Wellness Matters

08/02/2025

https://drjewilliams.com/blog/the-incredible-health-benefits-of-urolithin-a-discover-the-power-of-this-natural-compound/

Explore Urolithin A’s incredible health benefits for cellular health and longevity in our latest blog post.

07/24/2025

Can We Change Our Brains? All About Neuroplasticity

AUTHOR
Caitlin Holmes, MS, CNS
Can We Change Our Brains? All About Neuroplasticity
DATE PUBLISHED
July 9, 2025

The Brain Is Not Fixed

Your brain grows rapidly in the first five years of life, responding to various physical, social, and environmental factors that influence its development, including brain structure and function. Early life experiences and exposures can even shape your future health outcomes. For example, your childhood experiences shape your learning, skill development, and cognitive processing. This means that what happens in your early years doesn’t just shape your personality; it also sets the stage for how your brain and body respond later in life.

However, it is a myth that your brain stops developing after adolescence. In reality, your brain keeps evolving for your entire life. Every new experience, challenge, or habit helps it grow more adaptable, or “neuroplastic.” Neuroplasticity is the brain’s ability to rewire, adapt, and grow in response to your environment. Not only is this important for general wellness, but plasticity also has implications for mental health, learning, aging, and recovery from injury. Without the ability to respond to change, your brain would not be able to reorganize itself to adapt and compensate for changes. In a sense, your brain is like a whiteboard—it’s easy to write something new, but just as easy to erase and rewrite.

What Is Neuroplasticity?

If you can remember life before cell phones, you probably did not use your thumb in the same way as you do now to send a text. Additionally, if you ever became sick from eating a certain food, you may develop an aversion to that food. These are great examples of how the brain adapts to a specific context. Neuroplasticity is the brain’s ability to reorganize itself by forming new neural connections in response to experiences.

There are two types of neuroplasticity: structural and functional. Structural neuroplasticity means the brain is physically changing and growing new connections or even thickening in some areas, like muscle does with strength training. An example of this can be seen in musicians with dense auditory cortices. Additionally, people who practice meditation have been found to have increased cortical thickness. Functional neuroplasticity is the ability to shift between tasks to different brain areas. This is commonly observed in individuals who have experienced a stroke or traumatic brain injury (TBI). Thanks to these built-in adaptations, your brain doesn’t stop developing once you’re grown up—it keeps learning and changing.

What the Latest Research Is Saying

Although neuroplasticity is considered experience-dependent, there is some evidence that it is triggered by nutrition and lifestyle factors. For example, your diet, sleeping habits, and exercise routines are linked to how well your brain responds to change. To better understand how best to support brain health, neuroplasticity research is rapidly expanding in various areas of study.

Physical activity boosts neuronal survival through increased Brain-Derived Neurotrophic Factor (BDNF). BDNF is important for neuronal activity and synaptic plasticity. Recent studies have shown that moderate aerobic exercise increases hippocampal volume and memory performance in young adults and individuals with neurodegenerative diseases.

Sleep helps your brain sort, store, and strengthen your memories. A recent study found that REM sleep is critical for consolidating new skills and forming flexible cognition. However, daytime naps may also help the brain consolidate and process emotional memories.

Psychedelic compounds (like psilocybin) support neuroplasticity in the brain. A preclinical study found that mice exposed to psilocybin had increased levels of neuroplasticity, which was evident in the number of dendritic branches and density formed during exposure. Additionally, the brain built new connections (synaptogenesis), grew new neurons (neurogenesis), and activated BDNF pathways. In human studies, psilocybin administration had neuroplastic effects and caused positive changes to normal thought patterns.

Cognitive training studies show gains in working memory and executive function with targeted brain training platforms. One meta-analysis found that memory-oriented cognitive training improved working memory. Additionally, combining cognitive training may improve outcomes.
How to Support Neuroplasticity Naturally

1. Mental Stimulation

Learn a new language, instrument, or complex task.
Try dual-tasking exercises (e.g., memory + movement).

2. Physical Activity

Regular aerobic exercise (brisk walking, cycling) increases BDNF and cerebral blood flow.

3. Mindfulness & Meditation

Enhances the prefrontal cortex and hippocampus structure.
Reduces stress-related neurotoxicity.

