tea, or coffee to reduce cumulative exposure.

    If you notice reproducible symptoms such as headaches, mood changes, or gastrointestinal discomfort that consistently occur after consuming aspartame, several reviews suggest trial reduction or avoidance to see if symptoms improve.

    Take Home Message

    Aspartame is one of the most extensively researched food additives in the world. The majority of evidence supports its safety at current intake levels for the general population, with the clear exception of people with phenylketonuria.

    Concerns remain due to mixed findings in animal studies, observational research, and mechanistic theories, but these have not translated into consistent evidence of harm in humans at typical dietary exposures.

    For most people, the key issue is not avoidance but moderation and overall dietary pattern. High intake is very different from occasional consumption, and context matters more than single ingredients.


    References

    Magnuson BA, Burdock GA, Doull J, et al. Aspartame: A safety evaluation based on current use levels, regulations, and toxicological and epidemiological studies. Critical Reviews in Toxicology. 2007;37(8):629-727.

    Makar Abdel Messih N. The safety of aspartame. JAMA. 2015 Mar 30.

    Wojcieszonek A, Szpyt J, Pajor K, Hawryłkowicz V. Can aspartame-sweetened products safely help with weight loss? Journal of Education, Health and Sport. 2020 Sep 15.

    Biernikiewicz M, Biernikiewicz J, Wilewska A, et al. Aspartame in the diet: A contribution to the debate on safety and health impact. Journal of Education, Health and Sport. 2025 Feb 12.

    Zhang Y. Aspartame: A review of functional properties and physiology impacts of aspartame. Theoretical and Natural Science. 2024 Jul 26.

    Choudhary A, Pretorius E. Revisiting the safety of aspartame. Nutrition Reviews. 2017 Sep;75(9):718-730.

    Czarnecka K, Pilarz A, Rogut A, et al. Aspartame—True or False? Narrative review of safety analysis of general use in products. Nutrients. 2021 Jun;13(6):1957.

    Solmaz F, Dıraman E, Sezgin B. Current approaches to the use of artificial sweetener aspartame. 2021 Mar 30.

    Burh A, Batra S, Sharma S. Emerging facts on chronic consumption of aspartame as food additive. Current Nutrition & Food Science. 2021 Aug 12.

    Ali W, Mohammed SA, Abdullah EM, ElDeen EMS. Aspartame: Basic information for toxicologists. Sohag Medical Journal. 2019 Apr 1.

    Shaher SAA, Mihailescu D, Amuzescu B. Aspartame safety as a food sweetener and related health hazards. Nutrients. 2023 Aug;15(15):3410.

    Goodman J, Boon D, Jack MM. Perspectives on recent reviews of aspartame cancer epidemiology. Global Epidemiology. 2023 Aug;5:100109.

    El Doueihy N, Ghaleb J, Kfoury K, et al. Aspartame and human health: A mini-review of carcinogenic and systemic effects. Journal of Xenobiotics. 2025 Jul 7.

    Riess L, Huynh BQ, Nachman KE. Aspartame exposures in US population studies using NHANES data. Journal of Exposure Science & Environmental Epidemiology. 2024 May 9.

    Schorb S, Gleiss K, Wedekind R, et al. Assessment of aspartame occurrence in foods and beverages on the German market. Foods. 2023 May 26.

    Knezovic Z, Jurcevic Zidar B, Pribisalić A, et al. Artificial sweeteners in food products intake assessment. Nutrients. 2025 Mar 22.

    Trawiński J, Skibiński R. Stability of aspartame in soft drinks and toxicity evaluation. Food Research International. 2023 Aug;170:113996.

    Jones SK, McCarthy DM, Vied C, et al. Transgenerational transmission of aspartame-induced anxiety. PNAS. 2022.

    Fowler SP, et al. Early-life exposure to diet soda and autism outcomes. Nutrients. 2023.

  • Agility in combat sports is not simply about moving fast or running through footwork patterns. It is about rapidly changing speed and direction in response to an opponent, often under pressure, fatigue, and uncertainty. Because of this, agility development in sports like taekwondo, karate, judo, wrestling, fencing, boxing, and mixed combat settings is more complex than traditional speed or conditioning work.

    Research in combat sports consistently separates change-of-direction speed (COD) from true reactive agility, and this distinction is key for training design.

    Understanding Agility in Combat Sports

    A consistent finding across the literature is that agility and change-of-direction ability are related but not the same.

    Change-of-direction speed (COD) refers to pre-planned movement. The athlete knows exactly where they are going and simply executes the movement as efficiently as possible.

    Agility, in contrast, includes perception and decision-making. The athlete must react to an opponent, a stimulus, or an unpredictable situation.

    This distinction matters because improvements in COD do not automatically transfer to real fight situations where reaction and decision-making dominate.

    Reactive agility, where an athlete responds to an opponent or cue, is particularly important in combat and self-defence contexts. However, research suggests it is less commonly trained in structured programs compared to COD work.

    What Training Methods Improve Agility

    Research across taekwondo, karate, wrestling, judo, fencing, and mixed combat populations shows several effective training approaches, especially when the goal is improving speed, footwork, and COD ability.

    Plyometric Training

    Plyometric (jump-based) training is one of the most consistently supported methods for improving explosive performance in combat sports.

    Across studies in taekwondo, karate, judo, wrestling, fencing, and silat, 4 to 12 weeks of plyometric training (typically 2 to 3 sessions per week) leads to:

    • Improved change-of-direction speed
    • Increased lower-body power
    • Better jump performance
    • Improvements in sport-specific actions such as kicking and explosive movement patterns

    In karate and taekwondo populations specifically, plyometric programs have shown improvements in jumping ability, COD performance, and kick power. In wrestling, combining plyometrics with resistance training enhances explosive outputs such as jump height and force production.

    Overall, plyometric training appears more effective than general strength or stability work for improving speed and explosive movement qualities relevant to combat sports.

