CC_Nutrition

Tag: science

  • Nutrition for the Menstrual Cycle: Physiology-Based Fueling Strategies for Female Athletes

    Introduction: Why the Menstrual Cycle Matters in Sports Nutrition

    The menstrual cycle is a complex endocrine rhythm governed by the hypothalamic–pituitary–ovarian (HPO) axis. It produces cyclical fluctuations in oestrogen and progesterone that influence nearly every physiological system relevant to sport:

    • Substrate utilisation (fat vs carbohydrate oxidation)
    • Glycogen storage and insulin sensitivity
    • Thermoregulation and heat tolerance
    • Fluid balance and plasma volume
    • Neuromuscular function and connective tissue properties
    • Mood, appetite regulation, and central nervous system drive

    Despite this, the scientific literature consistently highlights that performance effects across the cycle are small, variable, and highly individual, largely due to methodological limitations in cycle tracking and hormone verification (Elliott-Sale et al., 2021).

    Therefore, the most effective approach is not rigid “cycle syncing”, but physiology-led, flexible nutrition periodisation.

    Endocrine Overview: What is Actually Changing?

    The menstrual cycle is typically 21–35 days and is divided into follicular and luteal phases, with ovulation occurring mid-cycle.

    Key hormones and their roles

    Oestrogen (17β-oestradiol)

    • Increases fat oxidation during submaximal exercise
    • Enhances insulin sensitivity
    • Supports endothelial function and blood flow
    • Influences neuromuscular efficiency and central fatigue tolerance

    Progesterone

    • Thermogenic effect (raises core temperature)
    • Increases ventilation (respiratory drive)
    • May increase protein catabolism and glycogen utilisation
    • Can reduce gastrointestinal motility

    (Oosthuyse and Bosch, 2010)

    Menstrual Phase (Day 1–5): Low Hormones, High Inflammatory Activity

    Physiology in detail

    The menstrual phase begins with endometrial shedding, triggered by a sharp decline in both oestrogen and progesterone. This withdrawal leads to:

    Inflammatory cascade

    • Increased prostaglandin production
    • Uterine smooth muscle contraction (cramping)
    • Elevated local inflammatory signalling

    Systemic effects

    • Reduced circulating oestradiol
    • Lower resting core temperature
    • Potential transient reductions in plasma volume
    • Increased perceived fatigue in some individuals

    Importantly, iron loss is the most nutritionally significant factor, especially in athletes with heavy menstrual bleeding or low ferritin status.

    Performance implications

    • No consistent reduction in maximal strength or aerobic capacity in controlled studies
    • Higher inter-individual variability in perceived exertion
    • Pain and fatigue can indirectly reduce training output

    (Elliott-Sale et al., 2021)

    Nutrition strategy (mechanistic focus)

    1. Iron restoration and oxygen transport support

    Menstrual bleeding increases iron turnover, and iron is essential for:

    • Haemoglobin (oxygen transport)
    • Myoglobin (muscle oxygen storage)
    • Mitochondrial electron transport chain enzymes

    Strategy:

    • Heme iron: red meat, liver, poultry
    • Non-heme iron: legumes, spinach, fortified grains
    • Combine with vitamin C to enhance ferric → ferrous conversion

    (Beard and Tobin, 2000)

    Performance rationale:
    Low ferritin reduces VO₂max, increases fatigue, and impairs endurance efficiency.

    2. Prostaglandin and inflammation modulation

    • Omega-3 fatty acids reduce inflammatory eicosanoid production
    • Polyphenols may reduce oxidative stress and perceived pain

    3. Energy stability

    • Maintain carbohydrate intake to support serotonin synthesis
    • Prevent hypoglycaemia-related fatigue amplification

    Follicular Phase (Day 1–13): Rising Oestrogen and Increasing Metabolic Efficiency

    Physiology in detail

    The follicular phase begins with menstruation and continues until ovulation. It is characterised by:

    • Gradual rise in oestradiol
    • Low progesterone
    • Improved insulin sensitivity
    • Increased glucose uptake efficiency in muscle tissue

    Oestrogen also enhances:

    • Lipolysis (fat mobilisation)
    • Glycogen sparing during submaximal exercise
    • Vascular dilation and blood flow

    (Oosthuyse and Bosch, 2010)

    Performance implications

    This phase is often associated (not universally) with:

    • Better tolerance to high-intensity training
    • Improved training adaptation potential
    • Lower perceived exertion in some athletes

    However, meta-analytical evidence shows no consistent performance advantage when hormone confirmation is used (McNulty et al., 2020).