4. Prioritize Deep Sleep

Memory consolidation and synaptic pruning occur during sleep cycles.
To promote better sleep hygiene, follow a consistent sleep schedule, ensure your room is dark and free of distractions, and avoid blue light before bedtime.

5. Positive Social Interaction

Enhances dopamine and oxytocin, critical for emotional learning and neural growth.

6. Nutrition for Brain Support

Malnutrition is considered a factor in secondary brain injury. A diet rich in omega-3 fatty acids, amino acids, vitamins, minerals, prebiotics, and probiotics supports the brain and may help the brain recover after a TBI.

Supplements That Support Neuroplasticity

A solid routine (i.e., good sleep, regular exercise, and diet) goes a long way for your brain, but certain compounds may also provide support and are worth exploring with your healthcare provider.

Pregnenolone

Pregnenolone is a neurosteroid that may play a role in memory, mood, and how easily your brain adapts. Neurosteroids are known to have anti-inflammatory, neuroprotective, and neurotrophic effects, which means they can support functional and structural changes in the brain. Additionally, pregnenolone may help brain cells grow and communicate better.

Alpha-GPC

Alpha-GPC is a special type of choline, an essential nutrient for brain health, that may help with memory and focus. It is a precursor to the neurotransmitter acetylcholine and may help boost its levels in the brain. Some studies suggest alpha-GPC may help with focus and memory, whether you’re trying to stay sharp or support healthy aging. Additional studies have shown that alpha-GPC may improve motivation.

Bacopa Monnieri

Bacopa monnieri has been used for centuries in Ayurvedic medicine to support memory and mental clarity, and research today is beginning to back that up. It may help with focus, memory, and learning, and some research shows it can calm the brain when it’s overstimulated. This suggests Bacopa monnieri may act as an adaptogen to reduce cognitive stress.

Magnesium L-Threonate

Magnesium L-Threonate (branded Magtein®) is a special form of magnesium that’s designed to reach your brain more easily, indicating its ability to cross the blood-brain barrier. Recent studies have found that Magtein® supplementation supports memory formation and retention, synaptic plasticity, and deep sleep.
Final Thoughts: You Can Reshape Your Brain

Neuroplasticity is a lifelong capacity, not a fixed trait. With the right environmental inputs, lifestyle habits, and supportive compounds, brain transformation is within reach. In other words, you can teach an “old dog new tricks” if the brain is supported and continually challenged to adapt to change.

Before beginning any diet, lifestyle, or supplement routines, talk to your healthcare practitioner to learn what’s best for you

07/21/2025

The Hidden Connection Between Erectile Dysfunction and Antioxidant Status
June 10, 2025 - 12:39

Erectile dysfunction (ED) is frequently perceived as a men’s sexual health concern. However, the physiological incapacity to achieve and sustain an er****on serves as a profound indicator of underlying systemic health issues, particularly those related to cardiovascular and metabolic health. Currently in the United States, the incidence of ED affects 25.9 men per 1,000 and rises with advanced age, with over 70% of men over 70 years of age impacted. Emerging research underscores the significant role oxidative stress plays in the pathology of ED, suggesting that antioxidant status may be a critical factor in both the development and management of this condition.

An er****on is a complex neurovascular event that heavily relies on healthy endothelial function, nitric oxide (NO) signaling, and healthy blood flow. Produced by the vascular endothelial cells lining the blood vessels, NO is a vasodilator that relaxes the smooth muscle in the corpus cavernosum of the p***s, increasing blood flow. The functional loss of NO production through the enzyme nitric oxide synthase (NOS) in the endothelial cells is termed “endothelial dysfunction.” It is considered the earliest stage in the development of hypertension. Endothelial dysfunction is also observed in conditions such as atherosclerosis and insulin resistance (IR), and can be associated with poor pe**le blood flow and erectile insufficiency.

ED often precedes cardiovascular events, acting as an early warning sign of systemic vascular dysfunction. This connection underscores the shared pathophysiological mechanisms of ED and cardiometabolic health, including endothelial dysfunction, inflammation, and oxidative stress.