    Ladder and Footwork Drills

    Ladder drills are commonly used to develop stepping patterns and coordination. In younger taekwondo athletes aged 9 to 12, ladder training has been shown to significantly improve stepping agility.

    When compared with plyometric training in karate athletes, ladder drills tend to improve agility and footwork, while plyometrics are more effective for speed and aerobic capacity. This suggests ladder drills may be particularly useful for refining coordination and movement efficiency, especially in developmental athletes.

    Combined Agility Training Programs

    Structured agility programs lasting around six weeks, incorporating multiple components including reactive tasks, have been shown to improve:

    • Agility performance
    • Reaction time
    • Power
    • Balance
    • Flexibility

    In taekwondo athletes, these combined programs appear more effective than general control training, highlighting the benefit of integrated approaches rather than isolated drills.

    Reactive and Decision-Making Training

    Reactive agility training introduces an opponent or stimulus-based element, requiring athletes to make decisions under pressure.

    Research in tactical and combat-related settings shows that combining reactive tasks with COD training improves:

    • Response speed
    • Agility in unpredictable situations
    • Decision-making under pressure

    Examples include light-based systems, partner cues, and combat-specific scenarios such as 1v1 or sport-relevant reaction drills.

    However, research also highlights a gap. While COD training is widely studied and consistently effective, there is still limited evidence on how best to develop true reactive agility. This has led researchers to suggest more use of small-sided games and 1v1 scenarios to better replicate real combat demands.

    Change-of-Direction vs Reactive Agility Why It Matters

    Most training methods used in combat sports such as sprint work, plyometrics, and mixed conditioning consistently improve COD tests like pro-agility and Illinois agility tests.

    However, improvements in COD do not always translate to reactive agility performance.

    This is an important distinction:

    • COD training improves physical execution of movement
    • Reactive agility training improves perception, anticipation, and decision-making

    Research suggests that to improve transfer to real combat situations, training must include reactive elements rather than relying solely on pre-planned drills.

    How Combat Sports Athletes Should Train Agility

    Most evidence-based programs in combat sports share a similar structure:

    • Duration: 4 to 12 weeks
    • Frequency: 2 to 3 sessions per week

    Effective programs typically combine three components:

    1. Explosive Development (Plyometrics and Sprint Work)

    Used to improve COD ability, lower-body power, and explosive actions such as kicking and striking.

    2. Footwork and Coordination Drills (Ladders and Cones)

    Used to improve stepping patterns, rhythm, and movement efficiency.

    3. Reactive Agility Training (Opponent-Based or Stimulus-Based Work)

    Used to develop decision-making speed and real-world responsiveness.

    Key Takeaways

    Agility in combat sports is not just speed. It is the integration of movement, perception, and decision-making under pressure.

    Research suggests:

    • Plyometric training is highly effective for improving explosive power and COD ability across multiple combat sports
    • Ladder and cone drills help refine footwork and coordination, particularly in younger athletes
    • Reactive agility training is essential for transferring physical ability into real combat situations
    • COD and reactive agility should be trained separately, as they develop different qualities
    • Most effective programs combine explosive, technical, and reactive components over 4 to 12 weeks

    Although agility work is often overlooked in favour of technical training, research consistently shows it is a very beneficial quality to develop for combat sport performance.

  • Telogen effluvium (TE) is one of the most common causes of sudden, diffuse hair shedding, particularly in women. It is usually non-scarring and often reversible. Rather than being a primary disease of the hair follicle, it represents a reaction to a systemic or physiological stressor that temporarily disrupts the normal hair growth cycle.

    TE occurs when a larger than normal proportion of hair follicles prematurely shift from the growing phase (anagen) into the resting phase (telogen). This leads to increased daily shedding, often in the range of 150 to 400+ hairs per day. The loss is typically diffuse across the scalp rather than localised, and people often notice reduced ponytail thickness rather than bald patches.

    Clinical Types

    Acute telogen effluvium usually begins around 2 to 4 months after a triggering event. It is the most common form and typically resolves within 3 to 6 months once the underlying cause is addressed. Hair regrowth generally follows within 6 to 12 months.

    Chronic telogen effluvium persists for longer than 6 months and may fluctuate over time. In some cases, the underlying trigger is unclear. This form can last for years, although it still follows a non scarring and potentially reversible pattern.

    Causes and Triggers

    Telogen effluvium is most often triggered by a significant systemic stressor. Common physiological triggers include pregnancy and postpartum hormonal changes, menopause, severe illness, surgery, trauma, hemorrhage, and sudden weight loss. Infections are also important, including high fevers and COVID 19, which has been strongly associated with post infectious shedding.

    Nutritional and metabolic factors play a major role. Deficiencies in iron, ferritin, vitamin D, vitamin B12, zinc, and protein can all contribute, particularly when combined with malnutrition, malabsorption, or rapid weight loss. Thyroid dysfunction is another well recognised cause affecting hair cycling.

    Medications can also trigger TE, including anticoagulants, anticonvulsants, retinoids, some antidepressants, and high dose hormonal contraceptives. Emotional stress is frequently reported, particularly significant life events, although everyday stress alone is less strongly supported as a direct cause. In a notable proportion of cases, no clear trigger is identified.

    Pathophysiology and Hair Cycle Disruption

    The central mechanism in telogen effluvium is a premature shift of follicles into the telogen phase. This is thought to occur in response to systemic stress that disrupts normal follicular activity. When multiple follicles enter telogen at the same time, shedding becomes noticeable several months later, reflecting the natural timing of the hair cycle.

    Across different triggers, the shared pathway is systemic stress whether physiological, nutritional, metabolic, or hormonal. This temporarily alters the normal balance of the hair cycle, leading to synchronised shedding of hairs that had previously been in the growth phase.

    Rapid Weight Loss as a Trigger

    Rapid weight loss is a well established cause of telogen effluvium and can occur with crash diets, bariatric surgery, or certain weight loss medications. The primary mechanism is metabolic stress rather than weight loss itself.

