Shockwave Therapy Calgary

09/10/2025

This is the reason why NAD is a good anti-aging supplement

The Wnt–NAD+ axis in cancer, aging, and tissue regeneration

The Wnt–NAD+ axis is a fundamental regulatory hub in which metabolic state meets developmental signaling and it acts as a metabolic sensor that coordinates tissue regeneration with cellular energy status through compartment specific NAD+ pools.

Wnt signaling regulates NAD+ metabolism by controlling the expression of key biosynthetic enzymes and NAD+ consumers, while NAD+ -dependent proteins modulate Wnt activity through direct interactions and epigenetic modifications.

Sirtuins exhibit tissue-specific and subcellular compartment-dependent roles in Wnt regulation where they function as activators or suppressors depending on the cellular bioenergetic state.

The Wnt–NAD+ axis maintains stem cell function and self-renewal capacity through metabolic/signaling integration, and its disruption during aging leads to declining regenerative capacity.

The progressive dysregulation of compartment-specific Wnt–NAD+ coordination contributes to stem cell exhaustion and multiple pathological conditions, indicating that therapeutic strategies must consider tissue-specific and subcellular targeting.

https://www.cell.com/trends/cell-biology/fulltext/S0962-8924(25)00172-2
https://sciencemission.com/Wnt%E2%80%93NAD-axis-in-cancer

08/18/2025

MASLD has become the most common chronic liver disease worldwide. Giovanni Targher, MD, Luca Valenti, MD, and Christopher D. Byrne, MB, ChB, review the features of the disease as well as pharmacotherapies targeting the associated liver and cardiovascular–renal–metabolic issues.

08/18/2025

Cysteinyl leukotrienes stimulate gut absorption of food allergens to promote anaphylaxis

A drug already FDA-approved for asthma was found to nearly eliminate life-threatening allergic reactions to food allergens in mice — a breakthrough that could lead to new protection for millions of people living with food allergies, reports a new study.

The findings will be published in the journal Science.

The discovery came after the scientists identified, in mice, a previously unknown role for a gene called DPEP1, which they found is essential in regulating anaphylaxis, a rapid and potentially fatal allergic reaction.

By using the asthma drug Zileuton to block the pathway involving this gene, the scientists nearly eliminated allergic responses in mice that were previously highly susceptible to food-induced anaphylaxis. The mice were given peanut extract orally shortly after receiving Zileuton while the team monitored for symptoms.

“It was actually shocking how well Zileuton worked,” said co-senior study author.

“After treatment with Zileuton, 95% of the mice showed almost no symptoms of anaphylaxis. The treatment reversed their risk from 95% susceptible to 95% protected,” added the co-senior author.

Once the scientists found that the DPEP1 gene controlled leukotrienes in the gut — inflammatory molecules already targeted by asthma drugs — they tested Zileuton, an FDA-approved drug that blocks their production.

The authors show that reduced DPEP1 activity causes leukotriene (LTC4 and LTD4) accumulation in the gut, acting on the CysLT receptors 1 and 2 (CysLTR1 and CysLTR2).

This promotes food allergen transport through goblet cells to the submucosa and bloodstream, where IgE-loaded mast cells are activated to trigger anaphylaxis.

https://sciencemission.com/leukotrienes-stimulate-gut-absorption-of-food-allergens

08/18/2025

Nature Reviews Neuroscience: Adverse experiences in early life affect brain development across species. In this Review, the authors discuss neuroimaging evidence for how these adversity-induced changes to human brain architecture alter developmental trajectories that may underpin adult psychopathology.

Link to the Review in the comments.

08/18/2025

Keto for Alzheimers

The ketogenic diet might be the most powerful tool we have against dementia. But 90% of people do it wrong for brain health. Here's what the science shows and what I've learned from patients who've used keto to protect their brains. Your brain has two fuel sources: Glucose (from carbohydrates) Keton...

07/27/2025

Triglyceride metabolism controls Alzheimer’s associated microglial phenotypes and inflammation

Neuroinflammation is central to Alzheimer’s disease (AD) pathogenesis and microglia plays a crucial role in AD..

Lipids are known to modulate microglia but the functional significance of these metabolic changes remains poorly understood.

The researchers establish that neutral lipid accumulation is necessary for microglial activation and that microglia expressing an Alzheimer’s risk gene (APOE4) hijack triglyceride biosynthesis to acquire a basal immune activated state.

Targeting triglyceride metabolism can modulate immune reactivity and disease phenotypes. In microglia harboring the Alzheimer’s disease risk APOE4 genotype, inhibiting triglyceride biosynthesis attenuates disease-associated transcriptional states.

https://www.cell.com/cell-reports/fulltext/S2211-1247(25)00732-6
https://sciencemission.com/Triglyceride-metabolism-controls-inflammation

07/27/2025

Body temperature affects Type 2 diabetes

Body temperature regulates glucose metabolism

Researchers have known for decades that the lower body temperatures observed during hibernation go hand in hand with lower metabolism. The metabolism of glucose, a sugar commonly used to generate the energy used by cells, produces heat, and maintaining lower body temperatures conserves energy when food is scarce. What researchers haven’t established, however, is whether metabolism determines body temperature or if body temperature changes the organism’s metabolism—until now.