Multifactorial Origins

It's essential to recognize that ED seldom occurs alone; rather, it's often a result of interconnected issues within the vascular, metabolic, neurological, and endocrine systems.

Metabolic and Vascular Factors

High levels of oxidative stress can impact both metabolic and vascular health, occurring when there is an imbalance between the production of reactive oxygen species (ROS) and the body’s ability to repair cellular tissues. Excessive ROS can degrade NO, leading to endothelial dysfunction, impaired vasodilation, and compromised blood flow. Contextually, both oxidative stress and diminished NO availability promote vascular inflammation and atherosclerotic changes in pe**le arteries.

Hormonal and Neurogenic Factors

Hormonal and neurogenic factors significantly influence the development of ED through decreased hormones, nervous system dysfunction, and metabolic disorders.

Decreased testosterone levels, commonly associated with advancing age and metabolic disorders, can reduce libido and hinder the expression of nitric oxide synthase (NOS) in pe**le tissue, which affects the vasodilatory mechanisms necessary for er****on.
Dysfunction of the autonomic nervous system, which regulates involuntary physiological processes, can disrupt the essential neurovascular coordination needed to initiate and maintain erectile function.
Peripheral neuropathy may further contribute by damaging the sensory and motor nerves of the p***s.
Lifestyle and Environmental Factors

Lifestyle and environmental factors play a pivotal role in the development and progression of ED through their influence on vascular, hormonal, and neurological pathways.

Smoking is a major contributor to endothelial dysfunction, promoting oxidative stress and vasoconstriction, which together impair the vascular flexibility needed for pe**le blood flow.
Excessive alcohol intake can disrupt liver detoxification pathways, interfere with hormonal balance, and impair neural signaling critical for sexual function.
A sedentary lifestyle and physical inactivity increase the risk of IR and obesity, both of which are linked to reduced testosterone levels and elevated systemic inflammation as key contributors to ED.
Chronic stress is a further compounding factor that increases cortisol levels and sympathetic nervous system activity, both of which diminish the parasympathetic signaling activity to initiate and maintain an er****on.
Inadequate or poor-quality sleep exacerbates oxidative stress and lowers testosterone production, which may impair both the libido and erectile function.
The Protective Role of Antioxidants

Antioxidants play a critical role in mitigating the development of ED by helping counteract oxidative stress, a major contributor to endothelial dysfunction. With the ability to scavenge free radicals, antioxidants contribute to the preservation of NO bioavailability and promote endothelial integrity.

Mitochondrial health, as a primary source of ROS production, is a vital aspect of metabolic health that can be supported through increased antioxidant intake, including polyphenols, CoQ10, and alpha-lipoic acid. Additionally, other nutrients, such as L-arginine, vitamin C, vitamin E, polyphenols, flavonoids, and carotenoids, have demonstrated vasoprotective effects by inhibiting inflammation through the NF-κB and NLRP3 inflammasome pathways, which are implicated in vascular injury and immune activation.

Beyond vascular health, antioxidants may also promote endogenous testosterone production by minimizing testicular oxidative damage through the modulation of inflammatory signaling pathways. Antioxidant-rich dietary patterns, such as the Mediterranean diet, have been associated with reduced ED prevalence, improved insulin sensitivity, and decreased systemic inflammation.

Enhancing endothelial function and reducing inflammatory mediators through increased antioxidant intake may support the health of vascular smooth muscle and may promote overall arterial compliance, both of which are essential for healthy erectile function.

Antioxidants Promoting Vascular Health

Vitamin C (ascorbic acid) is a powerful water-soluble antioxidant recognized for its role in endothelial function. By scavenging ROS, it enhances NO bioavailability, potentially improving vasodilation and blood flow. Furthermore, vitamin C aids in the regeneration of other antioxidants, such as vitamin E, and supports collagen synthesis, which is crucial for maintaining vascular integrity.

Vitamin E, made up of tocopherols and tocotrienols, is a fat-soluble antioxidant that shields cell membranes from oxidative damage by neutralizing free radicals. Its antioxidant effects may support vascular health by inhibiting LDL-C oxidation and by scavenging lipid radicals. Moreover, vitamin E may promote endothelial function by boosting NO production and reducing oxidative stress. A six-week, double-blind, parallel-group, placebo-controlled trial involving patients with ED (N = 52) aged 18 to 60 found significant improvement in erectile function with vitamin E and ginseng supplementation (combined) versus the placebo group.