    Severe calorie restriction reduces energy availability for the hair follicle, which has a high rate of cellular turnover. In this state, follicles may be pushed prematurely into the telogen phase. Protein energy deficiency further compounds this effect, particularly when weight loss is rapid or unplanned.

    Micronutrient deficiencies are also common in this context, including iron, zinc, vitamin B12, and folate. These deficiencies often develop alongside rapid weight reduction or malabsorptive states. Shedding typically appears 2 to 6 months after the period of weight loss and reflects the delayed nature of the hair cycle response.

    people using GLP 1 medications for weight loss are increasingly presenting with this type of hair shedding, alongside women in the postpartum period. In both situations, the combination of rapid physiological change, altered intake, and systemic stress appears to contribute to the development of telogen effluvium.

    Diagnosis

    Diagnosis of telogen effluvium is primarily clinical. A key feature is a history of a triggering event occurring approximately 2 to 4 months before the onset of diffuse shedding. The absence of scarring and the generalised pattern of loss are important distinguishing features.

    Supportive tests may include hair pull or wash tests and trichoscopy. In some cases, trichogram or scalp biopsy may be used to differentiate TE from other causes of hair loss such as female pattern hair loss. Blood tests are often performed to identify underlying contributors, including full blood count, ferritin, iron studies, thyroid function, and selected vitamin levels.

    Management and Prognosis

    Management focuses on identifying and correcting the underlying trigger. This may involve treating illness, addressing nutritional deficiencies, adjusting medications, or stabilising weight and metabolic status. In many acute cases, no specific pharmacological treatment is required.

    Reassurance is an important part of care, as telogen effluvium is non scarring and does not cause permanent follicular damage. Once the triggering factor is removed or resolved, hair typically begins to regrow over time.

    In persistent or distressing cases, supportive options such as topical or oral minoxidil, nutritional supplementation, and cosmetic approaches may be considered, although evidence varies. Emotional impact should also be acknowledged, as visible shedding can significantly affect quality of life despite the condition being medically benign.

    Take Home Message

    Telogen effluvium is a common, usually reversible cause of diffuse hair shedding triggered by systemic stressors such as illness, hormonal change, nutritional deficiency, medication, or rapid weight loss. It occurs due to a temporary disruption of the hair cycle, leading to synchronised shedding months after the trigger.

    Diagnosis is mainly clinical, supported by targeted investigations to identify underlying causes. Most cases resolve once the trigger is addressed, with gradual regrowth over several months. The key principles of management are identification of reversible factors, correction of underlying causes, and reassurance regarding the self limiting nature of the condition.

    Disclaimer

    This article is for educational and informational purposes only and is not a substitute for professional medical advice, diagnosis, or treatment. If you are experiencing hair loss or scalp changes, you should seek assessment from a qualified healthcare professional to determine the underlying cause and appropriate management.

  • Hair loss is something we have been covering quite a bit lately in UCD, and it made me realise how often it comes up not just academically but in real life too. It is something I see a lot, and something I have personally experienced as well.

    Dealing with hair loss myself has given me a completely different perspective on it. It is not just a physical change. It can affect confidence, how you feel day to day, and even how you see yourself. Because of that, I wanted to put together a clear, evidence-based overview of alopecia that actually makes sense without overcomplicating it.

    At its simplest, alopecia just means hair loss. In reality, it covers a wide range of conditions, all with different causes, patterns, and outcomes. Understanding those differences is what allows us to make sense of what is actually going on.

    One of the most important distinctions is whether the hair follicle is still intact. This determines whether the hair loss is potentially reversible or permanent.

    Non-scarring alopecia refers to hair loss where the follicle is still preserved. In these cases, regrowth is often possible once the underlying issue is addressed. This is where the majority of people fall.

    The most common type is androgenetic alopecia, more commonly known as pattern hair loss. This develops gradually over time and is driven by a combination of genetics and hormonal sensitivity. In men, it tends to present as a receding hairline and thinning at the crown, while in women it usually shows up as more diffuse thinning through the centre of the scalp, often noticed as a widening part.

    Another type that people are often familiar with is alopecia areata. This is an autoimmune condition where the body mistakenly targets the hair follicles, leading to patchy hair loss. It can remain as small, localised patches, or in more severe cases progress to complete scalp or body hair loss. What makes it particularly challenging is how unpredictable it can be.

    Telogen effluvium is different again. This tends to present as sudden, widespread shedding rather than defined patches or patterns. It is usually triggered by some form of stress on the body. This could be illness, surgery, significant weight loss, hormonal changes, or even prolonged psychological stress. Although it can feel quite alarming, it is often temporary once the underlying trigger is resolved.

    There are also other causes of non-scarring hair loss, including traction alopecia from prolonged tension on the hair, trichotillomania, fungal infections of the scalp, and hair loss associated with treatments like chemotherapy.

    In contrast, scarring alopecia involves permanent damage to the hair follicle. In these cases, the follicle is destroyed and replaced with scar tissue, meaning regrowth is no longer possible. Although less common, these types are important to recognise early.

    Conditions such as lichen planopilaris and frontal fibrosing alopecia fall into this category, along with central centrifugal cicatricial alopecia and certain inflammatory or autoimmune scalp disorders. These often involve underlying inflammation, and without early intervention, the hair loss can become permanent.

    Something that is often overlooked is that hair loss is not always just one condition. It is entirely possible to have overlapping types at the same time. For example, pattern hair loss combined with telogen effluvium. This can make things feel more confusing and is one of the reasons why a clear understanding of the different patterns is so important.

    Hair loss also does not affect everyone in the same way. Pattern hair loss becomes more common with age, while alopecia areata often appears earlier in adulthood, a significant amount of cases are diagnosed before the age of forty. Diffuse shedding conditions like telogen effluvium are particularly common in women, often linked to hormonal changes, nutritional factors, or stress.

    What is important to understand is that hair loss is rarely just cosmetic. It can be linked to hormonal imbalances, nutritional deficiencies, autoimmune conditions, or lifestyle factors that are often overlooked.