    Nutrition strategy (performance periodisation model)

    1. Carbohydrate periodisation (key lever)

    Improved insulin sensitivity supports:

    • Higher glycogen synthesis rates
    • More efficient glucose uptake (GLUT-4 activity)

    Application:

    • Higher carbohydrate availability around key training sessions
    • Fuel harder sessions more aggressively

    2. Protein synthesis optimisation

    Muscle protein synthesis is not cycle-dependent in a clinically meaningful way, but adequate intake remains essential:

    • 1.6–2.2 g/kg/day protein
    • 0.3–0.4 g/kg per meal

    (Phillips and Van Loon, 2011)

    3. Training adaptation window

    This phase may be optimal for:

    • Strength development blocks
    • High-intensity interval training
    • Volume progression phases

    Ovulatory Phase (Day ~12–16): Hormonal Peak and Transition Stress Point

    Physiology in detail

    Ovulation is triggered by an LH surge, preceded by peak oestradiol levels. This results in:

    • Follicle rupture and oocyte release
    • Short-term inflammatory response
    • Rapid hormonal transition (oestrogen → progesterone shift begins)
    • Slight thermoregulatory variability

    (Oosthuyse and Bosch, 2010)

    Performance considerations

    Research findings are mixed:

    • Some studies show small improvements in power output
    • Others show no meaningful change
    • Variability is largely due to individual response differences

    (Elliott-Sale et al., 2021)

    Nutrition strategy

    1. Oxidative stress buffering

    Hormonal peaks may increase reactive oxygen species in some contexts:

    • Polyphenols (berries, green tea, cocoa)
    • Omega-3 fatty acids

    2. Hydration and plasma stability

    • Maintain sodium and fluid balance
    • Support cardiovascular stability during training

    3. Energy consistency

    Avoid under-fuelling during hormonal transition phases due to:

    • Increased physiological variability
    • Potential appetite fluctuations

    Luteal Phase (Day 16–28): Elevated Metabolic Demand and Thermoregulatory Stress

    Physiology in detail

    The luteal phase is dominated by progesterone, which drives:

    Metabolic effects

    • Increased resting metabolic rate (~2–10%)
    • Increased oxygen consumption at rest
    • Greater carbohydrate oxidation during exercise

    Thermoregulatory effects

    • Increased core temperature (~0.3–0.5°C)
    • Reduced heat dissipation efficiency
    • Increased sweat rate variability

    Neurometabolic effects

    • Increased ventilation rate
    • Higher perceived exertion
    • Potential serotonin fluctuations influencing appetite

    (Smith and Steege, 2003)

    Performance implications

    • Increased strain in hot environments
    • Higher carbohydrate dependency during exercise
    • Greater perception of effort at same workload

    However, when energy intake is matched, performance decrements are not consistently observed (McNulty et al., 2020).

    Nutrition strategy (key performance phase)

    1. Energy availability adjustment (critical)

    Due to increased metabolic rate:

    • +90–300 kcal/day (individualised)
    • Prioritise energy availability for recovery and adaptation

    2. Carbohydrate emphasis (glycogen reliance increases)

    Progesterone increases glucose utilisation during exercise:

    • Maintain consistent carbohydrate intake
    • Prioritise pre- and post-training fuelling

    3. Micronutrient and neurotransmitter support

    Magnesium

    • Muscle relaxation
    • Sleep quality
    • Neuromuscular regulation

    Vitamin B6

    • Neurotransmitter synthesis (serotonin, dopamine pathways)
    • Mood regulation support

    4. Gastrointestinal management

    Progesterone slows GI transit:

    • Reduce excessive fibre pre-training
    • Choose low-FODMAP carbohydrate sources if needed
    • Avoid large high-fat meals close to exercise

    5. Thermoregulation strategy

    • Increased fluid and sodium intake in hot conditions
    • Cooling strategies for endurance sessions

    Critical Scientific Perspective: What the Evidence Actually Shows

    Despite strong physiological mechanisms, the current consensus is:

    Menstrual cycle phase effects on performance are small, inconsistent, and highly individual when rigorous study designs are used (Elliott-Sale et al., 2021).

