From Gut to Bone: A Crohn’s Disease Woman’s Bone Density Warning

This is the story of a 70-year-old woman who has been living with Crohn’s disease for more than two decades. She stands 158 cm tall and weighs 46.7 kg. After multiple surgeries and years of treatment, her intestinal inflammation finally stabilized. Yet, her recent bone density report has triggered a new health alarm.

As shown in the two images above, the lumbar spine (L1–L3) reading has dropped into the bright red osteoporosis zone, while the right femur total bone density curve has declined significantly in recent years — indicating a gradual increase in her risk of fracture.

In this case study, we’ll take a clear and simple look at her bone density results and explore the nutritionist’s perspective on targeted interventions — from dietary structure and calcium–magnesium–vitamin support to anti-inflammatory nutrition and lifestyle habits — showing how to rebuild the “energy highway” that runs from gut to bone.

• Why are people with Crohn’s disease more prone to osteoporosis?
• How can calcium and vitamin D be absorbed effectively — and reach the bones where they’re needed most?

Why Can Crohn’s Disease “Eat Away” the Bones? (Pathophysiology)

① What is Crohn’s disease and where does it attack?

Crohn’s disease is a form of chronic immune-mediated intestinal inflammation. In simple terms, the immune system “misidentifies” the intestinal wall as an enemy and mounts a long-term attack. Inflammation, ulcers, wall thickening, and scarring gradually damage both the structure and function of the gut.

Unlike a typical “stomach bug,” Crohn’s is not a brief infection but a long, internal war. It can affect anywhere from the mouth to the anus, but the most commonly involved areas are the terminal ileum (the last segment of the small intestine) and the beginning of the colon. Unfortunately, these two regions are also the body’s most important nutrient absorption hubs.

② Bones aren’t stone—they’re a “living factory”

Many people think bones are “dead,” but they are rebuilt every day. Bone cells continuously tear down old tissue and lay down new tissue—like a factory running around the clock. To keep bones strong, the body needs a steady flow of “construction materials”:

So when the small intestine’s “absorption factory” is burned by inflammation and the transport routes are blocked, the bones can’t get their raw materials—the worksite stalls before funding reaches the crew.

③ Fat-soluble nutrients need to “hitch a ride” with bile

Fat-soluble nutrients like vitamins A, D, E, and K need dietary fat to guide them. When we eat, bile released from the liver and gallbladder acts like detergent to emulsify fat— breaking large fat droplets into tiny particles so vitamins can mix in. Then bile salts package them into small transport spheres called micelles, which deliver nutrients into intestinal cells; they are then packed into chylomicrons and sent through the lymph into circulation.

After the job is done, bile acids aren’t wasted: they are reabsorbed in the terminal ileum and returned to the liver for reuse— a process called the enterohepatic circulation. It’s the body’s “bile recycling system,” ensuring each meal has enough bile to handle fats and fat-soluble vitamins.

When the ileum is damaged, the “bile cycle” breaks

The terminal ileum—often targeted by Crohn’s—is exactly where bile acids are reclaimed. When this area is inflamed, ulcerated, or surgically removed, three things happen:

Diarrhoea then accelerates the loss of minerals like calcium and magnesium. In the end, the bone “purchase order” can’t check off vitamins, minerals, or energy— bone weakening begins quietly.

④ Water-soluble and mineral nutrients are affected too

Even nutrients that don’t rely on fat for absorption—such as calcium, magnesium, iron, and vitamin B12—are not spared. Each is absorbed in specific segments of the small intestine:

When inflammation spreads or segments are resected, these “stations” are taken offline one by one: iron isn’t absorbed, calcium and magnesium are lost, and B12 supply is cut— the skeleton lacks both “bricks” and the energetic capacity to build.

⑤ Dysbiosis: adding insult to injury

A healthy gut microbiome produces vitamin K2 and short-chain fatty acids (such as butyrate), which help lock calcium into bone, repair the gut lining, and calm inflammation. In Crohn’s, chronic inflammation and medications reshape the microbiome, leading to:

From gut to bone: a clear “energy supply chain” failure

Crohn’s disease → ileal inflammation/resection → failed bile acid recycling → poor absorption of fat-soluble vitamins → vitamin D & K deficiency → calcium–magnesium loss + dysbiosis + inflammatory bone resorption → declining bone density and osteoporosis.

Therefore, recovery from Crohn’s isn’t only about “stopping diarrhea and controlling inflammation”— it must also restore the absorption system so the body can truly eat, absorb, and utilise nutrients. Only then can bones regain their strength.

Key Nutrient Gaps: Why Calcium Alone Doesn’t Work

Many people with Crohn’s see “low bone density” and their first reaction is—“I’ll just take more calcium.” The truth is: taking calcium alone is like pouring water into a bottomless bucket. If the body can’t absorb and utilize these nutrients, extra calcium tablets will simply “pass by.”

① Vitamin D: Calcium’s carrier—the first hurdle of fat-soluble absorption

Vitamin D’s job is to move calcium from the gut into the bloodstream. In Crohn’s disease, this step often gets stuck at the very beginning. Because vitamin D is a fat-soluble nutrient, it must be absorbed together with emulsified dietary fat. When bile acid recycling in the terminal ileum is impaired, vitamin D absorption drops sharply.

The result: even if you take calcium daily, it can’t enter the blood efficiently. Low serum calcium → elevated parathyroid hormone → calcium is “borrowed” from bone to correct blood levels. Over time, bones are gradually depleted.

② Vitamin K2: Calcium’s “navigator”—decides bone vs. blood vessel

If vitamin D gets calcium onto the truck, vitamin K2 is the GPS. It activates osteocalcin, a protein that helps calcium deposit precisely into bone. In Crohn’s, fat malabsorption and dysbiosis often mean low K2, so calcium gets “lost”—ending up in vessel walls and soft tissues instead of bones.

③ Magnesium: Calcium’s “balancer”—diarrhoea drains it fastest

Magnesium is a key part of bone and also required to activate vitamin D. Chronic diarrhoea causes substantial magnesium loss from the intestine; without magnesium, vitamin D can’t convert to its active form, so calcium is neither absorbed well nor effectively utilised.

Magnesium deficiency can also trigger muscle cramps and poor sleep— a common but overlooked issue for many with Crohn’s.

④ Protein & Iron: the “foundation” and the “oxygen” for bone

Bone’s basic framework is made of collagen. With inadequate protein intake, bone is like a concrete building without rebar. Iron supports heamoglobin to deliver oxygen, keeping bone cells active. In Crohn’s, malabsorption, low appetite, and chronic blood loss make these two chronically low—slowing bone repair even further.

Therefore, Crohn’s-related osteoporosis isn’t just “calcium loss.” It’s the combined result of multiple nutrient deficiencies + malabsorption + chronic inflammation. In the next article, we’ll break down, from a nutritionist’s perspective, how to repair step by step— from diet to supplementation—so nutrients truly reach the bones.