    From both a personal and professional point of view, I think it is something that deserves more attention. It is easy to dismiss it or assume it is just part of getting older or something you have to live with, but that is not always the case.

    In many situations, once you understand the underlying cause, there are ways to improve it or at least manage it more effectively. Even when it is not fully reversible, having clarity around what is happening can make a huge difference in how you approach it.

    Medical Disclaimer:
    This article is for educational purposes only and is not intended to replace medical advice, diagnosis, or treatment. If you are experiencing hair loss or any related symptoms, it is important to consult a qualified healthcare professional or dermatologist for an individual assessment.

    For more evidence-based content on hair loss, health, and performance, follow @sarahcurranfitpro

  • Melasma is a common form of facial hyperpigmentation characterised by symmetrical, irregularly bordered patches of increased pigmentation. While it is often discussed as a single condition, melasma is clinically and histologically diverse. Understanding its different types is essential, as both the distribution of pigmentation and the depth of pigment within the skin significantly influence prognosis and treatment outcomes.

    Clinical Pattern: Where Melasma Appears

    Melasma is classified into distinct types based on its anatomical distribution on the body.

    Centrofacial Melasma

    This is the most common presentation. It typically involves the forehead, cheeks, nose, upper lip, and chin. Its widespread distribution across central facial features often makes it the most noticeable and cosmetically concerning type.

    Malar Melasma

    Malar melasma is more localised, affecting the cheeks and the nose. This pattern is frequently seen in individuals with sun exposure concentrated on the mid-face.

    Mandibular Melasma

    This type presents along the jawline and chin. It is more commonly observed in older individuals and is often associated with cumulative sun damage.

    Extrafacial Melasma

    A less common variant, extrafacial melasma affects areas beyond the face, including the neck, sternum, forearms, and upper chest. This type may be linked to chronic environmental exposure and, in some cases, hormonal influences.

    Depth of Pigment: Why It Matters

    Beyond location, melasma is further classified based on how deeply pigment is deposited within the skin. This classification is critical, as it directly impacts treatment responsiveness.

    Epidermal Melasma

    Pigment is located in the upper layers of the skin. It often appears more defined under Wood’s lamp examination and typically responds well to topical depigmenting agents.

    Dermal Melasma

    Pigment is located deeper in the dermis and involves pigment-containing cells known as melanophages. This type is more resistant to treatment and often slower to improve.

    Mixed Melasma

    Mixed melasma includes both epidermal and dermal pigment. It is common in clinical practice and shows variable response to treatment depending on the dominant component.

    Indeterminate Melasma

    In this type, the depth cannot be clearly classified. It is more common in darker skin types or complex presentations and requires careful clinical assessment.

    Diagnostic Tools and Their Role

    Accurate classification of melasma type relies on a combination of diagnostic techniques.

    Wood’s lamp examination helps differentiate between epidermal, dermal, mixed, and indeterminate types by enhancing pigment contrast.

    Dermoscopy allows visualisation of pigment patterns, colour variation, and network structures, which supports assessment of pigment depth.

    Reflectance confocal microscopy and photoacoustic microscopy provide high-resolution imaging to assess pigment depth and identify additional features such as vascular involvement.

    Emerging Insights: The Role of Vascular Changes

    Recent advances suggest that melasma is not solely a pigmentary disorder. Photoacoustic microscopy has introduced refined subtypes based on both pigment depth and vascular involvement.

    These include epidermal pigment only, epidermal pigment with vascular changes, mixed pigment, and mixed pigment with vascular involvement. Increased dermal blood vessels may contribute to the persistence of melasma and may influence treatment strategies in resistant cases.

    Why Correct Classification Is Essential

    Identifying the specific type of melasma has direct clinical relevance. It helps predict treatment response, guides therapy selection, supports realistic patient expectations, and informs long-term management planning.

    Take Home Message

    Melasma is a condition I see very frequently when doing facials and treatments and also teaching, and while it is medically benign, it can be really bothersome and distressing for many individuals due to its impact on facial appearance and confidence. It is a multifactorial and heterogeneous condition best understood through its clinical distribution and the depth of pigmentation. Clinical patterns include centrofacial, malar, mandibular, and extrafacial types. Histological classification includes epidermal, dermal, mixed, and indeterminate forms. Emerging imaging techniques add further refinement by identifying vascular involvement.

    Accurate classification is fundamental to optimising treatment outcomes and improving long-term management of this chronic and often recurrent condition.

    Medical Disclaimer

    This article is intended for educational and informational purposes only and does not constitute medical advice, diagnosis, or treatment. Melasma is a complex dermatological condition, and individual cases may vary. Always consult a qualified healthcare professional or dermatologist for personalised assessment and treatment recommendations.

    Connect with Me

    For more evidence-based content on skin, health, and aesthetics, follow me on
    Instagram: sarahcurranfitpro

  • Binge eating doesn’t just end when the episode finishes.

    For most people, what follows is the harder part. Guilt, frustration, and the urge to fix it quickly by eating less, training more, or starting over.

    The issue is that response is often what keeps the cycle going.

    Research consistently shows that what actually helps is not punishment. It is returning to structure, building better coping skills, and changing how you respond to yourself in that moment.

    This is something I come across regularly in my work. I recently completed a Level 9 in Behaviour Change in UCD, and binge and restrict patterns are one of the most common things I see with clients, be it general fat loss clients or athletes.

    It is also something I have experienced myself, particularly during periods of bodybuilding style training after a cut. When calories are low for a long time, both your body and your mindset are primed for a rebound.

    I see similar patterns in fighters as well, especially around weight cuts, where restriction followed by overeating can become very normalised.

    Something I would recommend for everyone is to not just plan for the restriction phase of their deficit, but also how they plan to come out of it and eat at maintenance again when it finishes.

    Why the all or nothing approach does not work

    After a binge, the instinct is usually to tighten everything up

    Eat less the next day
    Cut out certain foods
    Train harder

    It feels like discipline, but in reality it just sets up the next binge.

    You end up stuck in a loop of restriction, cravings, bingeing, guilt, then back to restriction.

