rewrite this title Could Vitamin B12 Protect Your Pancreatic Cells?

• Genetic analyses show benefits of vitamin B12 — By studying natural genetic variations linked to vitamin B12 levels, the researchers determined that people genetically predisposed to higher levels of vitamin B12 were significantly less likely to develop acute pancreatitis. This was apparent after accounting for factors like lifestyle or diet that usually complicate observational studies.

• Animal models support human analyses — The researchers specifically targeted acinar cells, the pancreatic cells responsible for secreting digestive enzymes, which become severely damaged during acute pancreatitis.

For their experiment, the team used genetically modified mice lacking the transcobalamin receptor for vitamin B12, which helps regulate vitamin B12 uptake. Without the receptor, cells could no longer absorb and utilize B12 efficiently, replicating conditions similar to deficiency in humans.

• Supplemental vitamin B12 produced immediate results — Within a few hours of B12 administration, mice showed substantially reduced pancreatic injury. The levels of digestive enzymes such as amylase, which skyrocket during severe pancreatitis, dropped quickly back toward normal.

• B12 effectively halted the progression of cellular destruction — Under a microscope, pancreatic tissues treated with B12 showed remarkably preserved cellular structure. The destructive cellular breakdown known as necrosis is dramatically reduced:

“Based on our findings, ATP supplementation did not significantly increase the level of inflammation but effectively prevent cell necrosis during the progresses of induced acute pancreatitis in both VB12 uptake deficiency mice and wild‐type mice. Thus, VB12 restores the pancreatic structures and protects the acinar cells in the early phase of pancreatitis in mouse models via the ATP production pathway.”1

• Timing is a significant factor — Administering vitamin B12 at the onset of inflammation provided the greatest benefit, rapidly halting or even reversing early cellular damage. However, even delayed treatment still slowed the destructive processes.

• Certain groups will benefit the most from increased vitamin B12 — The researchers noted individuals who are genetically predisposed to absorbing less vitamin B12 or who have limited dietary intake are likely to see the most pronounced improvements. Because these populations typically start with lower baseline B12 levels, supplementation provides a critical boost exactly when cellular demands peak during acute pancreatitis episodes.

• How vitamin B12 protects your pancreatic cells at the molecular level — Central to the protective benefits of vitamin B12 is adenosine triphosphate (ATP), the primary energy powering every cell in your body. When pancreatitis strikes, ATP production plummets, leaving cells starved of the energy required to maintain structural integrity and normal function.

Vitamin B12 rapidly reversed this issue by replenishing ATP levels through enhancing mitochondrial energy pathways, specifically converting methylmalonyl-CoA to succinyl-CoA, a critical step that revitalizes energy production.

This restoration of ATP is essential because maintaining healthy ATP levels directly prevents pancreatic enzymes from prematurely activating inside the cells, which, as mentioned earlier, is a key event that triggers the destructive cascade of acute pancreatitis. Without adequate ATP, pancreatic cells weaken and collapse, digestive enzymes escape prematurely, and the pancreas essentially begins digesting itself.

By ensuring rapid ATP replenishment, vitamin B12 stabilizes cell membranes and maintains intracellular integrity, keeping destructive enzymes safely contained within their proper compartments.

• Vitamin B12 works straight toward the pancreas — The researchers ruled out indirect metabolic pathways commonly associated with B12, such as the regulation of homocysteine levels. Instead, their experiments confirmed a direct mitochondrial mechanism:

“[R]esults indicate that folate and homocysteine are not associated with acute pancreatitis in humans, excluding the possibility that VB12 displays a protective role in the progress of acute pancreatitis via homocysteine or folate pathway. Most likely, VB12 restores the pancreatic structures and protects the acinar cells in the early phase of pancreatitis in mouse models via succinyl‐CoA‐based energy metabolism involved in ATP production.”

• Dramatic improvement in overall pancreatic health occurred — Researchers saw clear reductions in oxidative stress markers that accumulate rapidly in pancreatitis:

“As expected, VB 12 suppressed the increase in intracellular ROS caused by NaT treatment in a dose-dependent manner. Various transcription factors in the antioxidant system are regulated by Nrf2 to maintain the redox homeostasis of cells and protect cells from oxidative damage. Western blot analysis showed that VB 12 inhibited the decrease of Nrf2 expression in acinar cells exposed to NaT.

Similarly, p-P38, a marker of oxidative stress, increased in the NaT treatment group, while VB 12 inhibited its expression. These results indicate that the occurrence of oxidative stress in acute pancreatitis may be due to the lack of CBS and could be improved by VB 12.”3

• Vitamin B12 promotes better mitochondrial function — Normally, acute pancreatitis severely damages mitochondria, causing energy production to plummet. However, vitamin B12 administration quickly improved mitochondrial health, stabilizing energy output and ensuring that the pancreas had the fuel needed to repair itself. This improvement in mitochondrial function was seen within 24 hours after treatment:

“[W]e presume that VB 12 could improve mitochondrial impairment related to CBS deficiency in acinar cells … Parkin, the main regulator of mitochondrial autophagy, was significantly reduced, and the expression of autophagy-related protein LC3II and autophagy adaptor protein P62 was increased after NaT loading, while VB 12 treatment increased the expression of Parkin and decreases the levels of LC3II and P62.