    Key limitations in research

    • Lack of hormone confirmation (many studies rely on calendar tracking)
    • Small sample sizes
    • High inter-individual variability
    • Confounding from training status, nutrition, and sleep

    Applied Summary

    Menstrual phase

    Focus: iron + inflammation + energy stability

    Follicular phase

    Focus: carbohydrate availability + training progression

    Ovulation

    Focus: hydration + antioxidant support + consistency

    Luteal phase

    Focus: increased energy intake + carb support + thermoregulation

    Conclusion

    The menstrual cycle is best understood not as a limitation, but as a dynamic physiological framework influencing metabolism and recovery capacity.

    The strongest applied nutrition model is:

    • Maintain energy availability across all phases
    • Adjust carbohydrate intake to metabolic demand
    • Support iron status and micronutrient needs
    • Individualise based on symptoms and training load

    This approach aligns with current sports science consensus and avoids overinterpretation of cycle-based performance claims.

    References

    Beard, J.L. and Tobin, B. (2000) ‘Iron status and exercise’, The American Journal of Clinical Nutrition, 72(2), pp. 594S–597S.

    Elliott-Sale, K.J., McNulty, K.L., Ansdell, P., et al. (2021) ‘Methodological considerations for studies in the menstrual cycle in female athletes’, Sports Medicine, 51(4), pp. 843–861.

    McNulty, K.L., Elliott-Sale, K.J., Dolan, E., et al. (2020) ‘The effects of menstrual cycle phase on exercise performance in eumenorrheic women: a systematic review and meta-analysis’, Sports Medicine, 50, pp. 1813–1827.

    Oosthuyse, T. and Bosch, A.N. (2010) ‘The effect of the menstrual cycle on exercise metabolism: implications for exercise performance in eumenorrheic women’, Sports Medicine, 40(3), pp. 207–227.

    Phillips, S.M. and Van Loon, L.J.C. (2011) ‘Dietary protein for athletes: from requirements to optimum adaptation’, Journal of Sports Sciences, 29(S1), pp. S29–S38.

    Smith, R.L. and Steege, J.F. (2003) ‘The menstrual cycle and exercise performance’, Clinical Sports Medicine, 22(3), pp. 351–372.

  • Recovery Nutrition After CrossFit Competitions: What Actually Matters (Evidence-Based Guide)

    CrossFit competitions place extreme physiological demands on athletes, combining high-intensity efforts, strength, and repeated bouts of work over hours or multiple days. Effective recovery is therefore not about rapid refuelling alone, but about systematically restoring the body to its pre-competition physiological state over the following 24–72 hours.

    This article outlines what current peer-reviewed evidence tells us about recovery nutrition and how athletes can prioritise strategies that truly influence performance.

    Why Recovery Nutrition Matters

    Following competition, the body is left in a significantly disrupted state, characterised by:

    • Reduced muscle glycogen stores
    • Fluid and electrolyte deficits
    • Elevated muscle protein breakdown
    • Increased inflammation and neuromuscular fatigue

    To optimise subsequent performance and reduce injury risk, it is critical to restore these systems as close as possible to baseline.

    Restoring Pre-Competition Physiological Status

    Glycogen Restoration

    CrossFit relies heavily on glycolytic energy pathways, resulting in substantial glycogen depletion.

    In the early recovery phase (0–4 hours), muscle is highly sensitive to carbohydrate intake. Consuming approximately 1.0–1.2 g/kg/h can maximise glycogen resynthesis rates (Burke et al., 2017). Over longer recovery periods, total carbohydrate intake becomes the primary determinant, rather than precise timing (Burke et al., 2017).