    Breaking that cycle starts with doing the opposite of what your instinct is telling you.

    What to do in the next 24 hours

    Go back to regular eating

    One of the most important things you can do is return to normal meals and snacks.

    Not skipping meals. Not saving calories. Just eating in a structured, consistent way.

    This helps bring things back to baseline and reduces the chances of another binge.

    Do not try to undo it

    Extra training or cutting food to compensate might feel productive, but it reinforces the cycle.

    Your training should stay the same
    Structured
    Planned
    Not used as punishment

    You are not trying to erase anything. You are just getting back to your routine.

    Change how you speak to yourself

    This is a big one and it is backed by research.

    People who respond with more self compassion are less likely to binge again, feel less out of control, and handle setbacks better.

    That does not mean ignoring it. It means not attacking yourself over it.

    A simple shift can help
    That happened. I am getting back on track now.

    The bigger picture

    Binge eating is very closely linked to how people deal with emotions.

    Most binges do not come out of nowhere. They are usually preceded by stress, low mood, or feeling overwhelmed.

    Food becomes a quick way to switch off or escape, even if it is only temporary.

    Common patterns that make it worse are overthinking what happened, blaming yourself, thinking in extremes, and trying to ignore how you feel.

    These tend to increase the chances of it happening again.

    What helps is building better ways to respond in those moments

    Noticing what you are feeling without reacting straight away
    Allowing discomfort without trying to escape it immediately
    Stepping back from all or nothing thoughts
    Having alternative actions ready

    These are skills and they improve with practice.

    Approaches that work

    Different approaches tend to come back to similar principles.

    CBT style approaches focus on getting eating patterns consistent, identifying triggers, challenging unhelpful thoughts, and having a plan for setbacks.

    DBT style approaches focus more on handling intense emotions, managing urges, and staying present instead of reacting.

    Self compassion and mindfulness help reduce harsh self criticism, shame, and automatic reactions. Even short interventions can make a noticeable difference.

    Structured training can help, but only when it is not used as a way to compensate. It should support your routine, not punish you for going off track.

    For athletes and high performers

    This tends to come up more in people who are disciplined and goal driven.

    Whether it is bodybuilding, fighters making weight, or people holding themselves to high standards, there is often pressure to stay lean, rigid rules around food, and an all or nothing mindset.

    After a binge, the focus should stay simple

    Eat normally
    Train as planned
    Do not compensate

    Longer term, it helps to shift focus from appearance to performance, be aware of high risk periods like cuts or stress, and build more flexibility into your approach.

    One of the biggest drivers here is self critical thinking.

    That voice that says that was not good enough is often the same one driving both restriction and bingeing.

    It is something I see constantly in both clients and athletes.

    Take home message

    Getting back on track after a binge is not about being stricter.

    It is about returning to structure, staying consistent, managing emotions better, and dropping the self criticism.

    Long term progress comes from responding better, not reacting harder. Having a plan in place for after any kind of cut can really help, and the most important thing is to give yourself grace.

    Disclaimer

    This article is for educational purposes only and is not a substitute for individual medical or psychological advice. If you are experiencing frequent binge eating or feel out of control around food, it is important to seek support from a qualified professional.

    For more evidence based coaching and education, you can find me on Instagram at @sarahcurranfitpro.

  • When we think about hair growth, most people jump straight to nutrition, hormones, or topical treatments. But there is a really interesting and still emerging area of research looking at how light, specifically blue light, interacts with proteins in the hair follicle to influence growth.

    This actually came up in tonight’s skin science lecture, and it is one of those topics that really sticks with you because it links together so many areas we do not always think about, including light exposure, cellular biology, and hair growth.

    At the centre of this is cryptochrome 1 (CRY1), a blue light sensitive protein traditionally known for its role in circadian rhythms. Recent dermatology research now shows that CRY1 is not only present in human hair follicles, but may actively regulate the hair growth cycle.

    What Are Cryptochromes?

    Cryptochromes are proteins that respond to blue light and help regulate the body’s internal clock. They have been studied for years in relation to sleep, metabolism, and cellular timing.

    What is newer, and particularly relevant for us in aesthetics, skin, and hair science, is that these same proteins are active in the skin and hair follicles, where they appear to influence cell behaviour, growth, and regeneration.

    CRY1 in the Hair Follicle

    CRY1 is strongly expressed in anagen, the active growth phase of the hair cycle. It has been identified in key areas of the follicle, including:

    • Epithelial stem cell regions
    • Outer root sheath (ORS) keratinocytes

    These are critical zones that drive hair growth. So when a protein is highly active here, it is likely playing a functional role.

    How Blue Light Influences Hair Growth

    Research using 453 nm blue light, a specific wavelength, has shown some really interesting effects on hair follicle biology:

    • Increased CRY1 protein levels in keratinocytes and whole follicles
    • Prolongation of the anagen growth phase
    • Delayed transition into catagen, the regression phase
    • Increased metabolic activity and proliferation in ORS cells at low doses

    In simple terms, low dose blue light appears to support hair staying in the growth phase for longer.

    CRY1 and Hair Cycle Control

    When researchers manipulate CRY1 directly, the effects become even clearer.

    Silencing CRY1 leads to:

    • Earlier transition into catagen
    • Reduced cell proliferation

    Activating CRY1 using compounds like KL001 leads to:

    • Prolonged anagen phase
    • Increased expression of growth related genes

    CRY1 also appears to regulate genes involved in:

    • Cell cycle progression, for example CDK6
    • Apoptosis, or programmed cell death

    This supports the idea that CRY1 helps maintain a pro growth, anti regression environment within the follicle.

    It Is Not Working Alone: OPN3 and Light Signalling

    CRY1 does not act in isolation. Another protein called OPN3, a blue to green light sensitive opsin, is also involved.

    Both CRY1 and OPN3 are expressed in ORS cells, and research shows:

    • Knocking down either protein reduces cell proliferation
    • Both are required for the full effect of blue light on hair growth

    This suggests a coordinated light sensing system within the follicle, where multiple photoreceptors work together to influence growth and cell behaviour.