The conventional view in the hibernation field suggested that body temperature was controlled by the heat generated by metabolism. The direct relationship between the two couldn’t be determined, however, because there was no method to safely lower mammalian body temperature independently of any changes to the animal’s metabolism.

To address this issue, a group of researchers employed a recently developed mouse model of hibernation, known as Q-neuron-induced hypothermia and hypometabolism (QIH). This model enabled the team to safely induce hypothermia in mice and isolate the effect of body temperature on metabolism.

Remarkably, the team found that mice in the QIH state exhibited elevated fasting glucose and insulin levels in their blood, two hallmarks of insulin resistance. Insulin resistance occurs when cells do not respond appropriately to insulin and are unable to transport glucose into the cells for energy. The condition can eventually lead to type 2 diabetes.

To reverse the hypothermia, the research team simply warmed mice to normal body temperature by increasing ambient temperature. Both the insulin and glucose levels in the hypothermic mice normalized after rewarming.

“The key message is simple but powerful: lowering body temperature alone, without drugs or genetic manipulation, can reversibly induce a diabetes-like state in healthy animals. Just by rewarming, normal metabolism is rapidly restored. This demonstrates that body temperature is not a passive output, but an active regulator of systemic glucose metabolism,” said the first author of the research study.

Closer analysis of specific organs revealed that glucose metabolism in brown adipose tissue, a heat-generating organ; skeletal muscle; heart and brain were significantly lowered in hypothermic mice, which paralleled decreases in animal movement and energy consumption. Importantly, the reversal of the high glucose and insulin levels in rewarmed mice suggests that that temperature is directly affecting glucose metabolism rather than activation of Qrfp neurons.

https://sciencemission.com/Body-temperature-regulates-glucose-metabolism-9012

07/27/2025

Scientists gave mice Parkinson's through p**p. Then cured it with antibiotics. The gut-brain connection is more powerful than we imagined. This study changed everything I thought I knew about Parkinson's disease. Caltech researchers made a stunning discovery. Mice genetically predisposed to Parkinso...

07/14/2025

Reduction in amino acid cysteine triggers weight loss

Consuming fewer calories is largely accepted as a way to improve health and lose weight, but a recently published study in Nature Metabolism points to a specific sulfur-containing amino acid cysteine as a key component in weight loss.

The researchers discovered that when study participants restricted their calorie intake, it resulted in reduced levels of cysteine in white fat.

The researchers contributed to the study in which they examined cysteine and discovered that it triggered the transition of white fat cells to brown fat cells, which are a more active form of fat cells that burn energy to produce heat and maintain body temperature.

When researchers restricted cysteine in animal models entirely, it drove high levels of weight loss and increased fat burning and browning of fat cells, further demonstrating cysteine’s importance in metabolism.

“In addition to the dramatic weight loss and increase in fat burning resulting from the removal of cysteine, the amino acid is also central to redox balance and redox pathways in biology,” said one of the author’s in the study. “These results suggest future weight management strategies that might not rely exclusively on reducing caloric intake.”

https://sciencemission.com/cysteine-triggers-weight-loss

06/17/2025

New research reveals that people can consciously remove specific information from their memories by dampening the brain circuits that initially stored it.

06/17/2025

Iron in s*x determination of mammalian embryos

The Y chromosome-located mammalian s*x-determining gene Sry, required for the formation of te**is, is activated only within a narrow time window during embryogenesis. However, the processes behind the activation of Sry remain uncertain.

Now, in a recent publication from Nature, a research team has discovered that iron plays a crucial role in male mammalian s*x development.

The Sry gene directs s*xually undifferentiated go**ds to differentiate into te**es rather than ovaries. The Sry gene is initially inactive because of a modification added to DNA-wrapping proteins called histone methylation. In males, a protein called KDM3A is responsible for removing this histone methylation, allowing the Sry gene to become active.

The researchers established mice lacking Tfrc, a gene crucial for cellular iron incorporation. Loss of Tfrc prevented the removal of the histone methylation, leading to reduced Sry expression. When inspecting the ge****ls of these mice, it was found that some XY mice developed as female, despite being genetically male.

The team also established an organ culture system for gonadal cells in which they could manipulate the levels of available iron. This confirmed that iron deficiency reduces the activity of KDM3A and activation of Sry. Therefore, the reduced Sry suppression under iron-deficient conditions was caused by the failure of KDM3A to remove histone methylation.

Perhaps most significantly, they then showed that maternal iron deficiency – whether induced by diet or by pharmacological intervention – could lead to altered histone methylation of the Sry gene because of reduced KDM3A activity. Some population of XY offspring derived from iron-deficient pregnant females were shown to undergo male-to-female s*x reversal, potentially due to the impaired Sry activation.

https://sciencemission.com/Iron-in-s*x-determination

06/02/2025

New research from the USA

New research affirms the national value of chiropractic care. A 2025 study published in the Journal of General Internal Medicine found that with low back pain who received care were 23% less likely to receive an opioid prescription within one year, compared to those who did n...