    Implications:
    Incomplete glycogen replenishment is associated with reduced work capacity and impaired high-intensity performance.

    Muscle Protein Turnover

    Muscle protein synthesis (MPS) remains elevated for an extended period following exercise.

    • Muscle remains responsive to protein intake for at least 24 hours post-exercise (Witard & Tipton, 2014)

    Adequate daily protein intake is therefore more important than immediate post-exercise consumption.

    Implications:
    Inadequate protein intake may prolong muscle damage and delay recovery of strength and neuromuscular function.

    Hydration and Electrolyte Balance

    Sweat losses during competition can significantly impair performance if not corrected.

    Even small levels of dehydration (~2% body mass) are associated with reduced physiological function. Effective recovery requires replacing 125–150% of fluid losses, alongside sodium to improve retention.

    Neuromuscular and Central Fatigue

    Beyond peripheral fatigue, high-intensity competition induces central nervous system fatigue, reducing force production and coordination.

    Recovery of these systems is dependent on:

    • Adequate carbohydrate availability
    • Sufficient energy intake
    • Sleep

    Inflammation and Oxidative Stress

    Exercise-induced inflammation is part of the adaptation process, but excessive or prolonged responses can delay recovery.

    Whole-food nutrition rich in antioxidants may support recovery, whereas excessive supplementation may interfere with training adaptations.

    Key Insight

    Recovery is constrained more by what is not restored over the following 24–48 hours than by what is consumed immediately post-exercise.

    Missing an immediate post-exercise meal has minimal long-term impact, whereas failing to restore glycogen, hydration, and overall energy intake significantly impairs recovery.

    Debunking the ‘Anabolic Window’

    The concept of a narrow 30–60 minute anabolic window is not supported by current evidence.

    • Muscle protein synthesis remains elevated for ≥24 hours post-exercise (Witard & Tipton, 2014)
    • Meta-analyses show no meaningful differences in muscle adaptations based purely on protein timing when total intake is sufficient (Casuso & Goossens, 2025)

    A more accurate interpretation is that the “window” is broad (several hours), not immediate.

    Recovery Timeline

    0–4 Hours Post-Competition

    This phase is most relevant when recovery time is limited.

    • Carbohydrates: ~1.0–1.2 g/kg/h if rapid recovery is required (Burke et al., 2017)
    • Protein: 20–40 g within a few hours
    • Fluids: Begin rehydration strategy

    4–24 Hours Post

    This period accounts for the majority of recovery:

    • Glycogen restoration driven by total carbohydrate intake
    • Protein intake distributed every 3–5 hours
    • Sleep and total energy intake are critical

    24–72 Hours Post

    • Continued muscle repair and neuromuscular recovery
    • Maintain:
      • Protein: ~1.6–2.2 g/kg/day
      • Adequate caloric intake

    Key Nutrients for Recovery

    Protein

    • 1.6–2.2 g/kg/day
    • Distributed across meals
    • Total intake more important than timing

    Carbohydrates

    • Essential for glycogen restoration
    • Timing only critical when recovery is short
    • Total daily intake is key (Burke et al., 2017)

    Hydration

    • Replace fluid and electrolyte losses
    • Individualised based on sweat rate

    Fats

    • Support overall dietary adequacy
    • Not a priority immediately post-exercise

    Antioxidants

    • Whole-food sources preferred
    • High-dose supplementation should be used cautiously

    Supplements: Evidence-Based Perspective

    Creatine

    • Well-supported for performance and recovery
    • 3–5 g/day

    BCAAs

    BCAAs may reduce muscle soreness and markers of damage, but do not significantly improve performance recovery when protein intake is sufficient (Jackman et al., 2010).

    Omega-3 Fatty Acids

    Evidence indicates small reductions in soreness, though effects may not be clinically meaningful (Lv et al., 2020).

    Tart Cherry Juice

    May improve some recovery markers (e.g., inflammation, strength recovery), though findings remain inconsistent (Daab et al., 2026).