    The Circadian Connection

    One of the most interesting aspects of CRY1 is its link to the circadian rhythm.

    Hair follicles appear to have their own clock system, involving genes like:

    • BMAL1
    • CLOCK
    • PER1
    • CRY1

    These genes oscillate over a 24 hour cycle and are linked to:

    • Timing of the hair growth phase
    • Stem cell activity
    • Cellular turnover

    There is also evidence from animal models, such as seasonal hair growth in goats, showing that light exposure and photoperiod can influence hair cycling via these clock genes.

    So this is not just about light hitting the skin. It is about light acting as a timing signal for hair growth itself.

    What This Means for Treatments

    From a practical perspective, this research opens the door to light based therapies for hair growth.

    The key takeaways so far:

    • Low dose blue light may enhance hair growth by increasing CRY1 activity
    • CRY1 supports the anagen phase and reduces premature regression
    • There is a clear biological mechanism, not just a cosmetic effect

    However, this is important. Most of the current evidence comes from:

    • In vitro, cell based studies
    • Ex vivo, isolated human follicle models

    We still need well designed human clinical trials to determine:

    • Optimal wavelengths and dosages
    • Safety over long term use
    • Real world effectiveness

    Take Home Message

    CRY1 is emerging as a key regulator in hair follicle biology, linking light exposure, circadian rhythms, and hair growth.

    The current evidence suggests:

    • CRY1 is highly active in growing hair follicles
    • Blue light at 453 nm increases CRY1 levels
    • This helps prolong the growth phase and support proliferation
    • CRY1 works alongside other photoreceptors like OPN3
    • Light based therapies show potential but are not fully clinically established yet

    From my perspective, this is a great example of where lifestyle, environment, and cellular biology all intersect. It also reinforces something I always come back to. Small, often overlooked factors like light exposure can have a much bigger impact on the body than we realise.

    And as always, the key is staying evidence based while keeping an open mind as the research evolves.

    Medical Disclaimer

    This article is for educational purposes only and is based on current research evidence. It is not intended to replace medical advice, diagnosis, or treatment. If you are experiencing hair loss or any scalp condition, you should consult with a qualified healthcare professional or dermatologist before starting any new treatment, including light based therapies.

  • One of the most important topics we are covering in skin science is the impact of UV rays on the skin. When we talk about skin aging, most people think of time as the main driver. In reality, ultraviolet (UV) exposure is the dominant external factor, responsible for up to 90 percent of visible skin aging in exposed areas.

    This is where the concept of photoaging comes in. Photoaging refers to premature aging caused by chronic sun exposure. While intrinsic or chronological aging is inevitable, UV exposure significantly accelerates and amplifies these changes.

    Photoaging vs Normal Aging

    Intrinsic aging is driven by genetics and time. It leads to gradual thinning of the skin, fine lines, and reduced elasticity.

    Photoaging is externally driven and largely preventable. It overlaps with intrinsic aging but progresses faster and presents differently. Common features include deeper wrinkles, skin laxity, uneven pigmentation, rough texture, and visible blood vessels known as telangiectasias.

    In simple terms, sun exposure does not just age the skin, it changes how the skin ages.

    UVA vs UVB: Not All UV Is Equal

    Understanding the difference between UVA and UVB is essential when it comes to prevention.

    UVA, which ranges from 320 to 400 nanometres, makes up about 95 percent of the UV radiation that reaches the earth. It penetrates deeply into the dermis and is primarily responsible for collagen breakdown, pigmentation changes, and deep wrinkle formation. UVA is present all day, all year, and can pass through clouds and glass.

    UVB, which ranges from 280 to 320 nanometres, has higher energy but mainly affects the epidermis. It is responsible for sunburn, direct DNA damage, and mutations associated with skin cancer.

    Both contribute to skin aging, but UVA is the main driver of long-term structural damage, while UVB is the primary cause of acute injury.

    The Biological Mechanisms Behind Skin Aging

    UV radiation accelerates skin aging through several interconnected biological pathways.

    DNA damage is one of the primary mechanisms. UV exposure leads to the formation of DNA lesions such as cyclobutane pyrimidine dimers and 8-oxoG. This results in cellular dysfunction, mutations, and an increased risk of carcinogenesis.

    Oxidative stress also plays a major role. UV exposure generates reactive oxygen species that damage lipids, proteins, and DNA. This oxidative damage contributes significantly to visible aging.

    Collagen breakdown and extracellular matrix degradation occur as UV exposure increases matrix metalloproteinases and reduces TGF beta signalling. This leads to collagen degradation, loss of elasticity, and thinning of the dermis, which presents clinically as wrinkles and sagging.

    Cellular senescence and inflammation are also key contributors. Damaged cells enter a senescent state and release inflammatory signals known as the senescence associated secretory phenotype. This drives chronic low grade inflammation, often referred to as inflammaging.

    UV exposure also alters immune function. It suppresses normal immune responses in the skin, reducing repair capacity and increasing susceptibility to skin cancer.

    Clinical Presentation of Photoaging

    Over time, cumulative UV exposure leads to a range of visible skin changes. These include fine and deep wrinkles, dryness, rough texture, skin laxity, pigmentation changes, telangiectasias, elastosis, and slower wound healing.

    It is important to recognise that damage begins long before it becomes visible on the skin.

    Skin Type and UV Vulnerability

    Skin response to UV exposure varies depending on skin type.

    Lighter skin types, classified as Fitzpatrick I to III, have much lower intrinsic protection, with an approximate SPF of 3.3. This makes them more vulnerable to UV induced DNA and collagen damage.

    Darker skin types have higher intrinsic protection, with an approximate SPF of 13.4. However, they are more prone to pigmentation issues and skin cancers are often detected later.

    UVA plays a particularly important role in pigmentary aging, especially in individuals with darker skin tones.

    Why Sunburn Matters

    Sunburn is more than temporary redness. It is a clear indicator of significant biological damage.