Polyphenols are a broad category of plant-derived compounds, including flavonoids, phenolic acids, and lignans. By modulating endothelial function, polyphenols may exert vasoprotective effects, reducing oxidative stress and inflammation. They may also enhance NO availability and support healthy lipid profiles, contributing to better vascular health.

Flavonoids are a diverse group of polyphenolic compounds found in various fruits, vegetables, and beverages, including tea and wine. They exhibit strong antioxidant properties, scavenging ROS and upregulating endogenous antioxidant defenses. Flavonoids may promote endothelial health by enhancing NO synthesis and supporting a healthy inflammatory response, both of which may promote healthy erectile function.

Carotenoids, including β-carotene, lycopene, lutein, and zeaxanthin, are present in colorful fruits and vegetables. They have antioxidant properties that may guard against lipid peroxidation and oxidative damage in vascular tissues, while supporting endothelial integrity and arterial elasticity.

Clinical Implications

Given the interplay between oxidative stress and ED, evaluating and managing antioxidant status should be central to addressing concerns related to erectile insufficiency. Integrative approaches may include:

Dietary Modifications: Increasing antioxidant-rich foods, such as berries, leafy greens, nuts, and whole grains, aligned with Mediterranean dietary principles.

Lifestyle Modification: Promoting regular physical activity, smoking cessation, and stress management techniques to reduce oxidative stress and improve vascular health.

Nutraceutical Support: Consider targeted antioxidant supplementation for individuals with identified deficiencies or elevated oxidative stress markers.

In conclusion, erectile function serves as a sensitive indicator of overall vascular health, intricately linked to endothelial integrity, nitric oxide availability, and systemic oxidative stress. Addressing oxidative stress through increased antioxidant intake, targeted supplementation, and lifestyle optimization represents a powerful strategy to enhance both vascular health and sexual well-being.

To learn more about nitric oxide, cardiovascular health, and supportive nutrients:

Exploring the Dual Pathways and Nutrients for Enhanced Nitric Oxide Production

Lifestyle Choices for Cardiovascular Wellness: The Latest Clinical Research

Vitamin C: Fueling Nitric Oxide for Healthy Blood Vessels

Vitamin E Tocotrienols: The Ultimate Cardiometabolic Solution

Nitric Oxide: The Key to Healthy Blood Pressure

By Rachel B. Johnson, MS, CNS, LDN

07/21/2025

The Latest on Allergic Response and Gut Microbial Composition
March 19, 2024 - 14:08

The body’s response to allergens is a complex process that involves immune and inflammatory pathways. It often manifests as conditions such as allergic rhinitis, atopic dermatitis, and food allergies, and is estimated to affect more than 20% of the general population.

The incidence of pathologies associated with the allergic response is on the rise. Some researchers have proposed a link between gut dysbiosis and allergic diseases. This is due to the important role the gut microbiome plays in the development of the immune system. Studies have shown that gut microbiota can influence certain aspects of the immune system and inflammatory responses. For example, a meta-analysis involving data from over 340,000 individuals reported that antibiotic use in children under 2 years old was associated with a higher risk of developing certain allergic diseases later in life, including food allergies, allergic rhinitis, asthma, and atopic dermatitis.

Recent clinical and preclinical research suggests that certain probiotics may support a healthy allergic response. A review article by Cukrowska and colleagues explored the role of different species within the Bifidobacterium genus in the presence of allergy in studies focused on infancy. In the early stages of life, the dominance of Bifidobacterium is thought to facilitate the development of certain aspects of the immune system related to the allergic response. Study conclusions indicate that the species Bifidobacterium breve in particular may support a healthy allergic response.

One animal study included in the review by Cukrowska and colleagues explored the effects of the administration of Bifidobacterium breve M-16V with certain prebiotic molecules on a murine population. The study reported a protective effect against an acute allergic skin response and other signs of allergy. Cytokine analysis was performed and an intestinal Th1/Th2 balance was reported to be the underlying cause for this protective response.