These results confirm our conjecture that VB 12 may repair mitochondrial function by promoting mitophagy.”

• Timing matters — Similar to the MedComm study, the researchers observed the most substantial benefits in animals that received early and higher doses of vitamin B12. Administering B12 at the onset of acute inflammation resulted in the most effective reduction of cellular damage. But even at later stages, supplementation continued to deliver notable improvements.

• Vitamin B12 exerts its protective effects by activating the CBS/SIRT1 pathway — CBS (cystathionine-β-synthase) is an enzyme that regulates your body’s antioxidant defenses by influencing glutathione levels:

“CBS regulates homocysteine metabolism and contributes to GSH (glutathione) biosynthesis through which it plays multifunctional roles in the regulation of cellular energetics, redox status, DNA methylation, and protein modification. Clinically, patients with untreated CBS deficiency suffer from various diseases, including hyperhomocysteinemia, thrombosis, osteoporosis, and mental retardation.”4

• Vitamin B12 significantly increased CBS activity — By doing so, it boosted glutathione production, enhancing your cells’ ability to neutralize oxidative stress effectively, which means your pancreas is better equipped to handle inflammation and repair damaged tissues.

Simultaneously, vitamin B12 enhanced the activity of SIRT1, which improved the cells’ ability to recover from oxidative damage by initiating repair mechanisms within mitochondria, helping damaged mitochondria recover their normal function.

• SIRT1 is vital for cell survival and longevity — In relation to the finding above, blocking SIRT1 activity erased most of the beneficial effects of B12, further proving that this specific biochemical pathway is essential.

When the CBS/SIRT1 pathway was disrupted experimentally, the protective effects of vitamin B12 nearly vanished, underscoring how important these enzymes are in B12’s protective mechanism. Thus, it’s clear that optimizing CBS and SIRT1 functions through vitamin B12 supplementation supports your pancreas when inflammation and cellular stress strike.

1. Test your levels first — If you’ve over 50 years old or feel unwell, ask your doctor for a vitamin B12 test. Regular blood checks every six to 12 months will also allow you for early intervention to maintain optimal vitamin B12 levels.

2. Increase your vitamin B12 intake — Start boosting your intake of vitamin B12-rich foods like grass fed beef liver, pastured eggs, and wild-caught sardines. Consider taking supplemental B12 as well to ensure you’re getting enough to stabilize your mitochondria and rapidly reduce inflammation.

Oral supplementation is generally effective for mild to moderate deficiency, with dosages ranging from 1,000 to 2,000 micrograms daily. Intramuscular injections, typically administered monthly, are more suitable for patients with severe deficiency or those with malabsorption issues.

3. Use dimethyl sulfoxide (DMSO) — Aside from B12, dimethyl sulfoxide (DMSO) dramatically enhances your antioxidant defenses, helping neutralize oxidative stress quickly for pancreatitis. DMSO improves cellular oxygenation and helps deliver antioxidants right where your pancreas needs them most, rapidly restoring tissue health and energy balance.

In one study, researchers conducted a double-blind trial involving 78 patients with chronic recurring pancreatitis. From that population, 26 of them received a rectal administration of 10% DMSO; at least 57% of this subset were free from pain after 12 hours compared to 17% of the control group. By 24 hours, all were pain-free. All DMSO subjects were discharged after three days, while 22% of the control group were discharged after five days of hospitalization.5

4. Minimize your linoleic acid (LA) intake — If your diet includes foods high in LA, you’re adding fuel to the inflammatory fire in your pancreas. Thus, removing these damaging oils helps stop inflammation at its source, reducing oxidative stress and allowing your mitochondria to recover quickly.

I recommend minimizing your LA intake below 5 grams, but if you can get it to below 2 grams, that’s even better. To help you achieve this goal, be sure to download my Mercola Health Coach app — the beta version will be released on the first week of June, while the full version is coming in July. It contains a useful feature called the Seed Oil Sleuth, which will track your LA intake to a tenth of a gram.

5. Start exercising — Another useful adjunct to managing pancreatic health is getting regular exercise. In a study published in PLoS One, researchers noted that people with higher leisure screen time (LST) have an increased risk of pancreatitis because they usually have unhealthy eating habits that lead to gallstones, which commonly trigger acute pancreatitis.6

That said, I recommend you start going for a walk, as it’s one of the best exercises you can do for your health. In my interview with Dr. James O’Keefe, he noted that your risk of mortality decreases by 10% to 15% for every 1,000 steps you take. More importantly, he noted that it also helps your all-cause survival rate two times better than vigorous exercise. For an in-depth discussion on this topic, read “The Benefits of Walking — How to Get More Steps in This Summer.”