    Frequent sunburns are strongly associated with increased skin cancer risk. Studies show that repeated sunburns can increase melanoma and squamous cell carcinoma risk by around 50 percent or more. Childhood sunburn is particularly significant, and repeated episodes can double the risk of basal cell carcinoma.

    Sunburn also causes immediate tissue and immune damage. It is an acute inflammatory response characterised by redness, pain, and swelling. DNA damage begins within hours, and immune suppression occurs at the level of the skin.

    Repeated sunburn accelerates visible aging by contributing to wrinkles, pigmentation changes, and structural skin damage. It is also important to note that significant damage can occur even without visible sunburn.

    Prevention: The Most Effective Anti Aging Strategy

    If UV exposure is the primary driver of skin aging, then protection becomes the most effective intervention.

    Limiting exposure and seeking shade is the first step. It is recommended to avoid peak UV times, particularly around midday and when the UV index is three or higher.

    Physical barriers such as clothing, hats, and sunglasses are highly effective. UPF clothing, long sleeves, wide brimmed hats, and UV blocking sunglasses significantly reduce UV exposure.

    Daily use of broad spectrum sunscreen is essential. A minimum of SPF 30 is recommended, with SPF 50 or higher advised for higher risk individuals. Sunscreen should protect against both UVA and UVB, be applied adequately, and reapplied every two hours or after swimming or sweating. Regular use has been shown to reduce photoaging, DNA damage, and skin cancer risk.

    It is also important to consider factors beyond UV. Visible light and pollution contribute to pigmentation and oxidative stress. Tinted sunscreens containing iron oxides and the use of antioxidants such as vitamins C and E or plant compounds can provide additional protection.

    Emerging Areas in Skin Protection

    Ongoing research is exploring strategies to mitigate UV induced damage. These include enhancing DNA repair pathways, supporting autophagy, and the use of compounds such as retinoids, metformin, and plant derived antioxidants.

    While these approaches are promising, UV protection remains the most effective and accessible strategy.

    Final Takeaway

    Ultraviolet radiation is the single most significant external driver of premature skin aging. It accelerates aging through DNA damage, oxidative stress, inflammation, and collagen breakdown.

    Protecting the skin from UV exposure is the most effective step you can take to preserve skin health, maintain appearance, and support long term skin function.

    Disclaimer

    This article is for educational purposes only and is not intended to replace medical advice, diagnosis, or treatment. Always consult with a qualified healthcare professional or dermatologist for individual concerns or conditions related to your skin.

    Follow for More Evidence Based Content

    For more evidence-based guidance on skin health, nutrition, and fitness, follow me on Instagram @sarahcurranfitpro where I share practical, science-backed advice you can actually apply.

  • Skin infections remain one of the most common and disruptive issues in combat and contact sports, including wrestling, Brazilian jiu-jitsu, judo, MMA, and rugby. These environments create ideal conditions for the transmission of bacterial, fungal, and viral pathogens, often leading to missed training, withdrawal from competition, and wider team outbreaks. I covered the microbiome of the skin recently in my skin science course, and it is really relevant to combat sports due to the prevalence of skin infections in this area.

    Current research consistently highlights that while the risk cant be eliminated, it can be significantly reduced through structured hygiene practices, early detection, and coordinated team protocols.

    Infection Risk in Combat Sports

    The high incidence of skin infections in combat athletes is multifactorial. Key contributing factors include:

    • Repeated skin-to-skin contact
    • Frequent abrasions, cuts, and mat burns
    • Sweat accumulation and friction, particularly in occluded areas
    • Use of shared equipment and facilities

    Additionally, a proportion of athletes may carry organisms such as Staphylococcus aureus asymptomatically, increasing the potential for silent transmission within teams.

    Most Common Infections

    Across the literature, three categories dominate:

    • Bacterial: Methicillin-resistant Staphylococcus aureus (MRSA) and other Staphylococcal infections
    • Fungal: Tinea corporis (ringworm)
    • Viral: Herpes gladiatorum

    These infections are highly transmissible in contact settings and can escalate quickly if not identified and managed early.

    Core Prevention Strategies

    Evidence supports a multi-layered approach to infection control. No single intervention is sufficient in isolation, and consistent implementation across several domains is required.

    Personal Hygiene

    • Shower immediately after training or competition
    • Maintain regular hand hygiene
    • Keep fingernails short
    • Avoid sharing personal items such as towels, razors, clothing, or water bottles

    Clothing, towels, and training gear should be washed in hot water at or above 50°C, and athletes should change out of sweat-soaked clothing promptly.

    Wound Management

    • Clean all cuts, abrasions, and mat burns immediately
    • Cover wounds appropriately during training
    • Monitor for early signs of infection

    Athletes with suspicious lesions should be removed from contact activity until assessed and no longer considered contagious.

    Environmental Hygiene

    • Implement structured cleaning protocols for mats and equipment
    • Regularly disinfect shared spaces including showers and changing areas
    • Use effective disinfectants with residual activity where possible

    Research shows that appropriate mat disinfection and hand hygiene measures can significantly reduce microbial load.

    Screening and Early Intervention

    • Routine skin checks, particularly before competition
    • Early reporting of suspicious lesions
    • Prompt isolation of affected athletes

    This is critical in preventing isolated infections from developing into outbreaks.

    Education and Protocols

    Education is consistently identified as a key factor in reducing infection rates. Athletes and staff should understand:

    • How to recognize common infections
    • The importance of hygiene and wound care
    • When to seek assessment and temporarily withdraw from training

    Clear, enforceable hygiene protocols within teams are essential.

    The Skin Microbiome and Infection Risk

    From a skin science perspective, the skin microbiome is highly relevant. There is a growing body of research showing its role in infection susceptibility and spread in combat sports.

    In athletes, particularly those in contact sports, the microbiome is constantly challenged by sweat, friction, frequent washing, antiseptic use, and shared environments. This can lead to microbial imbalance or dysbiosis, where protective organisms are reduced and opportunistic pathogens become more dominant.