Another review explored the role of Lactobacillus in support of a healthy allergic response. One included study involving supplementation with Lactobacillus acidophilus L-92 reported significant alleviation of nasal symptoms. Another study reported 33% fewer episodes of rhinitis in the presence of supplementation with Lactobacillus. Other species of Lactobacillus were shown to modulate the presence of Th2 cytokines interleukin (IL)-4 and IL-5. In addition, L. paracasei was shown in laboratory studies to induce IL-12 and inhibit IL-4. IL-12 is associated with Th1 activity and IL-4 with Th2; Lactobacillus may therefore help balance Th1/Th2 cytokine levels.

Additionally, clinical studies indicate that the presence of Bifidobacterium longum and certain Prevotella species during pregnancy may influence certain qualities related to the development of food allergies during childhood. The administration of probiotics such as Lactobacillus rhamosus has been correlated with a higher level of achieved tolerance to non-IgE cow’s milk allergy in some infant studies. Improvements in colic and symptoms related to skin or food allergies were observed in children following the administration of Lactobacillus reuteri. In adult populations, decreases in eczema severity have been observed following the administration of certain probiotic strains.

More research is needed, particularly in the clinical setting with larger treatment populations and with more varied microbiome considerations. However, research indicates a link between gut microbial health and a healthy response to certain allergens. Evidence also suggests that certain microbiome therapeutics may help support aspects of immune health.

By Cory Ambrose, ND, MAT

07/20/2025

Rusting On The Inside: How Sulforaphane Combats Oxidative Stress

img
David Roberts
Jul 07, 2025
3 min read
Sulforaphane and Reactive Oxygen Species (ROS): What Biohackers Need to Know

If you’re interested in optimizing cellular health, you’ve probably heard about sulforaphane—the potent phytochemical found in broccoli sprouts. But how exactly does sulforaphane interact with reactive oxygen species (ROS), and why does this matter for your health and longevity? Let’s break it down.

What Are ROS and Why Should You Care?

Reactive oxygen species (ROS) are highly reactive molecules produced as natural byproducts of cellular metabolism. At low to moderate levels, ROS play essential roles in cell signaling and immune defense. However, excessive ROS can damage DNA, proteins, and cell membranes - a process called oxidative stress - which accelerates aging and contributes to chronic diseases like cancer, neurodegeneration, and cardiovascular disease.



Sulforaphane: A Master Regulator of Redox Balance

1. Activating the Body’s Antioxidant Defenses
Sulforaphane is best known for activating the Nrf2 pathway, a genetic “switch” that ramps up your cells’ own antioxidant and detoxification systems. When sulforaphane enters the cell, it modifies the KEAP1 protein, releasing Nrf2. Nrf2 then moves to the nucleus and triggers the expression of dozens of antioxidant genes, including those that produce glutathione and other ROS-neutralizing enzymes.

2. Direct ROS Scavenging
Sulforaphane itself can directly neutralize certain ROS through hydrogen atom transfer and other chemical mechanisms, providing immediate protection against oxidative insults.



Dual Role: Friend and Foe to Cancer Cells

Rusting On The Inside: How Sulforaphane Combats Oxidative Stress

img
David Roberts
Jul 07, 2025
3 min read
Sulforaphane and Reactive Oxygen Species (ROS): What Biohackers Need to Know

If you’re interested in optimizing cellular health, you’ve probably heard about sulforaphane—the potent phytochemical found in broccoli sprouts. But how exactly does sulforaphane interact with reactive oxygen species (ROS), and why does this matter for your health and longevity? Let’s break it down.

What Are ROS and Why Should You Care?

Reactive oxygen species (ROS) are highly reactive molecules produced as natural byproducts of cellular metabolism. At low to moderate levels, ROS play essential roles in cell signaling and immune defense. However, excessive ROS can damage DNA, proteins, and cell membranes - a process called oxidative stress - which accelerates aging and contributes to chronic diseases like cancer, neurodegeneration, and cardiovascular disease.



