Creatine is best known as a muscle supplement, but a new study examined whether it can also support immune cells involved in cancer defense. The researchers focused on dendritic cells, a type of immune cell that helps alert the immune system by presenting antigen fragments from viruses, bacteria, and tumors to T cells, which can then mount responses against infected or abnormal cells.

The work combined cell experiments with an animal tumor model. In mouse dendritic cells, the researchers tested whether the ability to take up creatine affected cell survival, immune signaling, and the activation of T cells. They did this by comparing cells with and without the protein that transports creatine into cells, and by examining how the cells responded to additional creatine. Human dendritic cells made from blood samples from healthy donors were then used to see whether creatine could produce similar immune-supporting effects in human cells. Finally, mice implanted with melanoma cells received creatine injections to determine whether these cellular changes were accompanied by differences in tumor growth and immune activity within tumors.

• Mouse dendritic cells grown in the lab increased activity of the gene for the creatine transporter after immune stimulation, and dendritic cells taken from tumors also showed high activity of that gene.
• Mouse dendritic cells without the creatine transporter were less likely to survive, produced fewer inflammatory signals, showed weaker immune-alert markers, and had lower ATP, the molecule cells use as a direct energy source.
• Creatine-treated dendritic cells survived better, showed stronger immune-alert markers, turned on more inflammatory-response genes, and had higher levels of ATP.
  
• Human dendritic cells treated with creatine turned on more genes for inflammatory immune signals and were better able to activate T cells engineered to recognize a tumor antigen.
• In the melanoma model, creatine-treated mice had slower tumor growth, and dendritic cells inside the tumors showed stronger signs of immune activity, especially in a subtype that helps present tumor material to T cells.

The results suggest that creatine may help supply the energy needed for dendritic cell activation. Once inside cells, creatine can be converted into phosphocreatine, a stored form of energy support that helps maintain ATP availability. That extra energy support may help dendritic cells send inflammatory signals, display tumor material more effectively, and activate T cells.

Because the study was only conducted in cells and mice, it does not show whether creatine would have the same effects in human cancer patients. If confirmed in clinical trials, creatine could become a simple and inexpensive way to support immunotherapy strategies for cancer treatment. In episode #100, Dr. Darren Candow breaks down the optimal creatine protocol for supporting strength, brain health, and longevity.

Alzheimer's disease gradually erodes memory, language, and independence, leaving few treatment options once the condition becomes severe. Researchers explored whether psilocybin, a naturally occurring psychedelic compound in certain mushrooms, could affect abilities that had been severely impaired for years.

The case report focused on one Japanese-American woman in her 80s with a clinical diagnosis of advanced Alzheimer's disease and about 10 years of progressive decline. For about five years before the intervention, she had mostly one-word replies, long-term loss of bladder control, difficulty walking without help, swallowing problems, flat emotional expression, and high dependence in daily activities. She received a supervised 5-gram oral dose of psilocybin-containing mushrooms, followed one month later by a supervised 3-gram session. Changes in her condition were described through clinical observations rather than formal cognitive tests, brain scans, lab measures, or sleep monitoring.

• Speech improved in a striking way. After years of mostly one-word replies, the woman began talking spontaneously about her past roughly 19 hours after the first dose. This period of autobiographical conversation lasted about four hours.
• After years of chronic incontinence, bladder control returned within days of the first session and persisted for at least one month.
• In the week following the session, she also became more alert, recognized family members, was able to walk without assistance, dressed herself, showed more initiative, and engaged more socially through eye contact, smiling, and responses that showed awareness of people, surroundings, and social context.
• After the second psilocybin session, the woman was described as more verbally expressive, emotionally responsive, humorous, and agile while walking.
• The first session also came with some short-term safety concerns. In the first 12 hours, she experienced suspected overheating, heavy sweating, and a prolonged sleep-like state. However, no severe lasting complications were reported.

Psilocybin is converted in the body to psilocin, which activates serotonin receptors in the brain. That activation can make brain activity less locked into its usual patterns, allowing networks involved in memory, attention, emotion, and self-awareness to interact in less rigid ways. At the cellular level, psychedelics can also trigger plasticity-related programs that help neurons remodel connections between nerve cells. In advanced Alzheimer's disease, these effects would not rebuild lost brain tissue or remove the underlying disease process. A more plausible explanation is that psilocybin may temporarily alter access to still-surviving circuits that were no longer being used effectively.

This was a single uncontrolled case, so it cannot prove efficacy or safety of psilocybin for people with Alzheimer's disease. However, the observations raise the possibility that psilocybin may temporarily restore access to some abilities that appear lost in advanced dementia. In episode #30, the late Dr. Roland Griffiths discusses the effects of psilocybin on the human brain.

Melatonin is best known for regulating sleep timing, but it also has strong antioxidant properties that may support DNA repair. Since night shift work can suppress normal melatonin secretion and has been linked to lower repair of oxidative DNA damage, researchers tested whether taking melatonin before daytime sleep could improve a DNA repair marker.

The 4-week study included 40 night shift workers who were randomly assigned to take either 3 milligrams of melatonin or a placebo 1 hour before daytime sleep following a night shift. Urine was sampled after daytime sleep and during the following night shift, both before and near the end of the supplementation period. The researchers then measured two urine markers: a melatonin marker to confirm that the supplement raised melatonin levels, and 8-OH-dG, which they interpreted as a marker of oxidative DNA damage repair and cleanup. Sleep was tracked with a wrist-worn activity monitor, and participants rated how sleepy they felt during work.

• The supplement group had much higher levels of the melatonin marker in urine collected after daytime sleep (90.8 vs. 1.5 ng/mg) than the placebo group, but that difference had largely narrowed by the next night shift (3.3 vs. 1.3 ng/mg).
• Melatonin raised 8-OH-dG during daytime sleep by about 80% compared with placebo, but it fell just short of the study's threshold for a statistically clear result. During the following work period, 8-OH-dG showed no increase compared with placebo.
• When participants whose melatonin marker levels were low despite supplementation were excluded from the analysis, the daytime 8-OH-dG signal became stronger and reached statistical significance.
• Melatonin did not clearly improve sleep, making it less likely that the DNA repair signal was only a byproduct of better sleep.

Night shift work has been linked to higher cancer risk, and one proposed reason is that working at night can suppress or mistime the secretion of melatonin, a hormone that helps regulate the sleep-wake cycle and is involved in antioxidant defense. Oxidative stress can damage DNA and produce lesions such as 8-OH-dG. One way cells handle this lesion is to recognize the damaged piece, cut it out, and clear the removed material into urine. Melatonin could influence this pathway at two distinct points: upstream, by neutralizing reactive oxygen species and stimulating antioxidant enzymes, and downstream, by turning up genes in a DNA repair pathway that helps remove 8-OH-dG after it has formed. That is why higher urinary 8-OH-dG in this trial was interpreted as a sign of increased repair and cleanup of oxidative DNA damage.

The main limitation is that this was a small, short trial that focused on a single biomarker, so it cannot show whether melatonin improves long-term health in night shift workers. If larger, longer trials confirm the observed signal, melatonin could become a targeted way to support DNA damage cleanup in shift workers. In Q&A #54, I discuss melatonin's antioxidant properties and whether it has therapeutic potential beyond its role in promoting sleep.