    Research shows that combat sport athletes often have altered microbial profiles compared to non-athletes, and dysbiosis is associated with increased susceptibility to bacterial, fungal, and viral infections. Disruption of the skin barrier alongside microbiome imbalance facilitates pathogen entry and transmission. While hygiene is essential, overly aggressive or excessive use of antiseptics may further disrupt this balance.

    A balanced approach is recommended:

    • Effective hygiene practices
    • Protection of skin integrity
    • Avoidance of unnecessary overuse of harsh antimicrobial products

    Additional Considerations

    • Rapid weight loss practices may influence infection management
    • In high-risk settings, prophylactic antiviral or antifungal strategies may be considered
    • MRSA colonization may occur in asymptomatic athletes, and outbreak management may include screening and targeted decolonization under medical guidance

    Take-Home Message

    Combat sport athletes are at elevated risk of skin infections, but consistent and structured hygiene practices, proper wound care, environmental cleaning, routine screening, and ongoing education significantly reduce risk. Protecting the skin microbiome and barrier integrity while using antiseptics strategically further supports long-term skin health and infection prevention.

    Medical Disclaimer

    This article is for educational purposes only and is not intended to replace medical advice, diagnosis, or treatment. Athletes presenting with suspected skin infections should seek assessment from a qualified healthcare professional and follow sport-specific medical guidelines before returning to training or competition.

  • Combat sports place unique physiological demands on athletes, requiring a combination of power, endurance, repeated high-intensity efforts, and technical precision. Across the literature, a small group of supplements consistently demonstrates performance benefits. The most well-supported include caffeine, creatine, sodium bicarbonate, and β-alanine, with emerging evidence for beetroot juice. A well-structured, high-quality diet should always form the foundation of performance, with supplements used as a secondary strategy to provide a potential edge.

    Core Performance Supplements

    Caffeine -The Strongest Evidence Base

    Caffeine is the most consistently supported ergogenic aid in combat sports. Multiple systematic reviews and meta-analyses show that doses of approximately 3–5 mg/kg taken 30–60 minutes before competition improve combat-specific performance.

    These improvements include increased number of attacks and throws, enhanced handgrip strength, faster reaction time, greater power output, and improved time to exhaustion. Caffeine enhances glycolytic energy contribution and increases lactate tolerance.

    Research also shows small but clear improvements in handgrip strength and total judo throws, alongside increases in blood lactate and heart rate without a corresponding rise in perceived exertion. A network meta-analysis ranks caffeine, as well as caffeine combined with sodium bicarbonate, among the most effective supplements for improving power and technical actions such as kicks and throws in elite athletes.

    In taekwondo-specific research, doses of 3–5 mg/kg have been shown to acutely improve both physical performance and psychological state. Very high doses of caffeine (e.g. 9 mg/kg) are associated with a high incidence of side-effects and do not seem to be required to elicit an ergogenic effect.

    Creatine

    Creatine is well established for improving mean and peak power in combat-specific tests. Evidence from network meta-analyses shows that creatine, particularly when combined with sodium bicarbonate, produces large improvements in power output compared to placebo.

    Combat-sport-specific reviews demonstrate that creatine supplementation increases body mass, fat-free mass, maximal strength, and power. However, it has little effect on sport-specific endurance or fatigue. Importantly, creatine has a strong safety profile.

    Sodium Bicarbonate and Buffering Agents

    Sodium bicarbonate is a key buffering agent shown to improve repeated high-intensity efforts and glycolytic capacity across combat sports including judo, taekwondo, karate, wrestling, jiu-jitsu, and boxing.

    Both acute and chronic supplementation strategies have demonstrated benefits, particularly during later stages of competition when acidosis and fatigue accumulate. Sodium bicarbonate is often most effective in improving performance late in matches.

    β-alanine, another buffering-related supplement, increases intramuscular carnosine levels. This contributes to improvements in strength, power, and total work during high-intensity efforts in combat sports.

    Beetroot (Dietary Nitrate)

    Beetroot supplementation, a source of dietary nitrate, may enhance oxidative metabolism and improve isometric and isokinetic force, as well as balance. These adaptations are particularly relevant for grappling-based sports.

    However, results are variable and appear to depend on dosage, muscle group involved, and specific supplementation protocols. While promising, the current evidence base remains limited compared to core supplements.

    Micronutrient Support

    Position stands recommend the use of a daily multivitamin, vitamin D, omega-3 fatty acids, and minerals such as iron and zinc when required. These support overall health, recovery, and brain function alongside performance-focused supplementation.

    Practical Considerations

    You do not need to spend a fortune on supplements or buy into expensive, heavily marketed brands. Cheaper brands can be just as effective, as higher costs often reflect marketing rather than product quality.

    Where possible, choose supplements that are third-party tested. This is particularly important for athletes competing in tested federations, as contamination with banned substances can occur and may lead to a failed drug test.

    Summary of Supplement Use by Performance Goal

    Acute competition performance:
    Caffeine, sodium bicarbonate, β-alanine

    Power, strength, and fat-free mass during training camp:
    Creatine, β-alanine

    Repeated high-intensity efforts:
    Sodium bicarbonate, β-alanine, caffeine

    Aerobic capacity and balance:
    Beetroot

    Take home message

    Across combat sports, the most robust evidence supports the use of caffeine, creatine, sodium bicarbonate, and β-alanine for enhancing performance. Beetroot juice shows emerging potential as an additional strategy. A strong nutritional foundation should always come first, with supplements used strategically to provide a potential performance advantage.

    Supplement choice and dosing should be individualised, tested during training, and implemented alongside a well-structured nutrition and weight management plan.

    Follow @sarahcurranfitpro on Instagram for more evidence-based content on performance, nutrition, and health.

    Medical Disclaimer

    This article is for educational purposes only and is not intended as medical advice. Supplements may not be suitable for all individuals and can interact with medications or underlying health conditions. Always consult a qualified healthcare professional before starting any supplementation protocol.