Sulforaphane: A Master Regulator of Redox Balance

1. Activating the Body’s Antioxidant Defenses
Sulforaphane is best known for activating the Nrf2 pathway, a genetic “switch” that ramps up your cells’ own antioxidant and detoxification systems. When sulforaphane enters the cell, it modifies the KEAP1 protein, releasing Nrf2. Nrf2 then moves to the nucleus and triggers the expression of dozens of antioxidant genes, including those that produce glutathione and other ROS-neutralizing enzymes.

2. Direct ROS Scavenging
Sulforaphane itself can directly neutralize certain ROS through hydrogen atom transfer and other chemical mechanisms, providing immediate protection against oxidative insults.



Dual Role: Friend and Foe to Cancer Cells

In normal cells, sulforaphane’s activation of Nrf2 helps maintain redox homeostasis and shields against oxidative damage. However, in cancer cells, sulforaphane can have the opposite effect:

- At higher concentrations, sulforaphane increases ROS production in cancer cells, overwhelming their defenses and triggering apoptosis (programmed cell death).
- This selective pro-oxidant effect is one reason sulforaphane is being explored as a cancer therapy, as it can push cancer cells past their oxidative threshold while protecting normal cells.


Key Takeaways for Biohackers

- Sulforaphane reduces oxidative stress in healthy cells by both directly scavenging ROS and boosting your body’s own antioxidant defenses through Nrf2 activation.
- In cancer cells, sulforaphane can induce ROS to levels that cause cell death, making it a promising compound for cancer prevention and therapy.
- Maintaining optimal redox balance with sulforaphane may support longevity, protect against chronic disease, and enhance cellular resilience.


References

Dinkova-Kostova, A. T., & Talalay, P. (2008). Direct and indirect antioxidant properties of inducers of cytoprotective proteins. Molecular Nutrition & Food Research, 52(S1), S128–S138.
https://pubmed.ncbi.nlm.nih.gov/18327872/
Zhang, Y., Talalay, P., Cho, C. G., & Posner, G. H. (1992). A major inducer of anticarcinogenic protective enzymes from broccoli: isolation and elucidation of structure. Proceedings of the National Academy of Sciences, 89(6), 2399–2403.
https://www.pnas.org/doi/10.1073/pnas.89.6.2399
Myzak, M. C., & Ho, E. (2006). Sulforaphane and its effects on cancer, inflammation, and oxidative stress. Current Opinion in Clinical Nutrition and Metabolic Care, 9(6), 679–685.
https://pubmed.ncbi.nlm.nih.gov/17053418/
Juge, N., Mithen, R. F., & Traka, M. (2007). Molecular basis for chemoprevention by sulforaphane: a comprehensive review. Cellular and Molecular Life Sciences, 64(9), 1105–1127.
https://pubmed.ncbi.nlm.nih.gov/17396224/
Singh, S. V., et al. (2007). Sulforaphane induces cell death by ROS-dependent mechanisms in human leukemia cells. Free Radical Biology and Medicine, 43(8), 1328–1337.
https://pubmed.ncbi.nlm.nih.gov/18313257/
Tortorella, S. M., et al. (2015). The role of sulforaphane in cancer chemoprevention and health benefits: A mini-review. Journal of Cancer Prevention, 20(1), 1–7.
https://pmc.ncbi.nlm.nih.gov/articles/PMC5842175/
Yagish*ta, Y., et al. (2014). Nrf2 enhances resistance to oxidative and electrophilic stress by upregulating multiple antioxidant and detoxification enzymes. Antioxidants & Redox Signaling, 21(3), 423–436.
https://pubmed.ncbi.nlm.nih.gov/24483320/
Greco, V., et al. (2008). Sulforaphane induces apoptosis in human cancer cells through the ERK1/2 pathway. Cancer Letters, 269(2), 305–314.
https://pubmed.ncbi.nlm.nih.gov/18455346/
Angeloni, C., et al. (2012). Sulforaphane induces Nrf2 and protects against oxidative stress in human granulosa cells. Journal of Cellular Physiology, 227(2), 775–782.
https://pmc.ncbi.nlm.nih.gov/articles/PMC8665974/
Dinkova-Kostova, A. T., et al. (2015). The role of Keap1–Nrf2 pathway in protection against oxidative stress. Free Radical Biology and Medicine, 88, 284–295.
https://pmc.ncbi.nlm.nih.gov/articles/PMC9774434/

Bottom line: Sulforaphane is a powerful tool for anyone interested in fighting oxidative stress, supporting longevity, and even targeting cancer cells - thanks to its sophisticated, dual action on ROS.

