Wacky Hacky CBG

09/30/2026

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09/30/2026

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09/30/2026

⚠️ BREAKING: Ma*****na rescheduling has been halted.

A DEA administrative law judge has stayed the rescheduling proceeding for two weeks and ordered new briefing after a Government Accountability Office report on how federal agencies schedule drugs.

The entire rescheduling rests on HHS's "two-part test," which was created only after ma*****na failed DEA's long-standing five-part test. Now FDA has told GAO the two-part test "has not replaced other methods" and is only "an additional framework."

GAO also found:
• DEA has no policies or procedures for how its staff evaluate or schedule substances.
• FDA has no definition of "potential for abuse," the central question in every scheduling decision.
• The agreement governing how FDA consults NIDA on scheduling is more than 40 years old.

"An entire rescheduling was built on a shortcut its own authors call optional. That is not science. It is improvisation with a lab coat on, and the stakes are every kid in America." Dr. Kevin Sabet, President of SAM

Read the full release: https://learnaboutsam.org/2026/09/marijuana-rescheduling-proceeding-halted-after-federal-watchdog-report/

More reading: https://thedrugreport.org/2026/09/29/marijuana-rescheduling-paused-gao-report/

09/30/2026

09/30/2026

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09/30/2026

🧠 C*D & CBG May Protect Brain Cells Through a Newly Identified Target

For Educational Purposes Only. Not Medical Advice, Sales, or Encouragement of Substance Use.

A new 2026 study provides another clue to how C*D and CBG may protect neurons from mitochondrial damage.

Researchers exposed brain cells to rotenone, a chemical that damages mitochondria and increases oxidative stress.

What happened?

C*D and CBG helped protect the neurons.

But when researchers blocked the sigma-1 receptor (σ1R), that protection disappeared.

This suggests the sigma-1 receptor plays an important role in how C*D and CBG protect stressed brain cells.

Why is sigma-1 important?

The sigma-1 receptor helps regulate:

• Mitochondrial function
• Cellular energy
• Calcium balance
• Oxidative stress
• Cell survival during stress

Computer modeling also showed that C*D and CBG could bind stably to the sigma-1 receptor.

Interestingly, their neutral forms showed stronger predicted binding than C*DA and CBGA, supporting previous laboratory findings that C*D and CBG were protective while their acidic forms were not.

The bigger picture

C*D and CBG are often studied through the traditional cannabinoid receptors CB1 and CB2.

This research points toward another pathway:

C*D / CBG → Sigma-1 receptor → mitochondrial protection → improved neuron survival

This could help researchers better understand the potential role of cannabinoids in conditions involving mitochondrial dysfunction, oxidative stress and neurodegeneration.

However, this was a cultured-neuron study, not a human clinical trial. It identifies a promising mechanism that now needs further animal and human research.

Source: Oviedo-Pino V. et al. ChemMedChem. Published September 24, 2026.
DOI: 10.1002/cmdc.70510

09/28/2026

09/28/2026

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