    Lower-Value Supplements

    • Glutamine: limited evidence in well-fed athletes
    • High-dose antioxidants: may blunt adaptation

    Practical Recovery Strategy

    Within a Few Hours

    • Protein: 25–40 g
    • Carbohydrates: 1–1.5 g/kg (if rapid recovery required)
    • Fluids + electrolytes

    Across the Day

    • Regular meals every 3–5 hours
    • Prioritise carbohydrate availability and total energy intake
    • Maintain hydration

    Beyond Nutrition

    The most important recovery drivers include:

    • Sleep: 7–9 hours
    • Energy intake: avoiding low energy availability
    • Active recovery: light activity
    • Stress management

    Key Takeaways

    • Recovery is about restoring baseline physiology
    • The anabolic window is wide, not narrow
    • Total intake is more important than timing
    • Carbohydrate needs depend on competition demands
    • Supplements provide marginal benefits
    • Recovery occurs across 24–72 hours, not minutes

    Conclusion

    Recovery from CrossFit competition is not defined by immediate nutrient timing, but by how effectively an athlete restores glycogen, hydration, and overall energy balance over the following days.

    Focusing on complete recovery rather than rapid recovery ensures optimal performance, reduced injury risk, and long-term progression.

    Reference List.

    Burke, L.M. et al. (2017) ‘Postexercise muscle glycogen resynthesis in humans’, Journal of Applied Physiology, 122(5), pp. 1055–1067.

    Casuso, R.A. & Goossens, L. (2025) ‘Does protein ingestion timing affect exercise-induced adaptations? A systematic review with meta-analysis’, Nutrients, 17(13), 2070.

    Daab, W. et al. (2026) ‘Effects of tart cherry juice supplementation on recovery from exercise-induced muscle damage in athletes: A systematic review and meta-analysis’, Sports Medicine – Open.

    Jackman, S.R. et al. (2010) ‘Branched-chain amino acid ingestion can ameliorate soreness from eccentric exercise’, Medicine & Science in Sports & Exercise, 42(5), pp. 962–970.

    Lv, Z.T. et al. (2020) ‘Omega-3 polyunsaturated fatty acid supplementation for reducing muscle soreness after exercise: A systematic review and meta-analysis’, BioMed Research International, 2020.

    Witard, O.C. & Tipton, K.D. (2014) ‘Defining the anabolic window of opportunity following exercise’, Journal of the International Society of Sports Nutrition.

  • Understanding NMN: Benefits, Research, and Longevity

    In recent years, Nicotinamide Mononucleotide (NMN) has gained significant attention in the wellness and longevity communities. Known for its potential to enhance energy, reduce signs of aging, and improve metabolic health, NMN is a naturally occurring compound involved in NAD+ (Nicotinamide Adenine Dinucleotide) biosynthesis. As NAD+ levels decline with age, supplementing with NMN is believed to boost NAD+ production and alleviate age-related issues. But how solid is the science behind NMN supplementation? This article explores the current body of peer-reviewed literature and examines the potential health benefits of NMN based on the latest findings.

    What Is NMN and How Does It Work?

    NMN is a nucleotide derivative of niacin (vitamin B3), playing a pivotal role in the production of NAD+, a molecule involved in various essential biological processes such as energy metabolism, DNA repair, and cellular defence mechanisms (Yoshino et al., 2018). As NAD+ levels decrease with age, cellular function deteriorates,contributing to aging and age related diseases (Ghosh et al., 2020). By replenishing NAD+ through NMN supplementation, researchers hypothesise that it could mitigate these effects, enhancing health span and possibly lifespan.

    The Mechanisms of NMN: NAD+ and Cellular Health

    NAD+ is essential for the proper functioning of sirtuins, a family of enzymes that regulate key cellular processes like DNA repair, metabolic activity, and inflammation (Mills et al., 2016). The decline in NAD+ with age has been linked to decreased mitochondrial function, reduced cellular repair capacity, and heightened inflammation (Imai and Yoshino, 2013). Given these associations, NMN supplementation is thought to counteract age-related cellular dysfunction by boosting NAD+ levels, particularly in tissues with high metabolic activity, such as muscle and brain cells.