In normal cells, sulforaphane’s activation of Nrf2 helps maintain redox homeostasis and shields against oxidative damage. However, in cancer cells, sulforaphane can have the opposite effect:

- At higher concentrations, sulforaphane increases ROS production in cancer cells, overwhelming their defenses and triggering apoptosis (programmed cell death).
- This selective pro-oxidant effect is one reason sulforaphane is being explored as a cancer therapy, as it can push cancer cells past their oxidative threshold while protecting normal cells.


Key Takeaways for Biohackers

- Sulforaphane reduces oxidative stress in healthy cells by both directly scavenging ROS and boosting your body’s own antioxidant defenses through Nrf2 activation.
- In cancer cells, sulforaphane can induce ROS to levels that cause cell death, making it a promising compound for cancer prevention and therapy.
- Maintaining optimal redox balance with sulforaphane may support longevity, protect against chronic disease, and enhance cellular resilience.


References

Dinkova-Kostova, A. T., & Talalay, P. (2008). Direct and indirect antioxidant properties of inducers of cytoprotective proteins. Molecular Nutrition & Food Research, 52(S1), S128–S138.
https://pubmed.ncbi.nlm.nih.gov/18327872/
Zhang, Y., Talalay, P., Cho, C. G., & Posner, G. H. (1992). A major inducer of anticarcinogenic protective enzymes from broccoli: isolation and elucidation of structure. Proceedings of the National Academy of Sciences, 89(6), 2399–2403.
https://www.pnas.org/doi/10.1073/pnas.89.6.2399
Myzak, M. C., & Ho, E. (2006). Sulforaphane and its effects on cancer, inflammation, and oxidative stress. Current Opinion in Clinical Nutrition and Metabolic Care, 9(6), 679–685.
https://pubmed.ncbi.nlm.nih.gov/17053418/
Juge, N., Mithen, R. F., & Traka, M. (2007). Molecular basis for chemoprevention by sulforaphane: a comprehensive review. Cellular and Molecular Life Sciences, 64(9), 1105–1127.
https://pubmed.ncbi.nlm.nih.gov/17396224/
Singh, S. V., et al. (2007). Sulforaphane induces cell death by ROS-dependent mechanisms in human leukemia cells. Free Radical Biology and Medicine, 43(8), 1328–1337.
https://pubmed.ncbi.nlm.nih.gov/18313257/
Tortorella, S. M., et al. (2015). The role of sulforaphane in cancer chemoprevention and health benefits: A mini-review. Journal of Cancer Prevention, 20(1), 1–7.
https://pmc.ncbi.nlm.nih.gov/articles/PMC5842175/
Yagish*ta, Y., et al. (2014). Nrf2 enhances resistance to oxidative and electrophilic stress by upregulating multiple antioxidant and detoxification enzymes. Antioxidants & Redox Signaling, 21(3), 423–436.
https://pubmed.ncbi.nlm.nih.gov/24483320/
Greco, V., et al. (2008). Sulforaphane induces apoptosis in human cancer cells through the ERK1/2 pathway. Cancer Letters, 269(2), 305–314.
https://pubmed.ncbi.nlm.nih.gov/18455346/
Angeloni, C., et al. (2012). Sulforaphane induces Nrf2 and protects against oxidative stress in human granulosa cells. Journal of Cellular Physiology, 227(2), 775–782.
https://pmc.ncbi.nlm.nih.gov/articles/PMC8665974/
Dinkova-Kostova, A. T., et al. (2015). The role of Keap1–Nrf2 pathway in protection against oxidative stress. Free Radical Biology and Medicine, 88, 284–295.
https://pmc.ncbi.nlm.nih.gov/articles/PMC9774434/

Bottom line: Sulforaphane is a powerful tool for anyone interested in fighting oxidative stress, supporting longevity, and even targeting cancer cells - thanks to its sophisticated, dual action on ROS.

Stop by our store in downtown Casper Tuesday through Saturday. We’re happy to give you a free sample while they last. !!!!