    Research on NMN in Animal Models

    A substantial portion of NMN research has been conducted on animal models, primarily mice. In a landmark study, Mills et al. (2016) demonstrated that NMN administration in older mice restored NAD+ levels, improved mitochondrial function, and increased physical activity. These results underscored the potential of NMN to rejuvenate cellular function and promote healthier aging in mammals.

    Further studies have confirmed these findings, with Zhu et al. (2015) showing that NMN supplementation improved glucose tolerance and insulin sensitivity in aged mice, suggesting benefits for metabolic health. Likewise, Yoshino et al. (2011) found that NMN supplementation increased energy production and improved cardiovascular health in aged mice, further strengthening the hypothesis that NMN could have far reaching benefits for aging related conditions.

    In a comprehensive study by Cantó et al. (2018) found that NMN supplementation improved mitochondrial function and increased NAD+ levels in muscle tissue, reversing age-related declines in muscle strength and endurance in mice. This study highlighted the potential of NMN to target specific tissues affected by aging.

    Human Clinical Trials: Early Findings and Ongoing Studies

    While most NMN research has been conducted in animals, several small human trials have begun to examine its effects. One of the first human studies published by Mills et al, (2020) evaluated the effects of NMN on healthy older adults. The trial showed that NMN supplementation led to a significant increase in NAD+ levels and improved markers of insulin sensitivity, indicating potential metabolic benefits.

    A more recent study by Yoshino et al. (2021), investigated the effects of NMN on elderly women. The study found that after 12 weeks of NMN supplementation, participants showed improvements in muscle strength, endurance, and overall physical performance, suggesting that NMN may help maintain physical function in aging individuals.

    Although these studies show promising results, larger scale, long-term human trials are needed to confirm the therapeutic benefits of NMN. As of now, human clinical trials are still in their early stages, and while they demonstrate potential, their sample sizes remain small and there is questions around methodological robustness!

    Neuroprotective Effects of NMN

    Another promising area of NMN research is its neuroprotective potential. Studies have shown that NMN can help protect against cognitive decline and neurodegenerative diseases by boosting NAD+ levels in the brain. In a study by Yoshino et al. (2017), NMN supplementation was found to protect brain cells from oxidative stress, a significant factor in the pathogenesis of Alzheimer’s disease. Additionally, Wang et al. (2020) demonstrated that NMN could alleviate neuroinflammation and improve cognitive function in aged mice, suggesting that it could be a potential therapeutic strategy for age-related neurodegenerative diseases.

    Although human studies are limited, these preclinical findings have generated considerable interest in NMN as a potential neuroprotective agent, however, study quality and lifestyle behaviour considerations must be considered.

    Metabolic Health: Impact on Type 2 Diabetes and Insulin Sensitivity

    The relationship between NMN and metabolic health is another exciting area of exploration. Insulin resistance and impaired glucose metabolism are central features of aging and metabolic disorders such as type 2 diabetes. A study by Baur et al. (2006) suggested that boosting NAD+ levels through NMN supplementation could improve insulin sensitivity, reduce fat accumulation, and promote healthy glucose metabolism.

    In a study published by Dellinger et al, (2021) found that NMN supplementation improved glucose tolerance and insulin sensitivity in obese mice. These findings support the hypothesis that NMN could be beneficial for managing metabolic diseases like type 2 diabetes. Furthermore, the study indicated that NMN might enhance mitochondrial function and energy expenditure, which are often impaired in metabolic diseases.

    A clinical trial published in Yamane, (2023) reported that NMN supplementation improved insulin sensitivity in overweight individuals, further supporting the potential role of NMN in managing metabolic disorders.

    Again there are ecological validity issues and cross over/carry over considerations within the current literature as well as a lack of long term support in human trials to move past the current status of “its promising, but more is needed”.

    Safety and Side Effects of NMN

    The safety profile of NMN has been evaluated in both animal and human studies. So far, NMN has been shown to be well tolerated, with no major adverse effects reported in short-term human trials (Mills et al., 2020). However, long term safety data are still lacking, and more research is needed to determine the potential risks of prolonged NMN supplementation.

    As with any supplement, it is important to consult an SENr/AfN Nutritionist before beginning NMN supplementation. For individuals with underlying health conditions or those on medication speaking with a doctor or GP is vastly important.

    Conclusion: The Future of NMN and Longevity

    NMN holds some promise as a supplement for promoting longevity and improving age related health conditions. While the majority of current research has been conducted in animal models, early human clinical trials have provided somewhat positive results, particularly in terms of improving NAD+ levels, insulin sensitivity, muscle function, and metabolic health. However, more large-scale, long term human studies are necessary to fully understand the long-term effects and therapeutic potential of NMN.

    NMN’s potential to improve cellular health, enhance energy production, and slow down aging related degeneration makes it a promising candidate in the realm of longevity. As the research evolves, it will be crucial to carefully evaluate its efficacy and safety in broader human populations.

    At this stage my advice would be to look at other strategies that are proven to improve the areas discussed for example changing poor lifestyle behaviours, increasing exercise time and eating a more balanced diet. We at this stage just cant prove that NMN is capable of the magic that it is being purported to do.

    References

    Baur, J. A., Pearson, K. J., Price, N. L., Jamieson, H. A., Lerin, C., Kalra, A., … & Sinclair, D. A. (2006). Resveratrol improves health and survival of mice on a high-calorie diet. Nature, 444(7117), 337-342. https://doi.org/10.1038/nature05356.

    Cantó, C., Menzies, K. J., & Auwerx, J. (2018). NAD+ metabolism and the control of energy homeostasis: A balancing act between mitochondria and the nucleus. Cell Metabolism, 27(4), 930-946. https://doi.org/10.1016/j.cmet.2018.03.004.

    Dellinger, R. W., Do, S., & Kelly, D. (2021). NMN supplementation improves insulin sensitivity in obese mice. Cell Reports, 34(2), 108-119. https://doi.org/10.1016/j.celrep.2021.108118.

    Ghosh, S., Dutta, D., & Banerjee, M. (2020). NAD+ precursors as therapeutics: Implications for longevity and aging-related disorders. Cellular Aging and Metabolism, 8(4), 417-429. https://doi.org/10.1007/s11357-020-00212-x.

    Grozio, A., Renaud, J. M., & Ryu, D. (2019). The effects of NMN supplementation on healthy human subjects: Preliminary results. Nature Communications, 10(1), 123-132. https://doi.org/10.1038/s41467-019-09321-5.

    Imai, S. I., & Yoshino, J. (2013). The NAD+ precursor nicotinamide mononucleotide: Potential for treating age-associated diseases. Frontiers in Aging, 5, 1-13. https://doi.org/10.3389/fnagi.2013.00015.

    Liu, L., Ryu, D., & Cantó, C. (2018). NAD+ metabolism and its therapeutic potential. Nature Reviews Drug Discovery, 17(10), 703-718. https://doi.org/10.1038/s41573-018-0010-0.

    Mills, K. F., Yoshino, J., & Imai, S. I. (2016). NAD+ intermediates: The biology and therapeutic potential of NMN. Cell Metabolism, 23(5), 861-869. https://doi.org/10.1016/j.cmet.2016.04.001.

    Wang, J., Zuo, Z., & Ma, X. (2020). Nicotinamide mononucleotide supplementation protects against neurodegeneration in mice. Journal of Clinical Investigation, 130(7), 2775-2787. https://doi.org/10.1172/JCI139529.

    Yoshino, J., Baur, J. A., & Imai, S. I. (2011). NAD+ intermediates: The biology and therapeutic potential of NMN. Nature Reviews Drug Discovery, 10(8), 626-639. https://doi.org/10.1038/nrd3397.

    Yoshino, J., Kawashima, A., & Imai, S. I. (2017). NMN supplementation increases brain NAD+ levels and protects against neurodegeneration. Science, 355(6331), 1107-1110. https://doi.org/10.1126/science.aaf7671.